1

INDEX

President, IMA MS DR . BAKULESH S. MEHTA (022) 26832359 / 9820131926 dr.bsmehta@yahoo.inImm. Past President, IMA MS DR. ARUN B. PAWADE (07157) 223750 / 9373240703 arunpawade@gmail.comHon. State Secretary, IMA MS Dr. HOZIE D. KAPADIA (022) 23711051 / 9833793005 hozie.kapadia@gmail.comHon. Treasurer, IMA MS DR. SHIVKUMAR S. UTTURE (022) 24305373 / 9820089321 utture@yahoo.comSr. Vice President, IMA MS DR. M. S. PATWARDHAN (0233) 2232104 / 9423036173Vice President, IMA MS DR. T. C. RATHOD (07232) 245186 / 9422168300 tcrathod@yahoo.comVice President, IMA MS DR. RAVINDRA D. JAGTAP (02166) 222998 / 9921992168 jagtaprd@yahoo.co.inVice President, IMA MS DR. ANIL SUCHAK (022) 2889148 / 9820080151 anil.suchak@gmail.comHon. Jt. Secretary, IMA MS DR. ANIL LADDHAD (0712) 2765287 / 9822565225Hon. Jt. Secretary, IMA MS Dr. SANJEEV SHARANGPANI 9422429224 drsharangpani@gmail.com

doctorsanjeev1@rediffmail.comHon. Jt. Secretary, IMA MS DR. JAYESH M. LELE (022) 28823408 / 9819812996 drjayeshlele@gmail.comChairman, IMA MS SSS DR. ANIL J. TALATHI (02143) 252261 / 9422594236 anita_talathi@yahoo.co.inHon. Secretary, IMA MS SSS DR. SHRIKANT H. KOTHARI (022) 25171198 / 25001269 / drshkothari@yahoo.co.in

9821012970Hon. Treasurer, IMA MS SSS DR. SHAILENDRA C. MEHTALIA (022) 25132114 / 9820377174 drskcmehtalia@hotmail.comDirector of Studies DR. AKIL CONTRACTOR (022) 26127481 / 9892084360 raziakil@hotmail.comIMA MS CGP FacultyHon. Secretary, DR. DILIP G. DEODHAR (020) 24334136 / 9371005036IMA MS CGP FacultyHon. Jt. Secretary, DR. VIVEK BILLAMPELLY (020) 26832658 / 9822894963 drbillampellyvivek@gmail.comIMA MS CGP FacultyChairman, IMA AMS Chapter DR. RAVI S. WANKHEDKAR (02562) 246695 /94222 96495 raviwankhedkar@gmail.comHon. Secretary, DR. MAYA TULPULE (020) 25440530 / 9923709210IMA AMS Chapter

IMA MAHARASHTRA STATE OFFICE BEARERS 2009-10

EDITORIAL ....................................................................... 3PRESIDENT’S MESSAGE .................................................... 5HON STATE SECRETARY’S MESSAGE ................................... 7DR. ABDUL KALAM’S SPEECH ........................................... 9HAEMATOLOGY TODAY .................................................. 11ELECTIONS REPORT ....................................................... 13MASTACON - 2010 ......................................................... 14EVE C0N - 2010 - DHULE ................................................ 15AUTOMATION IN HAEMATOLOGY ................................... 17BLOOD COMPONENT THERAPY ...................................... 21AUTOLOGOUS BLOOD TRANSFUSION ............................. 23TREATMENT OF VENOUS THROMBOEMBOLISM .............. 25COMMONLY ASKED QUESTIONS IN ANAEMIA ................. 29NATIONAL THALASSEMIA CONTROL PROGRAM .............. 33INVESTIGATION & MANAGEMENT OF LEUCOCYTOSIS ..... 36HAEMATOPOIETIC STEM CELL TRANSPLANTATION .......... 39MARROW DONOR REGISTRY INDIA (MDRI) .................... 4550 YEARS IN HEMATOLOGY ............................................ 47INDUSTRIAL DISASTER MANAGEMENT ........................... 52SUPER SESSION OF MCI - THE PATH AHEAD ..................... 53IMA - ACTIVITIES REPORTS ............................................. 56IMA MS SOCIAL SECURITY SCHEME ................................ 60

DISCLAIMER : Opinions expressed in the various articles are those of the authors and do not reflect the views ofIndian Medical Association Maharashtra State Branch. The appearance of advertisement in MAHIMA is not aguarantee or endorsement of the product or the claims made for the product by the manufacturer.

EDITORIAL BOARDChairman : Dr. DEEPAK K. JUMANIEx.- Editor : Dr. ANIL SUCHAKEx.- Editor : Dr. P.N. RAOEx.- Editor : Dr. AJOY K. SAHA

MembersDr. RAJESH SUBHEDAR Dr. JAYESH LELEDr. BALKRISHNA INAMDAR Dr. Y. S. DESHPANDEDr. SUBRAMANIUM JAYARAM Dr. GOPINATHAN INDUMATIDr. NIRANJAN VAIDYA Dr. AVINASH BHONDWEDr. VYANKATESH METAN Dr. RAJENDRA GANDHIDr. SANJAY DESHPANDE Dr. KRISHNESHKARDr. RAVI PATEL Dr. GURUDATT BHATDr. AJAY TILWE Dr. GOVIND DHAWALE

Published by : IMA MAHARASHTRA STATEContact for write-ups, articles, interviews andadvertisements : Editor : Dr. Deepak Jumani

E-mail : deepak.jumani@gmail.com

IMA Bldg, 2nd Floor, J.R.Mhatre Marg, J.V.P.D. Scheme,Juhu, Mumbai - 400 049. Office : 2623 2965 / 6521 5756

E-mail : imamsmumbai@yahoo.co.inWebsite : www.imamaharashtrastate.org

Advertisement Cheques must be drawnin favour of IMA MAHARASHTRA STATE

2

1 Action Committee & Dr. Pt. RelationshipChairman Dr. DEVENDRA K. SHIROLEConvener Dr. VIJAY GHATE

MembersDr. KISHORE GANGURDE Dr. SALIM SACCHANIDr. ARSHAD G. MOHAMAD Dr. PRATAP JADHAV

2 Press PublicityChairman Dr. BAKUL S. MEHTAConvener Dr. HOZIE DARA KAPAIDAMembers Dr. ANIL LADDHAD

3 Professional Protection SchemeChairman Dr. ANAND KATEConvener Dr. KRISHNA PARATE

4 Medico Legal CommitteeChairman Dr. MILIND M. NAIKConvener Dr. NISAR SHAIKH GULABMembers Dr. DILIP PATILDr. RAJENDRA ABHYANKAR Dr. SUBHASH TIWARI

5 Mahima Editorial BoardChairman Dr. DEEPAK K. JUMANIEx.- Editor Dr. ANIL SUCHAKEx.- Editor Dr. P.N. RAOEx.- Editor Dr. AJOY K. SAHA

MemberDr. RAJESH SUBHEDAR Dr. JAYESH LELEDr. BALKRISHNA INAMDAR Dr. Y. S. DESHPANDEDr. SUBRAMANIUM JAYARAM Dr. GOPINATHAN INDUMATIDr. NIRANJAN VAIDYA Dr. AVINASH BHONDWEDr. VYANKATESH METAN Dr. RAJENDRA GANDHIDr. SANJAY DESHPANDE Dr. KRISHNESHKARDr. RAVI PATEL Dr. GURUDATT BHATDr. AJAY TILWE Dr. GOVIND DHAWALE

6 Resource & Finance CommitteeChairman Dr. ANIL PANCHNEKARConvener Dr. ANIL SUCHAKMembers Dr. SANJAY S. JOSHI

Dr. AKIL CONTRACTOR7 Membership Promotion committee

Chairman Dr. SUHAS PINGLEConvener Dr. JAYANT MAKARANDE

MemberDr. DEEPAK KHALANI Dr. ANIL D. KABRADr. SHRIDHAR G. SHANBAUG Dr. KIRAN V. NABARDr. BALIGA PRADEEP Dr. CHANDAK UMAKANTDR. GANGADHAR V. MAHESHWARIDr. YUVRAJ GEHLOT (Not Member) Dr. PATEL RAMESH

8 Rural Health CommitteeChairman Dr RAVI WANKHEDKARConvener Dr SAVITA S. NAIK

MembersDr. NARAYAN K. PURANIK Dr. BHARAT VALVIDr. SEHEJWAL Dr. YASH LOKHANDWALADr. NAPHADE NINAD EKNATH Dr. RAJKUMAR SACHDEV

9 Medical Education Committee & Medical Ethics CommitteeChairman Dr. TATYARAO. P. LAHANEConvener Dr. KISHOR TAORIMembers Dr. GIRISH THAKREDr. YASH LOKHANDWALAL Dr. SUDHAKAR TAMBE

10 Occupational Health / Service DoctorsCommitteeESIS/ LIC Sub Committee

Chairman Dr. YOGESH SHAHConvener Dr. MANGALA GOMARE

Dr. SANTOSH KADAMMembers Dr. RAJESH VASAVEDr. SAJAY SHINDE Dr. SUBHASH SHAH

11 Group Health & Insurance SchemeChairman Dr. DILIP DEODHARConvener Dr. DEVENDRA K. SHIROLE

12 Women Doctors WingChairman Dr. MAYA TULPULEConvener Dr. VIJAYA MALIMembers Dr. SUNITA KSHIRSAGARDr. VIDYUT SHAH Dr. SHRADDHA WALVEKAR

13 Constitution committeeChairman Dr. SHAILENDRA C. MEHTALIAConvener Dr. JAYESH LELEMembers Dr. NIRANJAN R. VAIDYADr. BHALCHANDRA WAGH Dr. DILIP SARDADr. PARTHIV SANGHVI Dr. PRASHANT NIKHADE

14 New Premises / Building CommitteeChairman Dr. ANIL PANCHNEKARConvener Dr. AJAY KATEMembers Dr. KAILASH GINDODIA

16 DASS CommitteeChairman Dr. Y. S. DESHPANDEConvener Dr. BAL INAMDARMember Dr. VANDANA GANDHI Dr. VILAS

BHOLE18 Award Committee

Chairman Dr BAKULESH MEHTAConvener Dr ARUN PAWADEMembers Dr R. D. JAGTAP

19 Projects committeeChairman Dr. PRAKASH DEOMember Dr. AKIL CONTRACTORDr. SUHAS PINGLE Dr. RAVI WANKHEDKAR

20 Co-ord. State H.Q. CommitteeChairman Dr. NIRANJAN VAIDYAConvener Dr. ANAND KATE

21 Anti Quackery cellChairman Dr. GHANSHAYAM UMREConvener Dr. BALDWA MAHESH

MembersDr. SANJAY DEORE Dr. SHRADDHA WALVEKARDr. SANDIP PHADKE Dr. PANKAJ GUPTADr. NITIN TURASKAR Dr. RAM SHIVEKDr. PRASAD MAGAR Dr. POLKAT

22 Information & CommunicationChairman Dr. JAYESH LELEConvener Dr. SATHAYE CHANDRASHEKHAR B,.Members Dr. JAYA DIGHE

23 Geriatric Cell CommitteeChairman Dr. DILIP DEODHARConvener Dr. PRAKASH J. KHALAPMembers Dr. RAMESH SHAH

25 Sports CommitteeChairman Dr. MANGESH GULWADEConvener Dr. SURESH GOKHALEMembers Dr. SACHIN PAWDE

Dr. CHARUHAS S. JAGTAP Dr. KISHOR GANDECHADr. ASHUTOSH KELKAR Dr. AMIT DEWAIKARDr. SANJAY DEOTALE Dr. UDAY PHUTEDr. RAJESH PATIL Dr. DILIP SHIRSHIKAR

26 BMW & Nursing HomeChairman Dr. SANJEEV SHARANGPANIConvener Dr. BAL INAMDAR

MembersDr. SANJAY DAMKE Dr. RAJENDRA JADHAVDr. VIPIN CHECKER Dr. AJAY TILWE

27 Advisory CommitteeDr. VIJAY PANJABI Dr. VASANT PAWARDr. R. G. JIMULIA Dr. RAM ARANKARDr. ASHOK ADHAO

28 Legal Advisory CommitteeChariman Dr. JAYANT NAVRANGEConvenor Dr. SUBHASH TIWARIMember Dr. ANIL LADDHAD

Dr. BHUJANG PANDURANG Dr. NIKHIL DATAR

SUB COMMITTEES

3

Pranaam to all my Respected teachers andall the members of Indian Medical Association.

In the 21st Century, the only skill that won’tbecome obsolete is the ability to learn. Nowadays,our ability to learn new processes can drasticallyimprove our earning potential. Learning is a lotlike exercising: it’s an activity that must be doneoften to attain maximum results.Success is not an accident...it’s a learnable skill

No matter what your dreams & aspirationsare, one thing is certain: To achieve them youmust have the right tools to guarantee yoursuccess. It’s time to think about what you’re goingto do today to make your life richer, happier, andmore successful

Enrich your personal and professional life.Unlock your full potential for success andachievement. Experience high levels of joy whileyou work in your clinics and beseech to getmaximum job satisfaction, then wealth andfinancial stability is not at all a problem.

You can only achieve your dreams when youbelieve in yourself! Learn how changing the way youthink will open new doors to unlimited possibilities.Successful people think and plan better thanunsuccessful people. I always say that Plan yourwork and then Work your plan, and To achievesomething you’ve never achieved before, you mustbecome someone you’ve never been before.

Success is simple. Do what’s right, the rightway at the right time.

Boat builders know that the deeper the keelof a sailing vessel, the more stable it will be instorms, squalls, and gusts of wind. The sameholds true for us. The deeper your keel - orstabilizing factors in your life i.e. the more youupdate, by reading or attending CME’s-the lesslikely it is that you will be blown over or offcourse when unexpected change occurs.

To be rich in admiration and free from envy,to rejoice greatly in the good of others, to lovewith such generosity of heart that your love isstill a dear possession in absence or unkindnessis a gem of a soul, a classified Haematologist of

EDITORIALour City and our GuestEditor, Dr Abhay Bhave. Hisbrilliant clinical acumen,simplicity and humblenessis beyond words and space.We are fortunate to have himenlighten our medical fraternity in this specialissue on hematology on common problems. Wehave also included articles by Dr Mammen Chandy,Dr Tapan Saikia, Dr Sunil Parekh and Brigadier VeluNair, eminent haematologists of our country whohave pioneered many useful therapies andprocedures for the benefit of patients. Indeed Indiais really proud of them.

Dr Mammen Chandy, Director, Tata MedicalCentre, Kolkata, West Bengal & Professor andHead, Hematology Department has beautifullyenlightened us on problems of thalassaemia,which speaks of his social commitment.

Dr Tapan Saikia, Head of Medical Oncology,Prince Aly Khan Hospital, has brilliantlydescribed leucocytosis and how to be vigilantwith the WBC reports, indeed a very very practicaland useful article.

Dr Sunil Parekh Chairman, MDRI (MarrowDonor Registry Programme, India) has been theMessiah of Bone Marrow Rigistry and has been aGuardian Angel for millions who may need Bonemarrow as life saving..

Brigadier Velu Nair Dean, Army College ofMedical Sciences, Delhi Cantt-110010 anotherpatriot son of our soil whose dreams are setingup a genuine functional Bone marrow transplantCenters and an ethnic registry to save our patientsby curing them from leaukaemias and giving thema good quality of life.

Your aim is to become a “change master,” toembrace change, to welcome change, to ride thetides of change, and to move toward theimprovements you desire. “Do not wait; the timewill never be “just right.” Start where you stand,and work with whatever tools you may have atyour command, and better tools will be found asyou go along.” said Dr Abhay Bhave.

4

W. Clement Stone, the billionaire and founderof Combined Insurance Company, was famousfor his attitude of being an “inverse paranoid.”He was convinced that everything that happenedto him was part of a conspiracy to help him to bemore successful. Whenever somethingunexpected occurred, he immediately said,“That’s good!” and then looked into the situationto find out exactly what was good about it.

Victor Frankl said that the last great freedomof man is the freedom to choose his attitude underany given set of circumstances. You cannotcontrol what happens to you, but you can controlyour attitude toward what happens to you, andin that, you will be mastering change rather thanallowing it to master you.

The life of every man is a diary in which hewrites his own story. Many such lives come andgo but the echoes of some remain, to touch oursouls in unthinkable ways. Lives of these heroesspeak to our hearts and give us strength forfinding the inspiration within ourselves to writethe story of our own life. It has been my heartywish in every endeavor of mine to see a change

in our readers and to act positive and bring tothem a great achievement and job satisfaction,through the wisdom of our teachers like Dr AbhayBhave and all the others. If something here makesyour heart smile and encourages the next boldstep of service and compassion in your journey,our mission is accomplished.

I have been getting many many encouragingsms’s, emails and telephone calls congratulatingme for the fineness of Mahima issues. I thank allof them and I pray and beseech all to bless mewholeheartedy and I shall always welcome everyinnovative idea or suggestion from all. Afterall Ibelieve No matter how physically you are, itdoesn’t matter until you share your knowledgewith others or show how beautiful you are fromthe inside. This surely will take you far as everyvalue has a value only if its value is valued.

With lots of love and light,

DR. DEEPAK K. JUMANI

FORTH COMING EVENTS1) EVECON 2010 at IMA Dhule Branch, 25th & 26th September 2010.2) 14th November 2010 – CGP Conference by IMA Maharashtra State CGP Faculty.3) Mastacon 2010 at Nashik on 19th, 20th & 21st November 2010.4) IMACON 2010 at Jaipur on 27th, 28th & 29th December 2010, Organising Secretary :

Dr. S. S. Aggarwal Mob. : 94140 55592

IMA MAHARASHTRA STATE CGP CONFERENCEIMA MS CGP faculty is organising CGP conference on Sunday, 14th November 2010;

at IMA Mumbai West branch Premises. This conference is dedicated to Late Dr K. Ramamoorthy,‘Teacher Par excellence’.

The detailed programme shall be sent at a later date. Please keep it blocked for thisconference. Some of the faculties who have confirmed participation are :Dr. Sanjeev Mehta, Dr. Umesha Khanna, Dr. Shivkumar Utture, Dr. Ketan Mehta, Dr. VishalGupta, Dr. Dilip Karnad, Dr. Sujeet Rajan

Dr Bakulesh Mehta Dr Hozie Kapadia Dr Akil ContractorPresident Hon State Secretary Director CGP IMA MS

Dr. Vivek Billampelly (Pune) Dr. Dilip G. Deodhar (Pune)Hon. Secretary Hon. Jt. Secretary

Dr Jayesh Lele Dr Anil Pachnekar Dr Sanjeev MehtaCoordinators

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Dear Members,

Namskar & Season’s Greeting

The festival season has started & we recentlycelebrated 63rd Independence Day in big way. WeIndians feel very proud & take pride to be calledIndians and for our, heritage /culture / rituals &customs. We strongly believe in our values whichplay very important role in our day to day life.

Even after 60 years of independence certainpeople & customs dominate in our daily life. E.g.The following (D):-

a: Dance b: Dowry c: Dacoity d: Dudhwala e:Disinvestment f: Dhaba.

We can not overcome above (Ds) in our dayto day life. There is every day festival (which iscelebrated some where in India). Dr. Kaka Kalelkarhas written that here are 365 days in calendar &we have 366 days festival.

We are basically emotional & God fearing people,& we accept/adjust/adopt many things in our life& we had compromising nature & let go policy.

The society’s values have changed & we areadopting more & more western culture. Jointfamily is on decline & we don’t have clear ideaabout which way our society is going & whichdirection our children should be given. Ourtolerance is decreasing & our demands areincreasing & every one of us have becomematerialistic & self centered.

Recently medical fraternity is passingthrough, a big wave & uncertainty & governmentis proposing many changes.

The past few months were hectic & haswitnessed many hassles some sour & some sweet.

The following major issues were discussed& were in limelight in media also

1) Proposed BRMS Course.2) Clinical Establishment Act.3) Dissolution of MCI.For above it is crystal clear that IMA has been

opposing these 3 bills & we had protest DHARNA atJantarmantar at New Delhi on 28th July 2010, whereabout 300 doctors participated from all over India.

1.Mediclaim Policy – Therecent announcement innewspapers (new policy) byfour major insurancecompany has created wavein the community. We atIMA platform is of opinionthat some applicable & practical solution shouldbe reached. We are following & studying thismatter. We are concerned about our members &patients (common policy holder).

2.Accreditation - procedure has started in fullswing. Some of the branches are alreadyrecognized by MMC & many have applied. Themore details & procedures are still awaited.

Doctor’s day celebration on 1st July wascelebrated by all our IMA branches.

We have received following Greetings /Quotes from our patients.1. Happy Doctor’s Day.2. We salute to the hand that cures.3. Honoring the hands that heal.4. We appreciate your kindness as well as your

thoughtfulness, & both which are priceless,during moments of darkness.We thank you in eagerness for you havealways been truly selfless.

5. We salute you for the sacrifice selfless service,& rent less effort towards the alleviate thepain & suffering of the patient.

6. Truly doctors you are amazing people whomakes the difference in our lives.

Friends reading above Greetings/Quotes showthat till today society respect, regards & are proudof us. At the same time it is our duty & responsibilityto maintain the dignity of the noble profession.

We are proposing 4 big events in near future.1) IMA Women’s Conference at Dhule on 25th &

26th September 2010.Please participate & to give encouragementto organizing committee which is workinghard under leadership of Dr. Mrs. Vijaya Mali,Dr. Ravi Wankhedkar & Dr. Maya Tulpule.

President’s Message

6

2) Workshop on Disaster Management proposedon 24th October 2010. Dr. Sanjeev Sharangpani& Dr. Yatin Jadhav are the convener & havealready started working.

3) 1st time CGP Conference to be held by IMA MSfaculty on 13th November at Mumbai West Branch.Dr. Akil Contractor, Director of CGP & Dr.Jayesh Lele, Joint Secretary IMA MS wants tohave organize it on large scale. The conferenceis going to be dedicated in name of Late Prof.Dr. K. Rammoorthy ‘A great teacher & clinician.

4) MASTACON 2010 at Nashik on 19th, 20th & 21st

of November, the preparation is in full swing.We are lucky that we have no Election for

the post of President & Vice Presidents.I Congratulate all of them for being elected unopposed.

PresidentDr. Jayghosh A. Kaddu (Wai)Vice Presidents1. Dr. Sunita K. Kshirsagar – Mumbai2. Dr. Sanjeev Sharangpani–Chiplun3. Dr. Anil C. Laddhad – Nagpur And4. Dr. Rajendra Kulkarni - Nashik (Nominated)

(Vice President Nomination from Host Branch)I also give compliments to Dr. Subhash

Behere, Dr. Jayant Pawar, Dr. Sanjeev Sharangpani& Dr. Jyesh Lele for withdrawal to avoid election.

We have achieved this through negotiations& meetings under leadership of Dr. Ashok Adhao.

We have already published 3 MAHIMA issuethis time & liked to publish 2 more before theMASTACON. I give compliments to Editorial board

of MAHIMA particularly to Dr. Jumani, our editorwho have changed the product.

We appeal to our members to join SocialSecurity Scheme, Medical Protection Scheme &Health Insurance Scheme for the benefit for you,your family members & help our members too.

We had 1st time successful blood donationdrive by our 48 local branches of IMAMaharashtra State who arranged the Camps. Icongratulate them, thankful to Dr. RajendraChavan from Boisar (Palghar) to take lead &initiate this project & also to Maharashtra StateBlood Transfusion Council & co-ordinators Dr.Anil Suchak & Dr. Jayesh Lele.

I suggest & appeal to all our members togive some donations to IMA MS. We want to createmore funds for betterment of State IMA office &more communication / functioning & projects.

Three big branches Mumbai West, Mumbai,Nagpur have already sent their help. The otherbranches should follow & do the needful.

Please make your friends Life Members ofIMA to make our association strong & torepresent & help our medical fraternity.

Long Live IMA!Yours sincerely

DR. BAKULESH S. MEHTAPresident, IMA MS

I would like to Congratulete you and allthe office bearers of IMA (HQ) for successfullyorganizing day long demonstration againstarbitrary dissolution of MCI, Bachelor of RuralHealth Care and Clinical Establishment Act aspassed by Government of India. It was verywell organize and successfully conducted.Representation fromall the state was very goodandwegot whole hearted support from all themembers. Now we haveto follow it up vigourslyand fight against it up to its logical conclusion.For that we need to ogranize same type ofdemonstration in all the states to increasepublic awareness about this. I.M.A. CalcuttaBranch has planned to similar day long Dharna ata prominent place in Kolkata on 15th July 2010.

Dr. R.D. Dubey, President, I.M.A. CulcuttaBranch 28th June 2010 will be remembered for ever,by Medical Fraternity, because of it has createdhistory in IMA by arranging Dharna (for 1st time).To protest our concern & show unity and strengthto government as well as public. It was verypeaceful and successful. Various leaders spokeand expressed their views. I must compliment andcongratulate IMA HQs. for this and particularlyDr. Dharna Prakash. The members were of opinionGovernment bureaucracy wants to rule MCI which willharm medical profession and public at large. Theprotest should continue till we approach our goaland if required “BANDH” one day should observe.

Dr. Bakulesh S. MehtaPresident, IMA Maharashtra State

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Dear friends,

Right now the medical profession is in aturmoil with huge challenges facing us.

1. Government of India promulgated anOrdinance on May 15, 2010 to supercedethe MCI and replace it with a six memberpanel which will remain for one year. TheGovernment is in process of proposing a draftbill “National Council of Human Resources inHealth” which may nullify the powers of MCI,DCI, Pharmacy Council of India and IndianNursing Council to a large extent. We stronglyprotest this government’s move which will takeaway our democratic rights to elect ourregulatory body.

2. The Clinical Establishment Act..Emergency medical care is made obligatoryunder the law. Even single doctor’s clinics arecovered under this Act. It will be under thesupervision of bureaucrats. The fines will bevery heavy.

3. We are fighting against the three year RuralBRHC course as it is discriminatory againstthe rural population. After a few years theBRHC Diploma holders will demand condensedMBBS course and finally PG courses openinga back door entry into the profession.

We had a protest dharna in New Delhi aswell as in local branches in Maharashtra.

We request all branches to comply with theaccreditation process of MMC as it will be a greatboost to the membership promotion drive. Alldoctors qualified in modern medicine will haveto become members of IMA.

We had a fantastic blood donation driveduring Doctors’ Day week in which 48 IMAbranches participated and collected 2378 bottlesof blood.

IMA, HQ had given five workshops on Con-traceptive Updates and Safe Abortion Techniqueswhich were held in IMA, Mumbai, IMA, MumbaiWest, IMA, Nashik,

IMA, Pune and IMA, Nagpur.

In Maharashtra State nowwe have three RNTCP units,Pune, Nagpur and Mumbai.

The proposed Patient’sRight Charter was printed inJune MAHIMA. It will be discussed in the SecondState Executive Committee Meeting on Sunday,August 22, 2010.

The cost of running our IMA State Branch isspiraling, cost of establishment, salaries, elec-tricity, postages, stationery, e-mails etc. Our re-sources are limited. Kindly suggest ways of aug-menting our income. We would like to have ourown IMA State Office building in future.

Our future programs are very interesting.1. IMA, Mah. State Women’s Conference at Dhule

on September 25 and 26, 2010.2. Workshop on Disaster Management. Proposed

date is October 24, 2010.3. First IMA, CGP State Conference to be held by

IMA, MS CGP faculty at IMA, Mumbai WestBranch on November 14, 2010. This confer-ence is to be dedicated in the name of a greatteacher and a wonderful human being Late Prof.Dr. K. Ramamoorthy.

3. MASTACON 2010 at Nasik, 19,20 & 21 Nov. 2010

Thankfully there were no elections this yearof the President and Vice Presidents due to mag-nanimity of the candidates who withdrew infavour of the elected candidates.

I hope and pray the same cumulative talent,tolerance and wisdom is used in tackling manyother problems facing IMA. For any help regard-ing IMA matters kindly contact me or the officebearers of IMA, MS.

DR. HOZIE KAPADIAHon. State SecretaryIMA, MS

Hon. State Secretary’s Message

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Why is the media here so negative?Why are we in India so embarrassed to recognizeour own strengths, our achievements?

We are such a great nation. We have so manyamazing success stories but we refuse acknowl-edge them--- Why?

We are the first in milk production. We arenumber one in Remote sensing satellites. We arethe second largest producer of wheat. We are thesecond largest producer of rice..

Look at Dr. Sudarshan, he has transferredthe tribal village into a self-sustaining, self-driv-ing unit. There are millions of such achievementsbut our media is only obsessed in the bad newsand failures and disasters.

I was in Tel Aviv once and I was reading theIsraeli newspaper. It was the day after a lot ofattacks and bombardments and deaths had takenplace. The Hamas had struck. But the front pageof the newspaper had the picture of a Jewish gentle-man who in five years had transformed his desertinto an orchid and a granary. It was this inspiringpicture that everyone woke up to. The gory detailsof killings, bombardments, deaths, were inside inthe newspaper, buried among other news. InIndia we only read about death, sickness, terror-ism, crime.

Why are we so NEGATIVE?Another question: Why are we, as a nation soobsessed with foreign things?

We want foreign T. Vs, we want foreign shirts.We want foreign technology. Why this obsessionwith everything imported. Do we not realize thatself-respect comes with self-reliance? I was inHyderabad giving this lecture, when a 14 year oldgirl asked me for my autograph. I asked her whather goal in life is. She replied: I want to live in adeveloped India. For her, you and I will have tobuild this developed India. You must proclaim.India is not an under-developed nation; it is ahighly developed nation.

The Past President of IndiaDR. A. P. J. Abdul Kalam's Speech

in Hyderabad.......

Do you have 10 minutes? Allow me to comeback with a vengeance.

Got 10 minutes for your country? If yes, thenread; otherwise, choice is yours.

YOU say that our government is inefficient.YOU say that our laws are too old.YOU say that the municipality does not pick

up the garbage.YOU say that the phones don't work, the

railways are a joke, The airline is the worst in theworld, mails never reach their destination.

YOU say that our country has been fed to thedogs and is the absolute pits.

YOU say, say & say. What do YOU do about it?

Take a person on his way to Singapore . Givehim a name - YOURS. Give him a face - YOURS. YOUwalk out of the airport and you are at your Inter-national best. In Singapore you don't throwcigarette butts on the roads or eat in the stores.

YOU are as proud of their Underground linksas they are. You pay $5 (approx. Rs. 60) to drivethrough Orchard Road (equivalent of MahimCauseway or Pedder Road) between 5.00 PM and8.00 PM.

YOU come back to the parking lot to punchyour parking ticket if you have over stayed in arestaurant or a shopping mall irrespective of yourstatus identity...

In Singapore you don't say anything, DO YOU?

YOU wouldn't dare to eat in public duringRamadan, in Dubai .

YOU would not dare to go out without yourhead covered in Jeddah .

YOU would not dare to buy an employee ofthe telephone exchange in London at 10 pounds(Rs.650) a month to, 'see to it that my STD and ISD

9

calls are billed to someone else. 'YOU would notdare to speed beyond 55 mph (88 km/h) inWashington and then tell the traffic cop,' Jaantahai main kaun hoon (Do you know who I am?).I am so and so's son. Take your two bucks andget lost.'

YOU wouldn't chuck an empty coconut shellanywhere other than the garbage pail on thebeaches in Australia and New Zealand.

Why don't YOU spit Paan on the streets ofTokyo ? Why don't YOU use examination jockeysor buy fake certificates in Boston ??? We are stilltalking of the same YOU.

YOU who can respect and conform to a for-eign system in other countries but cannot in yourown. You who will throw papers and cigarettes onthe road the moment you touch Indian ground. Ifyou can be an involved and appreciative citizenin an alien country, why cannot you be the samehere in India ?

Once in an interview, the famous Ex-munici-pal commissioner of Bombay, Mr. Tinaikar , had apoint to make. 'Rich people's dogs are walked onthe streets to leave their affluent droppings allover the place,' he said. 'And then the same peopleturn around to criticize and blame the authori-ties for inefficiency and dirty pavements. Whatdo they expect the officers to do? Go down with abroom every time their dog feels the pressure inhis bowels?

In America every dog owner has to clean upafter his pet has done the job. Same in Japan. Willthe Indian citizen do that here?' He's right. We goto the polls to choose a government and after thatforfeit all responsibility.

We sit back wanting to be pampered and ex-pect the government to do everything for us whilstour contribution is totally negative. We expectthe government to clean up but we are not goingto stop chucking garbage all over the place norare we going to stop to pick a up a stray piece ofpaper and throw it in the bin. We expect the rail-ways to provide clean bathrooms but we are notgoing to learn the proper use of bathrooms.

We want Indian Airlines and Air India toprovide the best of food and toiletries but we arenot going to stop pilfering at the least opportunity.

This applies even to the staff who is knownnot to pass on the service to the public. When itcomes to burning social issues like those relatedtowomen, dowry, girl child! and others, we makeloud drawing room protestations and continue todo the reverse at home. Our excuse?

'It's the whole system which has to change,how will it matter if I alone forego my sons' rightsto a dowry.' So who's going to change the system?What does a system consist of ? Very convenientlyfor us it consists of our neighbours, other house-holds, other cities, other communities and thegovernment.

But definitely not me and YOU. When it comesto us actually making a positive contribution tothe system we lock ourselves along with our fami-lies into a safe cocoon and look into the distanceat countries far away and wait for a Mr.Clean tocome along & work miracles for us with a majes-tic sweep of his hand or we leave the country andrun away.

Like lazy cowards hounded by our fears werun to America to bask in their glory and praisetheir system. When New York becomes insecurewe run to England. When England experiences un-employment, we take the next flight out to the Gulf.When the Gulf is war struck, we demand to berescued and brought home by the Indian govern-ment. Everybody is out to abuse and rape the coun-try. Nobody thinks of feeding the system. Our con-science is mortgaged to money.

Dear Indians, The article is highly thoughtinductive, calls for a greatdeal of introspectionand pricks one's conscience too.... I am echoing J.F. Kennedy 's words to his fellow Americans torelate to Indians.....

'ASK WHAT WE CAN DO FOR INDIAAND DO WHAT HAS TO BE DONE TO MAKE INDIAWHAT AMERICA AND OTHER WESTERN COUNTRIESARE TODAY'

Lets do what India needs from us.Forward this mail to each Indian for a change

instead of sending Jokes or junk mails.Thank you,

DR. ABDUL KALAAM

10

HAEMATOLOGY TODAYHaematology is a fascinating branch of

medicine that studies problems related to theblood, bone marrow and lymph glands andanalyses its disorders. This includes problemsof red blood cells (especially anemias), bloodbanking (red cells, plasma and platelets), whiteblood cells (especially blood cancers), plateletsand coagulation (bleeding or clotting). Manyexciting advances in research and developmenthave taken this field recently from nascence tothe heights of cutting edge medicine such as stemcell technology, blood banking and targeted andadoptive immunotherapy among several others.

Blood is madae up of components which areplasma (~55%), and the formed elements. Thelatter comprise of erythrocytes (RBCs) (~45%), theLeukocytes (WBCs) and platelets (~1%).

The role of a haematologist is to assesswhether any alterations in the plasma or formedelements of the blood are a result of disease inthe bone marrow (primary marrow disease) orreaction of the bone marrow to disease elsewhere(systemic causes). These alterations are often thefirst sign that disease is occurring in the body.

The most important and easiest test to detectthis change is an automated CBC report, whichgives us information about the red cell indices,white cell count and platelets. The automated CBCis preferred for reasons of rapidity, accuracy,reliability and reproducibility. Another importantaspect for assessing any change is theexamination of the peripheral smear underthe microscope. Many abnormalities ofhaemato-logical disorders can be diagnosed orsuspected by the smear itself. The automated CBCreport gives us some measured and some derivedvalues that can be used to analyze the givenpatients haematological problem and assure amore evidenced based approach to diagnosisand treatment. Each of the formed elements ofthe blood can be affected qualitatively orquantitatively (ie either in function or numbers)

Under normal conditions the production,release, and survival of blood cells is a highly

regulated process.Quantitative and/orqualitative hematologicabnormalities may resultwhen there is an imbalancebetween cell production,release, and/or survival.

Age, sex, and geographic location areinvolved in physiologic changes in normal valuesof the formed cellular elements

Pathologic changes in the values of the formedcellular elements occur with disease or injury.

Normal values for a group are determinedby calculating the mean for healthy individualsof the group and reporting the normal range asthe mean +/- 2 standard deviations

Hematopoiesis is a term describing theformation and development of blood cells. Cellsof the blood are constantly being lost ordestroyed. Thus, to maintain homeostasis, thesystem must have the capacity for self renewal.This system involves. proliferation of progenystem cells along with differentiation andmaturation of the stem cells into the functionalcellular elements. In normal adults, theproliferation, differentiation, and maturation ofthe hematopoietic cells (RBCs, WBCs, andplatelets) is limited to the bone marrow and thewidespread lymphatic system and only maturecells are released into the peripheral blood.

Hematopoiesis in the bone marrow is calledmedullary hematopoiesis, hematopoiesis inareas other then the bone marrow is calledextramedullary hematopoiesis ( liver and spleen)of an adult when the bone marrow cannot meetthe physiologic needs of the tissues. This canlead to hepatomegaly and/or splenomegaly(increase in size of the liver and/or spleen becauseof increased functions in the organs).

Bone marrow is located inside spongy boneand is considered to be the factory that producesblood. In a normal adult, ½ of the bone marrow ishematopoietically active (red marrow) and ½ is

11

inactive, fatty marrow (yellow marrow). Themarrow contains stem cells with self renewalcapacity. The bone marrow has cellularcomponents and a lattice like micro-environmentthat allows growth of the cellular elements.

Erythroids are the precursors to red cellsthat house the haemoglobin. Myeloids arethe precursors to white cells that preventinfection and are responsible for immunity.Megakaryocytes are the precursors to plateletsinvolved in haemostasis.

In certain pathologic states the bone marrowcan increase its activity to 5-10 times its normalrate. When this happens, the bone marrow issaid to be hyperplastic because it replaces theyellow marrow with red marrow. This occurs inconditions where there is increased or ineffectivehematopoiesis. The degree to which the the bonemarrow becomes hyperplastic is related to theseverity and duration of the pathologic state.Pathologic states that cause this include:

Acute blood loss in which there is atemporary replacement of the yellow marrow

Severe chronic anemia – erythropoiesis (RBCproduction) may increase to the extent that themarrow starts to erode the bone itself.

Malignant disease – both normal redmarrow and fatty marrow may be replaced byproliferating abnormal cells.

Hematopoietic cells can be divided intothree cellular compartments based on maturity:

Pluripotential stem cell capable ofself-renewal and differentiation into all bloodcell lines (cellular reserve for the stem cells)

Committed proginator stem cells destined todevelop into distinct cell lines (can differentiateinto any of the other hematopoietic cells)

Mature cells with specialized functions

IN THIS JOURNAL……..It is indeed my proud privilege to present in

this journal articles of interest to the communityby repute hematologists

Dr Mammen Chandy has discussed theextremely important community problem of

thalassaemia in our community and how we canreduce the risk of thalassaemic births.Thalassaemia major births have a aprofoundeffect on the economic, social and medicalaspects of our country

Dr Tapan Saikia has given an approach to acommon problem of leucocytosis in practice sothat we can logically come to a conclusion of itbeing benign versus malignant. He has given uspractical tips for routine practice.

Dr Sunil Parekh has dedicated his currentpractice to set up a most difficult task of anational bone marrow donor registry. ThisHerculean effort is most needed for patients inneed of a marrow donor outside the family.Importantly, bone marrow can cure some cancersbut in this country, non availability of HLA matcheddonors is vexing.

Brigadier Velu Nair has been an outstandingcontributor to our field from Army Hospital, NewDelhi. He has written on the role of bone marrowtransplantation in India. Its only when moretransplant centres are set up in India and anethnic registry is formed that more of our patientswill achieve cure and better quality of life.

I have included topics of routine practiceinterest in this journal and hope the readers willenjoy them.

I am grateful that these gentlemen have giventheir articles for this edition

Happy reading !

DR. ABHAY A. BHAVEMD, FRCPA (Australia), Haematologist

Lilavati Hospital & Research Centre,Bandra (W), Mumbai

Raheja Hospital & Research Centre,Mahim, Mumbai

Honorary Haematologist,BYL nAir Charitable Hospital, Mumbai Central

Chairperson (cancer detection & treatment Cell),Lions Club of Mumbai

12

02nd August 2010

To,The President / Hon. SecretaryIMA Maharashtra State

Sub : Report on Elections of President & Vice Presidents for the year 2010 – 2011.

Dear Sir,The Election Commission is happy to give report on Election of President & Vice Presidents

for the year 2010 – 2011.Three contestants for the post of President have withdrawn their candidature and one

contestant has withdrawn his candidature for the post of Vice President before the close ofwithdrawal date (i.e. 31/07/2010).

Since the no. of candidates left in the fray are as follows :1) One Post of President – One Candidate2) Three Post of Vice President – Three Candidates

Hence the candidates are declared as elected unopposed as follows :-For the post of PRESIDENT :

Name Nominating BranchDr. Jayghosh A. Kaddu IMA Wai

For the post of VICE – PRESIDENTS :Name Nominating Branch

1) Dr. Sunita K. Kshirsagar IMA Mumbai2) Dr. Sanjeev Sharangpani IMA Chiplun3) Dr. Anil C. Laddhad IMA Nagpur

Thanking you,Yours sincerely,

Dr. N. N. Murkey Dr. C. M. Gupta Dr. S. H. PingleChairman Member Member

Election Commission, IMA Maharashtra State

IMA PROTEST DHARNA

AT IMA MUMBAI WEST AT IMA HQ, NEW DELHI

13

MASTACON - 2010AT IMA NASIK

I am glad to inform the office of IMA Maharashtra regarding our MASTACON 2010.We at Nashik have formed an organising committee as follows-

Chairman Reception : Dr. Vasantrao PawarOrganising Chairman : Dr. Shrikant PurnapatreOrganising secretary : Dr. Rajendra KulkarniOrganising secretary : Dr. Satish Patil

(President IMA Nashik )Treasurer : Dr. Kishor Gangurde.

Dates of the Conference 19, 20 & 21 November 2010

Tentative programme

19/11/2010 : Social security scheme meeting - 9.00 am onwards: Office bearers' meeting: State executive Meeting: Lunch: State council meeting: Dinner

20/11/2010 : State council meeting--if remaining: Inauguration of the conference - 6.00 pm onwards: Installation of the new President: Scientific sessions: Banquet

21/11/2010 : Ordinary State Council Meeting: Scientific sessions: Valedictory function: Lunch

Venue on 19/11/2010 : Dr. Vasantrao Pawar Medical College Adgaon, NashikVenue on 20/11/2010 & 21/11/2010 : IMA House, Shalimar, Nashik

Registration chargesUpto 30/09/2010 : Rs. 1000/-From 1/10/2010 to 31/10/2010 : Rs. 1250/-1/11/2010 onwards---spot : Rs. 1500/-

Address for correspondence Dr. Rajendra Kulkarni

Organising Secretary, MASTACON 2010,IMA House, Shalimar, Nashik - 422001.

Phones--0253-2504887, 2502787, 2506994, 9823067946e-mail : rajakulkarni@hotmail.com

14

EVE CON-2010-DHULEFirst Maharashtra IMA Women Conference Host-IMA Dhule Branch

*Aim : To involve lady ima members n lady nonmedical spouses in imaTo adress specific women doctors issues

To sensitize women doctors on women health problems

*Venue : IMA house, DHULE*Dates : 25 th, 26 th Sept 2010(Sat,Sun)

PROGRAMMESaturday, 25th Sept, 2010

08.00 - 09.30 am : Registration and Breakfast09.30 - 10.00 am : Inauguration ceremony10.00 - 10.30 am : Guest lecture(Prominent Lady Doctor)10.30 - 11.00 am : Tea Break11.00 - 01.00 pm : Various competitions-debate,extempore,antakshari,ukhana etc01.00 - 02.00 pm : Lunch02.00 - 05.00 pm : Personality development workshop

1) Working women make up 2) Sari Draping3) Hair stying 4) Cosmetic Dentistry5) Low cal recipes n Quick breakfast 6) Hair n Skin Care

05.00 - 05.30 pm : High Tea05.30 - 07.30 pm : Mehndi, Rangoli, Poster presentation (Topic-Save The Girl Child),

Rangoli, funny games competions.Fun Filled events for MALES

08.00 pm onwards : Banquet, Cultural Prog, Talent Show (Singing, Dancing, mimickry etc)26 th Sept, Sunday

08.30 - 09.30 am : Breakfast09.30 - 10.30 am : Oration(on Common topic by prominent lady doctor)10.30 -12.30 pm : Symposium-HOME N HOSPITAL

*Stress Management & Meditation,*Financial Management, *Time Management,*Women & Law, *Electronics, etc

12.30 - 01.30 pm : Award ceremony n Validectory Function01.30 - 02.30 pm : Lunch02.30 - 5.00 pm : Public lecture on common women health problems

(eg-adolescent health/arthritis/menopause etc)05.00 pm : Tea n Disperse to meet next year

STATE LEVEL ORG COMTDr Bakulesh Mehata Dr Hozie Kapadia Dr Shivkumar Utture

President Hon.State Secretary Treasurer

Patron Org Chairperson Org SecDr. Mrs. Alka Mehta Dr Maya Tulpule Dr Vijaya Mali,

Mumbai-9323232378 Pune-9923709210 Dhule -9922251777

Joint Org Secs CordinatorDr Varsha Dhavle Dr Shradhha Walvekar, Dr Ravi Wankhedkar

Nagpur-9822204338 Nasik-937066222 Dhule-9422296495

15

LOCAL ORG CMTDhule IMA President Dr K R Gindodia Exctv Presd Dr C S Jagtap Sec Dr N C GalaniOrg Chairperson Dr Ashalata Bafna Org Sec Dr Vijaya MaliTreasurer Dr Chaya Bora Jt Org Sec Dr Mrs Date, Dr Archana Jakhete

Various sub comittee formed

* Males also should register for this conf n attend in large numbers* The participants in various competions will be only females* As far as posb guest speakers ,judges,org comt members will be females* Registration fee-Rs 300 only(inclusive of 2 lunches,2 breakfasts,banquet,entry fees,delegate kit)* A souvenir will b published* Funds-Local reception comt members,delegate fees,ima ms,help from bigger ima branches, adver-

tisements in souvenir,sponsorships,stalls etc

THANKS

Dr Ravi WankhedkarConsulting Surgeon & ColoproctologistMember-Maharashtra Medicasl CouncilChairman-IMA AMS MaharashtraChairman-IMA Rural Health Comt,MaharashtraHon Asso Prof of Surgery, SBH Govt Med Clg,Dhule

Dear Friends,

GREETINGS OF THE SEASON

IMA Maharashtra is proud to hold a state level Women Conference, FIRST OF ITSKIND at DHULE on 25th & 26th September 2010 (Sat, Sun) The aim is to strenghten IMAby involving lady IMA members & non medical lady spouses. We plan to adressvarious issues of working women including health awareness. The meet will a plethoraof competions, feast of cultural events, funfilled programs, felicitation of womenachievers, useful workshops, brainstorming symposium, orations by eminentspeakers & much more. A special session on Total Personality Development willbe held for MALE delegates. Dhule, a tranquil city & an Educational hub, boasts ofexcellent & warm hospitality. It is well connected by national highways & railwaysto major cities. The climate in September is pleasant & uplifting. The conference isopen to IMA members & their spouse (MALE/FEMALE). Participants in variouscompetions will be lady IMA members & non medical spouses only. Please mark thedate, 25 & 26 September in your diary. Circulate the information among friends &other IMA members. Detailed brochure & entry form follows shortly.

SEE YOU AT DHULE

Thanking you yours

Dr Bakulesh Mehta Dr Hozie KapadiaPresident Hon. State Secretary

16

INTRODUCTION :Automated analyzers dominate almost every

modern laboratory. These machines are capableof processing a large number of samples rapidly,with minimal human assistance and produceaccurate results. Some of the analysers used inmodern laboratory include the following.

1) Biochemistry Analyzers2) Immuno-based Analyzers3) Haematology Analyzers

a) Cell Countersb) Coagulometers

However, this article will only be limited tothe Electronic blood cell counters (CBC) which wereintroduced in 1955, and have remarkablereproducibility & respectability as compared tothe earlier manual methods of cell count analysis.

Blood cell counters operate on variousprinciples, the patented being the Coulterprinciple which states that particles pulledthrough an orifice, concurrent with an electricalcurrent, produce a change in impedance that isproportional to the size of the particle traversingthe orifice. A very small amount of the bloodsample is aspirated through a narrow tubing.Within this tubing, there are 2 types of sensorsi.e. are light detectors and electrical impedancedetectors . These sensors count the number of

Automation in Haematologycells going through and identify the type of bloodcell by its size. Characteristics of the cells areused to differentiate and categorize them.

Counters today give a CBC report that includes:1) Hb, PCV,RBC count, MCV, MCH, MCHC & RDW2) PLT count, MPV3) WBC count with differentials

Depending on the counter used, thedifferential may be a 3 part or 5 part machine.

A 3 part differential includes granulocytes,monocytes and lymphocytes .

A 5 part differential includes : neutrophils,eosinophils, basophils, monocytes & lymphocytes.

Parameters provided by automatedhematology analyzers

Measured parametersHemoglobin (Hb) Hematocrit (HCT)RBC count (RBC #) Platelet count (PLT #)WBC count (WBC #) WBC diff. (WBC %)

Derived parametersMCH (Hb/RBC #) MCV (HCT/RBC #)MCHC (Hb/HCT) RDW (RBC volume)MPV (Plt TV/PLT

In addition, the machine issues histograms (RBC,WBC & PLT)

DR. ABHAY AVINASH BHAVEHAEMATOLOGIST MD, FRCPA

MD INTERNAL MEDICINE, LTMGH AND SION HOSPITAL, MUMBAI, INDIAFELLOWSHIP IN HAEMATOLOGY FROM CMC VELLORE A PREMIER INSTITUTE IN INDIA IN HAEMATOLOGY.FELLOWSHIP IN HAEMATOLOGY FROM WESTMEAD HOSPITAL, SYDNEY, AUSTRALIA.HAS CARRIED OUT ANAEMIA & THALASSAEMIA DETECTION CAMPS & DVT AWARENESS PROGRAMMES.HAS GIVEN PUBLIC AWARENESS LECTURES ON ANAEMIA, BLOOD DONATION & BLOOD CANCERS.HAS INTERNATIONAL and several NATIONAL PUBLICATIONS TO HIS CREDITDistrict Chairperson for MDRI, Lions Club of Mumbai Carter roadChairperson, Cancer Detection and Treatment cell, Lions Club of Mumbai Carter RoadEkta Manch Awardee for community service 2007Member of the national panel for deep venous thrombosis guidelines for IndiaWRITTEN A CHAPTER ON AGRANULOCYTOSIS FOR THE 3RD EDITION OF MANUAL OF MEDICAL THERAPEUTICSMember- INDIAN MEDICAL ASSOCIATION,

ASSOCIATION OF MEDICAL CONSULTANTSMumbai Haematology Group

AFFILIATIONS - Lilavati Hospital and Research Centre, Bandra (W), Mumbai, IndiaRaheja Hospital, Mahim, Mumbai, IndiaHonorary Haematologist to BYL Nair Chritable Hospital (Teaching Institute)

17

POINTS WHILE UTILISING A LAB TEST1. NO TEST IS PERFECT2. CHOOSE THE TEST WHICH IS MOST LIKELY TO

DIAGNOSE THE PROBLEM3. ALL RESULTS ESP. ABNORMAL SHOULD BE

RECHECKED. PREFERABLY RESAMPLE4. VALUES OUTSIDE THE NORMAL RANGE DON’T

ALWAYS MEAN DISEASE5. VALUES INSIDE THE NORMAL RANGE DON’T

ALWAYS ELIMINATE DISEASE6. REPEAT TESTS PREFERABLY IN SAME LAB7. THE CLASSIC TEXT BOOK PICTURE IS NOT

ALWAYS SEEN8. GIVE INTERVAL BETWEEN TESTS TO ASSESS THE

PROBLEM9. DO TESTS ONLY IF IT WILL CHANGE THE MX OF

THE PATIENT

Please note that CLERICAL ERRORS MORECOMMON THAN TECHNICAL HISTORY,EXAMINATION ARE A MUST TO INTERPRET REPORTS

ASPECTS OF CBC INTERPRETATION1. INTERPRETATION OF VALUES2. INTERPRETATION OF SCATTERGRAM & GRAPHS3. IMPORTANCE OF SMEAR EXAMINATION4. REPORTING OF SMEARS5. COMMUNICATION

The major inroad into understanding theCBC was in the ability to best analyze the RBCindices viz. MCV, MCH & MCHC, Red celldistribution width (RDW), MPV, PCT, PDW, P-LCRetc. were added. These parameters, whichincidentally were first described by Wintrobe in1935 for classification of anemias, could be putto practical use. Technological progress in (1)the volumetric analysis of blood cells combinedwith (2) the development of special lyzers and (3)remarkable development in computers &microprocessors, transformed the ‘ordinary’ cellcounters to modern hematology analyzers.

The biggest victory came when accuracy forleukocyte differentiation was established. Highlyreproducible differentiation of white cells in –initially three and more recently five - normalsubtypes almost eliminated the need for amicroscopic evaluation of the peripheral blood film.

It is important to note that the machine isonly as good as the quality control that is run onit daily to ensure its appropriate working. Thereport generated must be issued only if it passesthe stringent quality control of the laboratory.

Once the CBC report is issued after satisfyingthe above criteria, then the interpretation of thereport can be appropriately done either by thetechnologist, pathologist, physician orhaematologist. In that all the three cell elements(RBC, WBS, Platelets) should be seen and inaddition depending on the generation of themachine issued, the various RBC indices,differential count and platelet size should beinterpreted in the light of the given situation.Undoubtedly, the machine cannot replace a pairof trained eyes behind the microscope, hence allabnormal slides should be reviewed by thepathologist or haematologist to confirm orexclude any obvious pathology on a well stainedsmear to get rapid answers to aid the clinician.For example the detection of malarial parasite,malignant cells, virocytes, etc on the smear caninitiate appropriate therapy.

Levels of Review:1. The medical technologist: The med tech, who

has demonstrated expertise in blood filmmicroscopy, performs the first level althoughthe criteria for this initial review vary fromlab to lab. In general, most labs will reviewblood smears on those samples where thehematology analyzer has either (a) failed to givea result, or (b) has flagged the presence ofabnormal WBCs or (c) has flagged for abnormalin RBC and/or platelet morphology. Blood filmsare examined and manual differential countsare performed as necessary.

2. Supervisor / Sr. Technologist: Every lab shouldinclude a supervisory review of blood films inselected cases. The criteria followed could beon following lines:a. All alert values (a.k.a. critical or panic

values) generated by hematology analyzerb. Any RBC morphology result of +++ or greater,

reported at level 1c. Reporting, at level 1, of either Blasts or

promyelocytes

18

d. More than 5% frequency of myelocytes &metamyelocytes, neutrophils either <10%or > 90%, Eosinophils > 20%, Basophils >3% OR more than 2% Nucleated RBCs inadults and > 5% in children.

e. Any congenital abnormality of white cells

3. Pathologist / Laboratory director: As the headof the lab holding responsibility for accuracyof data and as an expert morphologist, s/heshould provide the final level of review andconformation of the abnormal findings. Anyslide which has transited - from level 1 throughlevel 2 - without satisfactory conclusion onthe type of abnormality must be reviewed atthis level.

It is very useful to have an authoritative atlasof hematology as reference in the lab.

How to interpret the analyzer data?The hematology counters / analyzers output

mere numbers. These numbers must be convertedto an opinion which has a relation to the patient’scondition. Interpretation of numeric data &abnormality flags generated demands that theperson responsible for the final opinion on thepatient diagnosis is sufficiently familiar with theconcepts leading to the data generation. It is veryimportant that s/he has:

1. Knowledge of the technology employed (e.g.impedance, optical or fluorescent) to countthe blood cells and study their nuclear &cytoplasmic characteristics.

2. acquired basic understanding of how thehistograms and / or scatter plots are generatedby hematology analyzers. Operation manualsare a great help here.

3. Familiarity of the pre-analytical & analyticalfactors which give rise to false positive andnegative flags.

4. Clarity about the strengths and weaknesses ofthe analyzer used and thorough understandingof the abnormalities or lab artifactsassociated with each type of flag.

5. Information - whenever possible – of thepatient’s clinical history & condition, toefficiently correlate with the analyzer data.

6. A system to accumulate and update databaseof the abnormalities and their connection tomedical conditions

Conclusion:High reproducibility of the data favors wider

use of hematology analyzers. There is a significantvolume of literature now to support use ofautomated hematology analyzers in detection anddiagnosis of red cell, white cell and more recentlyplatelet disorders. However, data fromhematology analyzers is of diagnostic value onlyif the user is familiar with the basis & conceptsof flagging and learns to read the histograms andscatter plots generated by these automateddevices. It is important to prepare and strictlyfollow a protocol which is tailored specificallyfor the hematology analyzer under use in thelaboratory. It is of paramount importance to keepin mind the strengths, capabilities andimportantly also the limitations of thehematology analyzer. A well made smear and itsreview are equally important. Communicationwith the clinician in order to ascertain clinicalfacts and data is extremely helpful in abnormalreports so that the CBC can be appropriatelyanalysed and reported. All this will ensure bettercare for the patient.

Recommended reading material:1. Advanced Laboratory Methods in Haematology,

edited by R. Martin Rowan, Onno W. vanAssendelft and F. Eric Preston, published byArnold

2. Dacie & Lewis “Practical Haematology”, editedby Lewis, Bain & Bates, Ninth edition Publishedby Churchill Livingstone

3. Practical guide to – Modern HematologyAnalyzers, by Warren Groner & Elkin Simson,published by Wiley

ACKNOWLEDGMENTS:

Dr. Vijay Parekh,Ex-Director Scientific Affairs,Sysmex Asia Pacific Ltd, Singapore

Dr. Shrikant Kalmunkar,Director Unique Diagnostics

19

Understanding the underlying cause is animportant component (clinical assessment)of transfusion.Assess both quantity and quality of the bloodcells and coagulation parametersAvoid unnecessary transfusion and ‘quick fix’haematology

Points to keep in mind at the time o red cell transfusion• Minimise blood loss• Hb level is not the only deciding factor for

transfusion• Clinician should be aware of risks of transfusion• Transfuse only if clinical benefit• Justify transfusion need on paper• Monitor transfusion appropriatelyRational for blood transfusion

• Providing – the right blood product– in the right quantity– for the right patient.

Bridges the gap between demand and supplyof precious and limited blood / components orblood products.

Situation where transfusions are inevitable (Avoidsingle unit transfusion)

Cardiac compromiseElderlyRapid drop in hb-G6PD haemolysis, AIHA(autoimmune haemolytic anaemia)Active ongoing bleeding

Indications of Whole blood (usually notpreferred in today’s practice)

• Active bleeding• Intrauterine transfusion• Exchange transfusion in neonates• Autologous blood donation

Indications of packed red cells (BCSH guidelines)

1. Do not transfuse if Hb > 10 gm/dl2 Transfusion indicated if Hb < 7 gm/dl3 Transfusion essential if Hb < 5 gm/dl4 Hb 8- 10 gm/dl safe even if cardio-

respiratory problems5 Symptomatic patients should be transfused.

BLOOD COMPONENT THERAPY(evidence base appropriate use of blood components in clinical practice)

• Indications of Fresh Frozen Plasma

• (each bag of FFP over 30 mins with blood set.No irradiation needed. 10-15 ml /kg is std dose)

• For Factor replacement if factor notavailable or unaffordable

• Warfarin immediate reversal• DIC coagulopathy• Coagulopathy going for surgery• Post surgical consumption (bypass/liver

disease)• TTP

FFP NOT indicated in the following

• Hypovolemia correction• Immunodeficiency state• Volume expansion• Nutritional supplement• Prophylactically with massive blood

transfusion• Prophylactically following

cardiopulmonary bypass

• Indications of Cryoprecipitate

• (each bag of cryoppt over 15 mins with bloodset. No irradiation needed. 1-2 bags per 10kg is std dose)

• Hypofibrinogenemia• DIC• Trauma• Renal related bleeding• Fibrin glue (controversial)

• Indications of Platelets ( 4-6 random units isstd adult therapeutic dose)

• (transfuse each bag of random platelets over15 mins with blood filter) (Single DonorPlatelet over 1 hour)• Severe thrombocytopenia• DIC• Supportive during chemotherapy• Platelet dysfunction

• <10, 000 high risk of bleeding• 10-20,000 additional risk factors- fever,

haemostatic failure, spleenomegaly

20

• >50,000 operative fitness in qualitative(functional) plt problem or massivetransfusion DIC

Platelets are NOT indicated in the followingITP (unless bleeding)TTP (thrombotic thrombocytopenic purpura)HUS (haemolytic uraemic syndrome)Drug inducedNon-bleeding thrombocytopenia

Role of Leucocyte transfusions:Not used commonly in clinical practice due

to the advent of better and more effectiveantibiotics, availability of granulocyte colonystimulating growth factors. But most importantly,availability of granulocyte transfusion is verydifficult and costly. The donor has to be mobilizedwith steroids, GCSF or cyclophosphamide in orderto harvest adequate numbers of leucocytes. Manycenters do not have the ability to prepareleucocytes unless they have the apheresismachine. Moreover, there are a large number ofadverse events associated with leucocytetransfusion which could add to the deterrent forsuch transfusion. Once transfused the benefit istransient. Required dose is 1 – 2 x 10 11 cells.

Rationale for Irradiation of blood components(only packed cells and Platelets are irradiated)-To Prevent TAGVHD which is a life threateningreaction with almost 100% mortality

• Transfusion-associated GVHD (TA-GVHD) isan intensive immunologic reaction mediatedby transfused immunocompetentlymphocytes directed against animmunocompromised host.

• TA-GVHD has a rapid onset, severesymptoms, and a poor response totreatment, mortality being over 90%

• Very rare in immunocompetent patients

Patient population needing irradiatedcomponentsare

• Bone marrow transplant recipients• Treated with potent immunosuppressives,

e.g. Fludarabine• Hodgkins lymphoma• Babies, during or post iut• Some congenital immune deficiencies• Directed donations (related donors to be avoided)

Some of the common problems with transfusion ofcomponents that need to be AVOIDED at all costs are

• Blood kept in fridge pre-transfusion• Platelets kept in fridge pre-transfusion• Complete immersion of FFP/CRYO in water bath

during thawing- contamination of port of bag• Long periods of packed cells transfusion –

do not exceed 3 hours• Routine use of hydrocortisone pre-

Transfusion• Inadequate or excess transfusions

Novel rFVII ( activated FVII) drug for profuse bleeding.Indicated along with components in following

• Haemophilia with inhibitors• Acquired haemophilia• FVII deficiency• Glanzmann’s thrombasthenia

• Other extended indications for rFVII could be• PPH (post partum haemorrhage)• Bleeding secondary to Trauma• Post-surgical bleeding• ICH (massive or significant intra cerebral bleed)• Liver/UGI Bleeding• Anticoagulant (warfarin) toxicity reversal

Responsibility of Blood Bank• Donor quality control• Collection quality control• Methodology quality control• Addititonal procedural quality control• Stringent release criteria• Information of how to use the component to

clinicians (administration)• Appropriate use of components

TAKE HOME MESSAGE• Use components• Appropriate component for the appropriate

indication in the appropriate dose and frequency• Appropriate monitoring• Filtered / irradiated components as per

clinical situation• Encourage donation, discourage related

transfusion• Use autologous blood if possible• Avoid single unit transfusion

Dr Abhay A. BhaveMD, FRCPA, Haematologist

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Blood is a very important life saving tissue.In this country there is always a shortage, withpeople either not willing to donate or beleagueredby myths of donations. Hence whatever isavailable should be utilized properly for theproper indications and settings. This way we canensure that people who genuinely need blood getit at the right time to save lives

Autologous Blood transfusion is the collectionand re-infusion of the patient’s own blood.Recommended by the American MedicalAssociation’s Council on Scientific Affairs, anddescribed as the safest Blood product by Bloodbanks themselves, it clearly should be thetransfusion therapy of choice in certain clinicalsituations. The alternative, allogeneic Blood, on theother hand, is collected from a Blood donor otherthan the patient, and transfused into the patient.

Advantages of autologous blood are four fold,1. Avoid exposure to someone else’s blood that

can potentially cause transfusion transmitteddisease (your own blood is the safest blood)

2. Reduce or restrict the need of other’s blood tothe minimum by using most of your own blood(risk reduction),

3. Patients who have rare groups or have aconstitution of blood that makes it difficultfor them to have cross matched blood

4. (this advantage is actually a spin off of the benefitsof doing autologous transfusion) Allogeneic bloodwill be available for patients who genuinelyneed blood in an emergency, accident or forpatients who are on treatment for cancersneeding recurrent blood transfusions.

Five categories of autologous transfusionsare generally recognized

Preoperative autologous Blood donation,transfusion and storage (PABD): units of Bloodare drawn from a patient usually starting (in theshort term case) three to five weeks before anelective surgical procedure and stored fortransfusion at the time of the surgery.Intraoperative hemodilution: Blood iscollected at the start of surgery and the fluidvolume lost is replaced with appropriate IV

AUTOLOGOUS BLOOD TRANSFUSIONsolutions, and then finally, patient’s blood isreinfused after surgery.

Intraoperative Blood salvage: Blood issalvaged by advanced scientific gadgets from thesurgical area during the operation for re-infusionduring or after the surgical procedure. Washingand return of shed blood with machines that canseparate the red cells containing haemoglobinfrom the blood that is collected at the time ofsurgery on table provides the patient with anothersource of autologous blood. This is called redcell salvage.Postoperative Blood salvage: Blood iscollected after the surgical procedure is completeby drainage of the operative area and re-infusedAutologous self stored Blood (Blood banking):your own Blood is preserved in a frozen state foruse by you or your designee at a later time, incase your need of a Blood transfusion arises.

Anyone from age 18 to 70 can donate bloodfor themselves pre operatively as long as theyare fit to donate as per routine criteria for anydonor. In that they should have normal BP, normalsugar, no history of seizures (fits), should not bepregnant, have no fever or focus of infection andhave no cardiac or other organ problems. samestringent standards applied to the drawing ofautologous blood as allogeneic blood.

Since it is the patients own blood the risk isnon existent for transmitting any infection,however, the risk of a reaction during transfusiondue to bacterial contamination during collectionor allergic reaction exists.

This topic has been dogged by controversiesand lack of application in many centres all overthe world. Some of these are fears that the bloodmay be not properly stored, wrong labeling,excess work for blood bank staff to maintainseparate register, clerical errors of issuing thisblood to the homologous pool (ie instead ofpatient who donated for himself, it has gone outas a routine blood bag to some other patient),wastage of units of blood if not utilized and finallythe main problem of issuance of the blood unit tothe homologous pool (common pool) if the bloodhas not been utilized or transfused to the patient.Unfortunately, the medical community has not

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warmed up to the idea especially our surgicaland anaesthetic colleagues

In order to get adequate autologous bloodpreoperatively, we give iron replacement andsometimes erythropoietin injections.

Autologous donation would be appropriateonly for surgeries where blood loss is anticipatedto be one to two units of blood. Unnecessarysingle unit transfusion of allogeneic bloodshould be discouraged , as when the blood lossis less than one unit of blood, there is no need for

either autologous or allogeneic blood transfusionas the haemoglobin can be improved over a periodof time by non-transfusional methods.

This topic has specially been broached bythe editor to popularize this modality especiallyin certain situations such as certain cardiacsurgeries, orthopaedic surgeries, breast cancersurgery and surgeries with minimal vascularity.

Dr. Abhay A. BhaveMD, FRCPA

Report of Blood DonationBlood Donation Camps were arranged by IMA MS jointly with Maharashtra State Blood TransfusionCouncil through its IMA Local Branches on the occasion of Doctor’s Day. Total 47 branches arranged blooddonation camps and collected 2380 bottles of blood. The list of the IMA Local Branches is as follows :

AHMEDNAGAR ........................................... 30AKOLA ........................................................ 30AMRAVATI .................................................. 36AURANGABAD ............................................ 42BARSHI ........................................................ 3BARAMATI .................................................. 32BHUSAWAL ................................................. 27BOISAR ...................................................... 78BULDHANA ................................................... 4CHEMBUR .................................................. 72CHOPDA .................................................... 11DAHANU .................................................... 13DHARASHIV ............................................... 22DHULE ........................................................ 46DOMBIVALI ............................................... 82GONDIA .................................................. 102INDAPUR ................................................... 48KALLAM ..................................................... 24KARAD ........................................................ 25KARANJA .................................................... 28KARJAT ....................................................... 35KOLHPUR ..................................................... 5KOPARGAON .............................................. 15LATUR ......................................................... 50LONAND NEERA ......................................... 20

MIRA-BHAYANDAR .................................... 680MULUND .................................................. 110MUMBAI .................................................. 112MWS .......................................................... 22MWS (ANDHERI) ....................................... 18MWS (MALAD) .......................................... 19NANDURBAR .............................................. 14OMERGA .................................................... 20PANDHARPUR ............................................ 20PANVEL ....................................................... 76PARATWADA ............................................... 48PEN ............................................................ 40PUNE .......................................................... 20SATARA ....................................................... 26SHRIRAMPUR ............................................. 37UDGIR ........................................................ 21VASAI .......................................................... 44WARUD ...................................................... 60PALGHAR .................................................... 23VIKRAMGAD ............................................... 44WADA ......................................................... 25BADLAPUR .................................................. 21.......................................................................

TOTAL ................................................. 2380

We congratulate all the branches/Presidents, Hon. Secretaries and the membersfor their efforts and expects, same corporation in future.

Dr. B.S. Mehta Dr. Hozie Kapadia Dr. Anil SuchakPresident Hon. State Secretary Vice-President

Dr. Jayesh Lele Dr. Rajendra ChawhanHon. Jt. Secretary Convenor

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Great strides have been made in recent yearsin defining the optimal intensity and optimalduration of anticoagulant therapy. In addition,the demonstration that low-molecular-weightheparin (LMWH) is effective and safe whenadministered in weight-adjusted doses withoutlaboratory monitoring has the potential torevolutionize the way we treat patients withvenous thromboembolism.

In contrast, there has been very little progressmade in defining the role of thrombolytic therapyfor the treatment of deep venous thrombosis (DVT),although preliminary study results suggest apotential role for thrombolytic therapy in apreviously undefined subgroup of patients withpulmonary embolism (PE).

After years of use, one of the roles of venacaval interruption in the treatment of proximalDVT has been clarified by data from a well-designed randomized trial.

Finally, little progress has been made indefining the role of surgery in the treatment ofvenous thromboembolism.

Four treatment modalities are for thetreatment of DVT or pulmonary embolism (PE):(1) anticoagulant therapy, (2) thrombolytictherapy, (3) caval interruption, (4) surgery toremove thrombi or emboli.

AnticoagulantsThe most important recent major advances

in the use of anticoagulant treatment for VT andPE are summarized below and shown in Table I.Table I: Advances in Anticoagulant Therapy forVenous Thromboembolism

• Initial treatment with heparin is necessary;

• Reduction in duration of initial treatmentwith heparin from 10 days to 5 days;

• Importance of continuing adequateanticoagulant treatment after hospitaldischarge;

• Introduction of LMWH;

• Elucidation of optimal therapeutic rangewith coumarins; and

• Elucidation of optimal duration ofanticoagulant therapy.

Recent Advances in the Treatment of Venous ThromboembolismExcerpted from a CME by Prof Jack Hirsh Edited by Dr. Abhay A. Bhave

An Initial Course of Heparin Is NecessaryIn 1992, Brandjes and associates confirmed

the value of a longstanding clinical practice bydemonstrating that an initial course of heparinis required for the optimal management of DVT.In this study, patients with proximal DVT wererandomly assigned to receive either heparin orplacebo, followed by coumarin. Those assignedto receive coumarin had a significantly higherincidence of recurrence.

Reduction in the Duration of Induction PeriodWith Heparin

The optimal duration of heparin treatmenthas been evaluated in 2 randomized trials; bothdemonstrated that a 4- to 5-day course of heparinwas as effective as a 9- to 10-day course ofheparin. With the shorter regimen, oralanticoagulants were started within 24 hours ofthe heparin treatment and overlapped withheparin for 4 to 5 days. Reducing the treatmentduration with heparin is important because itallows patients to be discharged from the hospitalearlier and because it reduces the risk of heparin-induced thrombocytopenia.

Low-Molecular-Weight HeparinLMWHs are fragments of unfractionated

heparin produced by either chemical or enzymaticdepolymerization processes that yieldglycosaminoglycan chains with a mean molecularmass of approximately 5000 daltons. Because oftheir reduced size, LMWHs have a longerelimination half-life and a more predictable dose-response when compared with unfractionatedheparin. As a consequence, LMWHs can be givenonce or twice daily subcutaneously in weight-adjusted doses without laboratory monitoring.

Recent trials have shown that unmonitoredsubcutaneous LMWH is at least as safe andeffective as intravenous unfractionated heparinfor the treatment of DVT and PE. Two large trialsinvolving patients with DVT compared the effectsof LMWH given subcutaneously (withoutlaboratory monitoring) twice daily to outpatientsvs the effects of unfractionated heparin given by

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continuous intravenous infusion in-hospital. Therates of recurrent thromboembolism and majorbleeding were similar with both treatments. Otherstudies have shown that LMWH administered oncedaily subcutaneously is as safe and effective as atwice-daily regimen. The safety of outpatient useof LMWH for the treatment of DVT has the potentialto revolutionize the way these patients are treated.

Thrombolytic TherapyStudies have demonstrated that thrombolytic

therapy is superior to conventionalanticoagulation in achieving early resolution ofboth radiographic & hemodynamic abnormalitiesof acute PE when measurements were made withinthe first 24 hours. However, repeat perfusion scans5 to 7 days later revealed no significant differencebetween patients treated with thrombolytic agentsand those treated with heparin.

Based on these observations, there is a bodyof opinion that thrombolytic therapy should bereserved for patients who are hemodynamicallyunstable and that most patients with PE shouldbe treated with heparin (or LMWH). Thistraditional approach is being challenged by theresults of studies that suggest thathemodynamically stable patients with acute PEmight benefit from thrombolytic therapy if theyhave associated right ventricular cardiacdysfunction on echocardiography. Althoughimproved lysis of venous thrombosis on follow-up venography has been demonstrated whenthrombolytic therapy is compared with heparintreatment, insufficient evidence is available toconclude that thrombolytic therapy in patientswith DVT reduces the risk or severity ofpostphlebitic syndrome. In addition, withoutmore definitive evidence of clinical benefit, thereis reluctance to use thrombolytic therapy in thesepatients because its use is associated with a 4-fold increase in risk of bleeding.

Caval Interruption (IVC Filter)Placement of a caval vein filter is usually

considered in patients with a high risk of bleedingor in patients with objectively diagnosedrecurrent PE despite adequate anticoagulation.The risks and benefits of caval filter placementwere addressed in a recent randomized trial in

which 400 anticoagulant-treated patients withproximal DVT were randomly assigned to cavalfilter placement or no filter. The results of thisstudy showed that in patients treated with heparinor LMWH, the insertion of a caval filter reducedthe risk of early PE, but that this initial benefitwas counterbalanced by an excess of recurrentDVT at long-term follow-up. The practicalimplication of this study is that filters arethrombogenic and therefore are a relativeindication for long-term anticoagulant therapy.

Pulmonary EmbolectomyPulmonary embolectomy can be a life-saving

procedure in a patient with massive embolism,but the procedure is often impractical becausemost hospitals do not have the resources,personnel, or facilities to perform this type ofsurgery. Elective pulmonary thrombo-endarterectomy is performed in a limited numberof specialized centers and can be life-saving inselected patients with chronic large-vesselthromboembolic hypertension. The success ofthis procedure is highly dependent on the skilland experience of the surgical team, however.

Long-term Treatment of VenousThromboembolism

After initial treatment with heparin, there isa need for long-term anticoagulant therapy toprevent recurrent venous thromboembolism.Moderate intensity anticoagulation(international normalized ratio [INR] of 2.0 to 3.0)is as effective in preventing recurrent venousthromboembolism and produces less bleedingthan an INR of 3.0 to 4.5. Results of a number ofstudies indicate that patients with VT,complicating surgery, or limited medical illnesshave a relatively low risk of recurrence and shouldbe treated for 6 weeks to 3 months, or until theprecipitating factor resolves. In contrast, thosein whom VT develops in the absence of obviousrisk factors are at higher risk for recurrence onceanticoagulant therapy is discontinued, andshould be treated for 6 months or longer. Long-term therapy is indicated for patients withrecurrent VT and those with continuing riskfactors for recurrence such as metastatic cancerand certain hypercoagulable states (protein C

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deficiency, protein S deficiency, antithrombindeficiency, presence of an antiphospholipidantibody, homozygous factor V Leiden mutation).

SummaryPatients with venous thromboembolism

should be treated with an initial 5- to 7-day courseof heparin or LMWH. The latter can be given in anoutpatient setting. Patients with extensiveiliofemoral thrombosis, major PE, or concomitantmedical illness, as well as those at increased riskfor bleeding, should be treated as inpatients.

Thrombolytic therapy should be consideredin patients with massive PE and may be consideredin those with extensive iliofemoral thrombosis andno contraindications. Vena caval interruptionshould be considered in patients with a high risk of

hemorrhage or recurrent venous thromboembolismdespite adequate anticoagulation.

Oral anticoagulants can be started within24 hours of initiating heparin or LMWH at dosessufficient to achieve an INR of 2.0 to 3.0. Whileoral anticoagulant therapy is safe and effectivefor the long-term treatment of venousthromboembolism, fixed-dose LMWH is areasonable alternative.

Patients with idiopathic venousthromboembolism should be treated withanticoagulants for at least 6 months and probablylonger. Those with transient risk factors can be treatedfor between 6 weeks and 3 months. Indefinite therapyshould be considered in those with metastatic cancer,recurrent venous thromboembolism, and certainhypercoagulable states.

1st July 2010DOCTORS DAY

1st July 2010Camp at Panchawati Vruddha Ashram, Nagpur

8th July 2010Rally on “Exorbitant Hike in Water Bill”

along with Janakrosh.

10th July 2010Inauguration of “Road Safety Abhiyan”

by Hon’ble Mr. R. R. Patil,Home Minister, Maharashtra Govt.

Lt. to Rt. Dr. Anil Laddhad, Hon’ble Shri R. R. Patil,Home Minister, Govt. of Maharashtra,

Shri. Pravinji Dixit, Mr. JainDr. Prashant Nikhade, President, IMA

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What are the common causes of anaemia in thepopulation?Deficiency - iron , vitamin b12 , folic acidHaemoglobinopathies-alpha or betathalassaemia, sickle cell anaemia and otherhaemoglobinopathies Bleeding ( upper/lowergastro-intestinal/ menorrhagia) Anaemia ofchronic disease Rbc shape and size variation(eliptocytosis, spherocytosis, schistocytosis etc)Immune destruction

What is Hypochromic- Microcytic anaemia?When a blood sample is analysed by an

Automated CBC machine, it gives us the RBCindices. MCV (Mean Corpuscular Volume) is thesize of the cells, while MCH (Mean CorpuscularHaemoglobin) is the amount of haemoglobin perred cell. When the size is small and there is lessHb per cell, it is called a LOW MCH AND LOW MCVhypochromic – Microcytic anaemia.

What are the common causes of Hypochromic-Microcytic anaemia?Iron deficiencyBeta thalassaemia trait (minor)Sideroblastic anaemiaAnaemia of chronic diseaseLead poisoning.

How to diagnose Iron deficiency anaemia?• History of pica / worms / poor nutrition/

chronic blood loss / mennorhagia• Platynychia (flat nails) or koilonychias

(spooned out nails)• Hypo-micro anaemia on routine cbc test• Smear examination showing classic rbc changes• S. Iron studies• Low s .ferritin• Stool occult blood for gastro-intestinel blood loss

How to diagnose Iron deficiency anaemia on a CBCreport?Low Hb Low RBC countLow MCV Low MCHLow MCHC (Mean Corpuscular HaemoglobinConcentration) Raised RDW

How to diagnose Beta Thalassaemia trait on a CBCreport?

SOME COMMONLY ASKED QUESTIONS IN ANAEMIA.Dr Abhay A. Bhave, MD, FRCPA

Common in certain ethnic communityLow hb, low mcv, low mch (hypochromic- microcytic)Normal rbc count and normal mchcHb electrophoresis shows raised haemoglobin a2DNA analysis for specific gene mutation notalways necessary but is confirmatory

What is a Macrocytic anaemia?When the size of the RBC is big (raised MCV) it is amacrocytic anaemia.

What are the causes of a macrocytic anaemia?Megaloblastic anaemia (Vitamin B12 and Folatedeficiency) MDS (Myelodysplastic Syndrome)Haemolysis Hypothyroidism Liver diseaseAplastic anaemia, Myeloma and other marrowfailure syndromes

How to diagnose a Megaloblastic anaemia?Macrocytic anaemia with low RBC count andraised RDWPeripheral smear shows macrocytosis withhypersegmented neutrophils & macroovalocytesThe levels of S.B12 or S. FOLATE are lowThere is raised S.LDH, Low RETICS and raised S.IND BILIRUBINPernicious anaemia as a cause of B12 deficiencycan be diagnosed if Intrinsic factor antibody andor Parietal cell antibody is positive in the serum.Upper GI scopy may reveal Atrophic gastritis onappearance or biopsyS. Homocysteine may be high in vitamin B12 deficiency

How to diagnose Haemolytic anaemia?Low hb, normal / raised mcv Reticulocytosis,Raised LDH and indirect bilirubinLow serum haptoglobinIf the patient has positive DIRECT COOMBS TEST,then it is called AIHA (auto Immune HaemolyticAnaemia.

If the patient has an INDIRECT COOMBS TESTpositive then this is suggestive of analloimmunised anaemia most likely secondary toan alloantibody to a previous transfusion.

Haemoglobinopathy can be diagnosed by HBELECTROPHORESIS to diagnose thalassaemia, sicklecell anaemia and other haemoglobin disorders.

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How to approach a patient with anaemia inroutine practice?• Take a detailed history and examination for

possible cause of low HB• Bleeding versus non bleeding cause• Haemolysis (jaundice) versus non-haemolytic• CBC and identify type of anaemia (hypo-micro,

macro or normocytic anaemia)• Investigate causes as per differential

mentioned above for each category• Replacement therapy as per the diagnosis• CBC after 2 weeks to see response• If not responding- refer to specialist

What are the salient points with regard tomanagement of anaemia?

• Cbc is the best test for anaemia• Need to assess cause of anaemia

(pathophysiology)• Diagnose with relevant investigations

(evidence based medicine )• Many oral iron preparations available / use

at least 60-120 mg of elemental iron daily• Parenteral route of Iron whenever there is poor

compliance to oral therapy• Replace vit b12 / folate wherever the proof of

deficiency is available• Correct underlying cause• Avoid transfusion if possible, use

erythropoietin as alterrnative• Assess response at intervals

Algorithm for anaemiaLOW HAEMOGLOBIN

HYPO-MICRO LOW MCV LOW MCH)

RBC COUNT / MCHC

NORMAL RBC NORMAL MCHC LOW RBC LOW MCHC SMEAR EXAMINATION

THALASSAEMIA LIKELY IRON DEFICIENCY LIKELY BASOPHILIC STIPPLINGS. Iron studies

S. FerritinHB ELECTROPHORESIS LEAD POISONING

RAISED A2 NORMAL A2 S. LEAD LEVEL

B THALASSAEMIA á THALASSAEMIAMACROCYTIC ANAEMIA

B12 DEFICIENT NOT DEFICIENT

TREAT DCT POSITIVE DCT NEGATIVE

TREAT RULE OUT ALCOHOLISMLIVER DISEASE AND HYPOTHYROID

IF ABOVE NORMALBONE MARROW EXAMINATION

APLASTIC ANAEMIA MYELOMAMYELODYSPLASIA

INVESTIGATE ACCORDINGLY

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DONATION DRIVE AT VARIOUS IMA BRANCHES

Blood Donation Camp at Mumbai Blood Doantion Camp at Amravati Blood Donation Camp at Baramati

Blood Donation Camp at Gondia Blood Donation Camp at Pandharpur Blood Donation Camp at Saoner

Blood Donation Camp at Nandurbar Blood Donation Camp at Indapur Blood Donation Camp at Udgir

IMA KALAMB BRANCH

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Thalassemia is one of the commonest singlegene disorders representing a major healthburden in India and in the world. According tothe data in the executive summary of the Marchof Dimes Global survey on birth defect conductedin 2006, five common serious birth defects ofgenetic or partially genetic origin in 2001 were:(1) congenital heart defects (1,040,835 births);(2) neural tube defects (323,904 births); (3) thehemoglobin disorders, thalassemia, and sicklecell disease (307,897 births); (4) Down syndrome(trisomy 21) (217,293 births); and (5) glucose-6-hosphate dehydrogenase (G6PD) deficiency(177,032 births). Combined, these five conditionsaccount for about 25 percent of all of birth defectsof genetic or partially genetic origin.1 It isestimated that more than 200 million people arecarriers of the â thalassemia gene in the worldand about 30 million of them are in India. Everyyear about 10,000 children are born withthalassemia major in India accounting for 10%of thalassemia major births world wide2. Whilebone marrow transplant (BMT) is the onlycurative option, the available remedy formanaging thalassemia is lifelong bloodtransfusion and removal of iron by chelationtherapy. Both of these options remain elusive tomany children with thalassemia due to the highcost involved: RS 6lakhs for a BMT and a recurrentannual cost of about RS 2lakhs for transfusion

and chelation with desferrioxamine. Only 5-10%of children born with thalassemia in India receiveoptimal treatment due to non-affordability3.

Therefore, the emphasis is a shift fromtreatment to prevention of the birth of suchchildren in the future through carrier detectionand prenatal diagnosis.

CARRIER DETECTIONCarriers of Beta thalassemia do not have any

clinical abnormality and do not suffer from anysymptoms. Carriers can be suspected byestimation of Hemoglobin which is mildly reduced8.5-11g% (however carriers can have hemoglobinin the normal range). However most carriers havea reduced red cell volume (Mean CorpuscularVolume) and therefore a mild reduction inHemoglobin and a low MCV would make onesuspect that an individual is a carrier. Irondeficiency also results in a reduction in the Hband MCV and therefore in populations where irondeficiency is common one cannot be certain. Thereare various indices which have been used todistinguish beta thalassemia carrier state fromiron deficiency. Bessman index (RDW), Mentzerformula (MCV/RBC), England & Fraser formula(MCV-RBC-5 X Hb-3.4, Shine & Lal formula (MCV2X MCH/100), Ehsani formula (MCV-10 X RBC),Srivastava formula (MCH/RBC), Green & Kingformula (MCV2X RDW/ Hb X 100), red distributionwidth index RDWI (RDW X MCV/RBC), RDW/RBC,are some of the formulae used to separatethalassemia carriers from iron deficiency.

Dr. Mammen Chandy

DEVELOPING A NATIONAL THALASSEMIA CONTROL PROGRAM FOR INDIADirector, Tata Medical Centre,Professor and Head, Hematology DepartmentKolkata, West Bengal

1. Chairman: Task Force on Human Genetics and Genome analysis.Department of Biotechnology.Government of India. Ministry of Science and Technology. 2009

2. Member Medical Biotechnology Development Board Department ofBiotechnology.Government of India. Ministry of Science and Technology. 2005

3. Scientific advisory committee .Basic Medical Sciences Division. IndianCouncil of Medical Research.

4. Scientific advisory committee: Institute of Immunohaematology.5. Scientific advisory committee; Tata Memorial Hospital.6. Editorial Board. Indian Journal of Haematology.7. Reviewer : Indian Journal of Medical Research.8. Reviewer: National Medical Journal of India.

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However the sensitivity of around 90% and aspecificity of 85% mean that these cannot be usedfor a definitive diagnosis in a thalassemiascreening program. 4

NESTROFTThe naked eye single tube osmotic fragility

test has been used for thalassemia screening witha high sensitivity but a lower specificity. This isvery cheap but cannot reliably differentiatebetween thalassemia minor and iron deficiency.5,6,7 The DCCP test is useful for studying HbE butagain is not totally reliable.8,9

MEASUREMENT OF HB A2 LEVELSHb A2 can be measured by electrophoresis

and elution of the A2 band and quantitation byspectophotometry. However a precision of 0.5 to1% is required and this is difficult to obtainreliably on a mass scale by electrophoresis. 10

HPLC : This is the most reliable technique forquantifying the HbA2 levels. This can be doneusing a commercial or in house developed micro-column. However reproducibility is not good andmay vary depending on the skill of the laboratory.Automated systems dedicated to estimate HbA2are the most reliable and accurate way ofquantifying the HbA2. The BioRad platforms havebeen used extensively all over the world forreliable quantitation of the HbA2: the twomachines used are the Variant and the D10. Aone microliter sample in a transport buffer canbe sent to the reference laboratory and is stablefor 7 days at room temperature.11,12

PROPOSAL FOR CARRIER DETECTION FOR INDIAThe most sensitive and reliable method

should be used even if it is expensive sincenegative publicity from a wrong result canadversely affect the whole program: there HPLCshould be the preferred method and costs can benegotiated to around RS 100 per sample if thevolumes are large. Since Iron deficiency is amajor public health problem diagnosis ofscreening for iron deficiency by ZPP should becoupled to he carrier detection program so thattwo public health problems can be solved.13,14

Two ml of blood to be collected byvenupuncture using a disposable syringe. Oneml will be dispensed into an EDTA tube: this willbe used for Hb, MCV and RDW determinationusing an electronic cell counter at the collection

center or at the closest testing laboratory. Onemicroliter of blood will be taken from the EDTAsample using an automatic pipette andtransferred into one ml of buffer in an Eppendorftube and this will be sent by courier to the HPLClaboratory. ZPP will also be estimated at thereference laboratory. The other one ml will be putinto a plain glass tube, clotted and the separatedserum will be stored frozen for ferritin estimationin a proportion of the sample as QC for the ZPP.This will be done at the central laboratory. Hb A2will be estimated on the BioRad Variant using thebeta thal short program. Any sample with a value>3.5% A2 will be designated as a beta thal carrier.

All the results of the laboratory tests will becommunicated to the individual with appropriateadvice. If the person tested is found to be a carrierhe/she will be advised to test family membersand genetic counseling regarding antenataltesting will be provided.

Procedure for screening1. Individuals who seek testing as a result of the

TV documentary will go to designatedcollection centers where personal data willbe entered and the sample collected afterpayment of RS 50.

2. Screening facilities will be provided at allantenatal clinics in the state both in thegovernment and private sector. All women whocome for the antenatal check up before 20weeks will be screened. If found to be carriersthe obstetrician will communicate theinformation and the husband will be advisedand if both are carriers they will be counseledregarding antenatal diagnosis

3. Screening of college students will continuealong with information campaigns in allcolleges in the state.

4. Mobile vans will go to the villages equippedwith a cell counter and collect samples fromall those who are willing to be tested afterinformation have been provided by a film andpuppet show.

CREATING AWARENESSPRODUCTION OF A SHORT DOCUMENTARY

Modern mass media is a powerful tool toinfluence human behavior. Advertising throughtelevision can significantly alter individual’schoice and this is a multimillion dollar business

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used by manufacturers to sell a product. We needto develop a one minute documentary onthalassemia using film personalities, which isso powerful that anyone watching would like toknow his or her carrier status and seek laboratorytesting and be willing to pay for the same.

SHOWING THIS DOCUMENTARY ON TELEVISIONThis documentary should be shown three

times a week during prime time viewing,systematically for a period of two years and thecost of doing this will should bee met from thebudget of a national thalassemia control program.

VILLAGE OUT REACHVillages in a target state should be covered

systematically over the year with a short film/skit/puppet show followed by collection of bloodsamples. Results will be communicated back tothe people with counseling and iron replacementfor those who are deficient.

COLLEGE STUDENT PROGRAM/ CORPORATESPresentations followed by blood collection

and testing followed be communication of resultsand counseling should be done through the yearin colleges.. The mandatory testing order fromthe Saurashtra University can be used for thisand applied to other states also. Mailers can besent to all corporate organizations followed byorganized testing. All groups who are carryingout such activities should be used.

ANTENATAL CLINICSPosters should be displayed in all antenatal

clinics and a system of collection of samplesorganized. A campaign to educate obstetricianson the importance of testing the couple for carrierstatus will be started and implemented throughthe Obstetric Societies.

EXTENDED FAMILY TESTINGThis should be encouraged since this is a

very cost effective way of carrier detection in agroup who would be highly motivated.

CREATING INFRASTRUCTURE FOR MOLECULARAND ANTENATAL DIAGNOSIS

This is essential since a nationalthalassemia control program will be successfulonly if carrier couples have easy access toreliable antenatal diagnosis. One center whichcan do a comprehensive screen for the molecular

defect must be available in each state where theprevalence is high. This must be linked to allcenters in that state which are capable of doingchorionic villous sampling and adequate counseling.

Management of ThalassemiaChildren with thalassemia major are treated

in special clinics in some parts of the country andgood day care transfusion centers have beenestablished where the transfusion is free. Howeverthis is not the case in most parts of India wheretransfusion is erratic and many children have beeninfected with hepatitis viruses and a few with HIV. 15

Very few families can afford regular chelationwith desferal, while many receive sub-optimalchelation with kelfer. Over 70% of children dieprematurely with iron overload in their teens ifthey have been transfused. The Christian MedicalCollege Vellore has performed 120 transplantsfor children with thalassemia and 85% of childrenwho are well chelated and transfused are curedbut only 60% of poorly managed children surviveafter transplant.16 So the outlook for a child withthalassemia who is born into a lower middleclass or poor family in India is bleak, Hence thenational control program must also improve thequality of care for children with thalassemia.

ECONOMICS10,000 children born each year with

thalassemia and it costs RS 200,000 to transfuse& chelate a 30 kg body weight child for one year.Therefore the annual cost of looking after 500,000if all children born with thalassemia were tosurvive would be: 500,000 x 200,000 = RS 10,000crores and 100 crores if only 1% were to survive.

Therefore a national program with aninvestment of 100 crores per year will be adequatereturn of investment if the there is a reduction inincidence of new births of children withthalassemia by 10%

India now is claiming its own place amongthe nations of the world and a country which iscapable of putting a satellite into space, has athriving innovative pharmaceutical industry andsoft ware professionals who can competeglobally cannot afford to ignore this problem ofthalassemia: if there is political will a nationalthalassemia control program can be imitated andsuccessfully managed.

Dr. Mammen Chandy

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DR. TAPAN K. SAIKIAHead of Medical OncologyPrince Aly Khan Hospital

Mazagaon, Mumbai 400010&

Blood Stem Cell Transplant PhysicianJaslok Hospital & Research Centre

Mumbai 400026

INVESTIGATION & MANAGEMENT OF LEUCOCYTOSIS

In physiological condition the white cellproduction in the bone marrow and their releaseinto the peripheral blood is tightly controlled bymolecular mechanisms. As it is a very dynamicsystem, a diurnal variation of total leucocytecount occurs. To define leucocytosis a WBC count>11,000/ìL is required; however laboratories mayhave their own standardization. It is one of themost common hematologic abnormalities (nextonly to anemia) encountered in clinical practice.There is no guideline how long this high countshould remain before it can be defined asleucocytosis. A practical decision could be todocument such a raised count at least 2 analyseson 3 days interval in an otherwise healthyindividual. In presence of acute bacterialinfection however, the dynamics could vary ondaily basis. Focus on the manual differentialcount is mandatory to identify the subtype ofleucocytosis. Leucocytosis may occur at any ageand could be acute, insidious, transient orsustained.

As multiple conditions may cause transientor sustained leucocytosis, it is imperative tofollow a guideline for relevant investigations andcorrect diagnosis.

1. A thorough medical history and clinicalexamination. There is no substitute for these.An acute or chronic infection could often besuspected on careful history elucidation and

physical findings. Hepatosplenomegaly,lymphadenopathy, purpura/ecchymoses, andsternal tenderness immediately raise thepossibility of hematological malignancies. Ageat leucocytosis could be informative. Forexample, though rare, leucocytosis of new bornand infants could be a self limitingmyeloproliferative condition or lead to a frankacute leukemia.

2. Laboratory investigations –a. Complete blood count (CBC) with manual

WBC differential counts & morphologicaldetails

b. Based on the manual differential countfurther investigationsi. Identification of an infective etiology

1. Bacterial, fungal, parasitic, etc

ii. Marrow studies1. Malignancies like leukemia,

myeloproliferative neoplasms,lymphoma, solid tumors, infections.

iii. LAP score (leucocyte alkaline phosphatase)1. To differentiate between chronic

myeloid leukemia and leukemoidreactions

iv. Cytogenetics & Molecular studies1. To identify pathognomonic abnormalities

of various hematological malignancies

v. Radiological investigations1. Infections, leukemia, lymphoma, solid

tumors

Involved in an Asia-centric program known as Asia CMLFoundation that will propagate research, patient care andeducation.

Involved in a patient oriented program called MyelomaIndia Foundation (MIF).

1. Patron–Deepsikha, an NGO, working for cancer patientsfrom N-E India

2. Patron–Brahmaputra Cancer Foundation, working forcancer patients

LIST OF PUBLICATIONS : 170 in peer reviewed journals.

CHAPTERS IN TEXT BOOKS : Regular contributor to the Chapterson Hodgkin’s Lymphoma, Chronic Myeloid leukemia

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vi. Lymph node or any other pathologicaltissue biopsy for histo-pathological& relevant special studies

1. Lymphoma, granulocytic sarcoma,solid tumors

vii. Others (based on the pathology)1. Tissue injury2. Allergy3. Vasculitis

Causes of leucocytosisA manual differential count immediately

hints a possible pathology. Based on this,leucocytosis can be subcategorized. Leukemoidreaction, a reactive condition where leucocytosiswith or without immature cells occur followingstimulation of the marrow by various cytokines.It usually subsides with control of basicpathology. Basically, leucocytosis can result froma normal marrow or an abnormal marrow. Inpresence of normal marrow the morphologicalchanges are absent or minimal. Table 1 showsthe details.

Table 1: Causes of leucocytosis1. Neutrophilia

a. Acute bacterial infections, speciallypyogenic

b. Fungal infections like invasive candiadiasisc. Sterile inflammation

i. Myocardial infarctionii. Burns

d. Solid tumors like lung cancer, hepatobiliaryneoplasms, stomach and colon. Thesetumors are known to produce hematopoieticgrowth factors like G-CSF

e. Drug induced – lithium, hematopoieticgrowth factors like G- or GM-CSF

f. Surgery – immediate after splenectomy

2. Eosinophiliaa. Allergic disorders

i. Bronchial asthmaii. Hay feveriii. Drug allergiesiv. Allergic skin diseases like Pemphigus,Dermatitis herpetiformis

b. Parasitic infectionsc. Malignancies

i. Hodgkin’s lymphomaii. Some subtypes of NHLiii. Some types of leukemia both acute andchronic

d. Systemic autoimmune diseasese. Some forms of vasculitisf. Cholesterol embolism

3. Basophiliaa. Chronic myeloid leukemia, systemic

mastocytosis

4. Monocytosisa. Chronic infections like tuberculosis,

bacterial endocarditis, rickettsiosis,malaria

b. Infectious mononucleosisc. Systemic autoimmune diseases like SLEd. Inflammatory bowel diseases like

ulcerative colitis

5. Lymphocytosisa. Chronic infections like tuberculosis,

brucellosisb. Viral infections like hepatitis, CMV infectionc. Malignancies like chronic lymphocytic

leukemia, other chroniclymphoproliferative disorders, multiplemyeloma or other plasma cell disorders

6. Immature cell leucocytosisa. Acute leukemia (increased blasts cells)

i. Acute leukemia (ALL, AML)ii. Chronic leukemia

1. CML2. Other myeloproliferative neoplasms

(MPNs) like polycythemia vera,idiopathic myelofibrosis, essentialthrombocytosis

iii. Lymphomas1. Mantle cell lymphoma

Management of leucocytosisOnce a correct diagnosis can be achieved,

the management should be of the primary cause.

InfectionsAppropriate antimicrobial therapy will lead

to normalization of leucocyte counts in acuteinfections. Many physicians follow the countsclosely for surrogate knowledge of infection

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control. This may be a practical approach butthe level of evidence has not been studiedcarefully. In chronic infections there is alwayssignificant delay in normalization of counts.Allergic conditions

Appropriate management of asthma, hayfever, autoimmune diseases should normalizeeosinophils within a few weeks. Similarly inparasitic infections antihelmenthic therapyeosionophils revert to normal level.

MalignanciesThis is where a need for specialized

investigations and care comes in. Based on thetype of malignancy various investigations wouldbe called for. For example, the chroniceosinophila of myeloproliferative disorders mayhave different molecular abnormalities. This isimportant as some of these could be treated veryeffectively with currently available smallmolecule tyrosine kinase inhibitors like imatinib.Certain acute lymphoblastic leukemia (ALL)present with associated eosinophila and itnormalizes after chemotherapy or otherindicated therapy like hematopoietic stem celltransplantation. In AML, eosinophilia is usuallyassociated with a good prognosis cytogeneticabnormality.

Current treatment of choice for CML is anoral tyrosine kinase inhibitor (TKI), imatinib 400mg once a day. This produces complete

hematologic response in >95% patients andmeaningful cytogenetic/molecular response in~80% and ~50% of patients. The event free survivalat 7 yr is 85% in responders. Newer TKIs are morepowerful and are being approved for use imatinibresistant cases or even as a first line therapy. InCML some patients receiving imatinib therapymay develop moderate eosinophilia. This is notharmful. Allogeneic hematopoietic stem celltransplant which can cure CML is now done onlyin selected cases. In Hodgkin’s lymphomaeosinophilia is usually associated with anadvanced disease but has no prognostic value.

Clinical tips1. A detailed medical history of present, past,

medications, known allergy, habits, and placesof residence (present & past).

2. A detailed physical examination.

3 A careful look at the full CBC. One shouldalways insist on a manual differential WBCcount. Currently, multiparameter counters giveplenty of information. For example, a mildleucocytosis with thromobocytosis may raisethe suspicion of a myeloproliferativeneoplasm which may not be seriousnonetheless helps in diagnosing the pathology.Immature cells should always raise thepossibility of hematological neoplasm.

DR. TAPAN K. SAIKIA

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Haematopoietic Stem Cell Transplantation

Brig Velu Nair, VSM**MD(Med), FACP(USA), FUICC (UK), MNAMS, FICP, FACA (USA),FIACM, FUICC (USA), FISHTM

Consultant (Medicine & Clinical Haematology)

Dept of Haematology & Bone Marrow Transplantation, Army Hospital(R&R), Delhi Cantt-110010

Dean, Army College of Medical Sciences, Delhi Cantt-110010

INTRODUCTION :Haematopoietic stem cell transplantation

(HSCT) is a life-saving procedure for a number ofmalignant and non-malignant diseases whichwere considered incurable in the past. The termbone marrow transplantation (BMT) is usedsynonymously with HSCT. Technically HSCT is thecorrect nomenclature as stem cells can besourced from the bone marrow (BM) for BMT, fromPBSC for peripheral blood stem cell transplant(PBSCT) and umbilical cord blood (UCB) for cordblood transplant (CBT). Stem cells areimmunophenotypically labeled as CD34+ cells. Inallogeneic (allo) HSCT the stem cells are harvestedfrom an HLA matched donor, either related orunrelated. In autologous (auto) transplants, thepatient’s own stem cells are harvested. In HSCT,the diseased marrow is ablated usingchemotherapy ± radiotherapy which is referred toas conditioning followed by stem cell rescue. Thereis high incidence of relapse in auto-HSCTs becauseit is difficult to achieve 100% ablation of themalignant clone. The relapse rates are lower inallo-HSCT due to the added immunological effectof graft versus tumor or graft versus leukemia (GVL)effect which is lacking in auto- HSCT.

HISTORICAL BACKGROUNDThe first use of BM in the present context of

HSCT was done by Schretzenmyr in 1937. Followingthe Hiroshima and Nagasaki disaster in 1945,radiation biologists Jacobson & Lorenz pioneered themice model demonstrating effect of radiation on BMand spleen. This stimulated further experimentedwork in the field of stem cell biology and HSCT.

E. Donnell Thomas, pioneered the techniquefor HSCT and Jean Daussett who discovered the

human leucocyte antigen (HLA) system whichrevolutionized the field of HSCT both were awardednobel prizesz for their path breaking reseach. Inthe 1970s, the Centre for International Blood andMarrow Transplant Research (CIBMTR) and theEuropean Group for Blood and MarrowTransplantation (EBMT) was set up. The 1980s sawthe entry of new drugs such as ciclosporine forGVHD prophylaxis, newer generation of antivirals,antifungals and antibiotics which helped reducetransplant related morbidity and mortality due toinfections. In the 1990s discovery of PBSC and cordblood stem cells was a landmark in establishingstem cell sources other than the BM.

Indications for HSCTsThe indications have been rapidly expanding

over the years (table 1). Besides high riskhaematological malignancies, various geneticdisorders and BM failure syndromes, it is alsobeing offered for autoimmune disease (AID).

Table 1.Indications for HSCTIndications for Allogeneic HSCTMalignancy: Acute myeloid leukaemia , acutelymphoblastic leukaemia, chronic myeloidleukaemia, chronic lymphocytic leukaemia,myelodysplasia, hodgkin’s disease, non-hodgkin’slymphoma, multiple myeloma

Immunodeficiency : Severe combined immunodeficiency,Wiscott-Aldrich syndrome, adenosine deaminasedeficiency, x-linked lymphoproliferative syndrome,cartilage hair hypoplasia.Defective Haemopoiesis:

Aplastic anaemia, acquired severe aplasticanaemia, congenital aplastic anaemia (Fanconi’sanaemia), post radiation injury, sickle cell

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disease, thalasaemia major, Kostmannsyndrome, chronic granulomatous disease,Chediak-higashi syndrome, adhesion moleculedeficiencies, platelet disorders, glanzmannthrombasthenia, Bernard-soulier syndrome,metabolic storage disease, osteopetrosis,familial haemophagocytic syndrome.

Indications for Autologous HSCT :Acute myeloid leukaemia, acute lymphoblastic

leukaemia, chronic myeloid leukaemia, lymphomaand hodgkin’s disease, multiple myeloma,neuroblastoma, breast cancer, germ cell tumor,autoimmune disorders, scleroderma, multiplesclerosis, rheumatoid arthritis, SLE

Autologous HSCT : Most commonly used formultiple myeloma and lymphoma patients. It hasalso been used for acute & chronic leukemiasand solid tumors (breast, neurobolastoma andlung neoplasms). BM or PBSC is harvested fromthe patient itself, while the disease is inremission. This graft is then cryopreserved at -800 C (freezers) or at -1800 C (liquid nitrogen).The harvested graft is stored in a cryoprotectantbag after mixing with DMSO which is acryoprotectant. Following this the marrow ismyeloablated with high dose chemotherapy and/or radiotherapy followed by reinfusion of thecryopreserved BM or PBSC.

Allogeneic HSCT : The chances of finding arelated donor (ideally a sibling) is 25-30% whileit increases to 50-70% in case of [matchedunrelated donor (MUD)] MUD transplants wherea donor is sought from a web based registry.Earlier allo-HSCTs were myeloablative but of late,non-myeloablative transplants are being doneincreasingly in older patients. This is thetreatment of choice for all high risk/ refractoryhaematogical malignancies, bone marrow failuresyndromes and several genetic disorders.

Source of HSCBone MarrowIn BMT, the haematopoietic stem cells (HSCs) arecollected from the pelvic bone (posterior iliacspine) of the donor using Jamshedi BM harvestneedles under general anesthesia.

Peripheral Blood Stem CellsThe advantages and disadvantages of PBSCT

are listed in table 2.PBSC represents the richest

source of stem cells and engraftment has beennoted to be earlier compared to BM or CB. As thelymphocyte content is higher in PBSC the incidenceof GVHD (especially chronic GVHD) is higher inPBSCT compared to BMT or CBT.Table 2: The advantages & disadvantages of PBSCT

Advantages D i s a d v a n t a g e s

Reci 1. Faster neutrophil recoverypient 2. Faster platelet recovery

3. Faster immunologic recovery Higher incidence of4. Less IV antibiotics chronic GVHD5. Shorter hospitalization6. Lower cost7. More GVL (?)

Donor 1. No general anesthesia 1. Venepuncture or central line

2. No marrow harvest 2. Side effect from growth3. No hospitalization stimulating factors of

citrate used & PBSC harvest

Umbilical Cord BloodNewer techniques using ex-vivo expansion of

cord blood units or the use of two cord blood unitsfrom different donors are being explored to allowcord blood transplants to be used in adults. Cordblood has a higher concentration of HSCs than inadult blood. They are naïve and less immunogenic,thereby causing less GVHD. Cytotoxic cells seemsto comprise mostly of a NK cell subset.

Engraftment: The presence of DNA pattern of thedonor type in the blood and BM cells of therecipient, confirms engraftment. It takes 2 to 3weeks for stem cells to re-grow (engraft) in theBM. Haematopoietic growth factor, G-CSF is usedpost transplant to enhance engraftment. Theengraftment is monitored by chimerism studies.Reconstitution of the immune system takes severalmonths predisposing these patients to infections.STEPS INVOLVED IN HSCTDonor Selection & HLA Matching : Ideally a siblingdonor with matched major HLA loci stands thebest chance for a successful HSCT. The outcomeof allo-HSCT is dictated by a set of immuneresponse genes clustered together as the HLAsystem which is analogous to the majorhistocompatibility complex (MHC) in animals.However, minor histocompatibility loci are notmatched and this can lead to GVHD and graft-rejection. HLA loci A, B and D R are done for all

37

related transplants and in addition HLA C, DPand DQ are also done for unrelated transplantedmolecular techniques.

Establishing a Venous Access: Since a long-termvenous access is required for several weeks, adouble or triple lumen central sialistic flexiblecatheter is used, double lumen being preferred.This is introduced through a subcutaneous tunnelin the pectoral region and then inserted into theinternal jugular or subclavian vein. Bloodsampling is also done using these lines.Meticulous care of these central lines is requiredto prevent catheter sepsis.

(b) Conditioning:Myeloablative: Conditioning or preparatoryregimens containing high dosechemotherapy ± radiotherapy are used toablate the abnormal clone of cells and createspace in the BM for the new graft. It alsosuppresses the patient’s immune system toprevent rejection of the new graft.Non-myeloablative : Reduced intensityconditioning, using lower doses of chemotherapyand radiation, is an evolving approach oftreatment which is less intensive and less toxicreducing transplant related mortality (TRM).

(a) GVHD Prophylaxis: For GVHD prophylaxisvarious protocols using combinations ofimmunosuppressive drugs are in use. Acombination of ciclosporine A (CSA) withMTX is a commonly used protocol. In casesof CSA intolerance, mycophenolate mofetil/tacrolimus can replace CSA.

(b) Stem Cells Harvest and Infusion: A target celldose of total nucleated cells of 3 or more x108 cells/kg or CD34 (stem cells) of 3 or morex 106 cells/kg is harvested followed byinfusion into the patient either directly, ifdone within 48 hours (stored at 40C) orfollowing cryopreservation when infusion isdone later than 48 hours.

(d) Supportive Care: Success of a transplantprogram relies heavily on an efficientsupport system, which includes blood bankfor blood component support, goodmicrobiological lab, molecular lab for HLAtyping and well trained transplant team ofmedical and nursing staff. In tropical

conditions, protective isolation is importantbecause of high risk of infections whenneutropenia occurs following myeloablation.However, In many centers in the west, HSCThas been successfully done withoutisolation.The nutritional status is often poorbecause of the underlying disease, occurrenceof GVHD, sepsis and psychosocial issues likedepression. Parenteral nutrition is resortedto, once the patient develops mucositis andis unable to take oral feeds.

ABO INCOMPATIBILITYHSCT can be performed despite ABO

incompatibility unlike solid organ transplantation,Major ABO incompatibility consists of the presenceof ABO antibodies in the recipient directed againstABO antigens of the donor e.g. O group recipientand A, B or AB donor.. Minor ABO incompatibility isthe presence of ABO antigens on recipient’s redcells which are lacking in the donor, who hasantibodies against the recipient’s red cells, e.g.group O donor into group A, B or AB recipient. It isreferred to as major and minor or ‘bidirectionalincompatibility’ if group A donor and group Brecipient or vice-versa is transplanted.

Blood Component Support: Haemolysis of donorRBCs by isoagglutinins in the recipient can causeimmediate haemolysis and formation ofisoagglutinins by donor lymphocytes againstrecipient’s ABO antigens can produce hemolysisafter engraftment in ABO mismatched transplantsas lifespan of residual recipient RBCs followingallo-HSCT is about 40 days whereas circulatingrecipient’s IgG and IgM antibodies have a half lifeof approximately 20 days and 6 days respectively.

COMPLICATIONS :The first 100 days post HSCT is referred to as

the early post transplant period. Considerablemorbidity and mortality is noted during this periodespecially in allo-HSCT. These early complicationsare often related to the conditioning regimen,metabolic, fluid &electrolyte disturbances,microbial infections secondary to the neutropenicstate, haemorrhagic episodes secondary tounderlying thrombocytopenia, VOD and acuteGVHD. Some of the complications, listed in table 3,will be discussed in more detail.

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Table 3. Early post-transplant complications1. Infections: Bacterial, viral, fungal, protozoal2. Gastrointestinal-

(a) Nausea, vomiting(b) Mucositis, oesophagitis & gastroduodenitis.(c) Diarrhoea and typhilitis.(d) Pancreatitis and cholecystitis

3. Hepatic veno-occlusive disease4. Interstitial Pneumonitis5. Renal and urinary tract complications

(a) Acute renal failure(b) Haemolytic uremic syndrome(c) Acute tumor lysis syndrome(d) Haemorrhagic cystitis

6. Cardiovascular complications: Pericarditis,endocarditis, hypertension

7. Metabolic complications(a) SIADH(b) Fluid and electrolyte imbalance

8. Neurological complication: Encephalopathy,seizures,CNS haemorrhage, thromboticthrombocytopaenic purpura

9. GVHD: Acute & chronic GVHD

Infections : The HSCT recipient isimmunocompromised both for humoral and cellmediated immunity. Once normal immunity is regainedthen the HSCT recipient has to undergo revaccinationas per an immunisation schedule provided there isno GVHD and patient is not on immunosuppressiveagents. There are three phases for opportunisticinfections to occur in a transplant patient.(a) Pre-engraftment phase (2-4 weeks post-

HSCT): Febrile neutropenia is commonly dueto gram positive and negative bacteriafollowed by candida and aspergillus fungalinfections. HSV viral reactivation is know tooccur during this period

(b) Early post-engraftment phase (< 100 day postHSCT): During this phase, viral (CMV, HSV)and fungal infections are common, besidesbacterial infections.

(c) Late post-engraftment phase (100 day post-HSCT): During this period with encapsulatedbacteria, fungi and viruses are known tooccur. This phase technically is a latecomplication of HSCT. However, forconvenience it has been included under thecategory of infection.

Hepatic Veno-Occlusive DiseaseVOD is clinical syndrome, presenting with

elevated levels of bilirubin, hepatomegaly and

fluid retention. There is now a greaterappreciation of obstruction in the hepatic venussinuses, hence it is also referred to as sinusoidalobstruction syndrome (SOS). In VOD, endothelialdamage due to the intensive conditioning leadsto a local hyper-coagulable state with initiationof a ‘cytokine storm’ (IL-1, TNF) which isresponsible for hepatocyte necrosis. VOD isassociated with renal failure, thrombocytopeniaunresponsive to platelet transfusion and hepaticencophalopathy. VOD occurs in the first 20 dayspost HSCT. 30-50% of patients undergoing HSCTdevelop VOD of varying severity andapproximately 5% of these are life threatening.Pulmonary Complications

The pulmonary complications commonlyencountered in HSCT are elaborated in table 4.

Table 4.Causes of pulmonary complications post- HSCTInfection

Bacterial ViralFungal Protozoal

Pulmonary oedemaFluid overloadCardiac dysfunctionAcute respiratory distress syndrome (ARDS)

Seps isDrug toxicity (e.g. CSA andcytosine arabinoside)

Idiopathic (toxic)Pulmonary embolism Pulmonary GVHD

Hemorrhagic CystitisThis is characterized by frequency, dysuria

and haematuria soon after administration of Cy.When severe it can pose a serious therapeuticchallenge. This occurs primarily due to damagebrought about by acrolein (a metabolite of Cy) tothe uroepithelium of the urinary bladder.

Prevention of haemorrhagic cystitis (HC)secondary to use of high dose Cy is done byadministering continuous infusion of MESNA (2-Mercaptoethanesulfonic acid sodium salt)starting 12 hours prior to and continuing 12 hoursfollowing cessation of cyclophospahamide alongwith hydration.Graft-Versus-Host Disease

GVHD is an inflammatory condition, uniqueto allo-HSCT, wherein, the donor immune cellsattack the recipient’s tissues. It is mainly, mediatedby T cells, when they react to foreign peptidespresented on the major histocompatibilitycomplex (MHC) of the host.

39

transplant for multiple myeloma. Apollo hospitalChennai has done over 249 HSCT’s withapproximately 60% of these being allo. At ArmyHospital Research and Referral, Delhi-Cantt, 207HSCT’s have been performed, of whichapproximately 66% have been allogeneic.Sahayadri Hospital Pune has done 314 HSCT’s ofwhich approximately 68% is allogeniec..

There is no functional donor registry for HSCTin India, while this is well established in Europe,North America and Japan. These registries improvethe chances of finding a fully matched HLA(unrelated) donor from 60%, to 80%, whereas, itis 25% to 30% when only siblings form the donorpool. There is a significant supply demandimbalance, necessitating more centers to meetthe requirement for a population of over a billionand to start a MUD program.Recommended Reading1. Schretzenmayr A. Treatment of anaemia by

bone marrow injection. Klin Wissenschaftschr1937; 16:1010-1012

2. M Chandy. Stem cell transplantation in India. BoneMarrow Transplantation (2008); 42: S81-S84

3. Velu Nair, Satyaranjan Das, Ajay Sharma.Hematopoietic Stem Cell Transplantation inChildren with Genetic Defects. IndianPediatrics; 46, 2009: 241-243

4. Russell JA, Chaudhry A, Booth K. Earlyoutcomes after allogeneic stem celltransplantation for leukaemia andmyelodysplasia without protective isolation:a 10 year experience. Biology of Blood andMarrow Transplantation 2000; 6:109-14.

5. Stern JM and Lenssen P. Food and nutritionservices for the BMT patient. In: Bone MarrowTransplantation. Administrative and ClinicalStrategies. PC Buchsel and MB Whedon (eds),1995 (London: Jones and Bartlett).

6. Billingham RE. The biology of graft-versus-hostreactions. Harvey Lectures 1966; 62: 21-78.

7. Deeg HJ. Graft-versus-host disease – host and donorviews. Semin Hematol 1993; 30 (Suppl 4) 110-118.

8. Velu Nair. Haematopoietic stem celltransplantation in autoimmune diseases.Indian Journal of Rheumatology 2008September, Volume 3(3): 101–109

9. Schmitz N, Barrett J. Optimizing engraftment-source and dose of stem cells. Semin Haematol2002;39:3-14.

10. Nair Velu. Stem Cell Transplantation. MedicineUpdate 2004; Association of Physicians ofIndia; Vol.14: 366-377

Acute GVHD:(a) It typically appears in the first 3 months

after allo-HSCT. It is known that theseimmunocompetent cells are T-lymphocytes.However, there is no clear evidence as to whichspecific subsets are involved in acute GVHD. CD8+lymphocytes act against class-I HLA antigens andCD4+ against class-II HLA antigens. GVHD isunderstood to be a multi-step process. Step onecauses tissue damage in the recipient which iscytokine (IL-1, IL-6 and TNFá) mediated. Skin, gutand liver ducts are the target organs as theyexhibit an increase expression of HLA molecules,adhesion molecules and other products with pro-coagulant activity. The next step involvesactivation of individual T-cells and expressionof IL-2 receptors and production of IFNg and IL-2.Activated T-lymphocytes undergo clonalproliferation and differentiation, elaborating IL-2 which stimulates mononuclear cells which inturn secretes IL-1, TNFá and IFNg producing acytokine storm. In addition the lymphocytes alsohave a cytolytic action.Chronic GVHD : Chronic GVHD is a latecomplications which occurs 100 days post -HSCTwith clinical manifestations closely mimickingAID such as skin dyspigmentation, xerosis,erythema, scleroderma, lichen planus,xerostomia, ocular keratitis, jaundice,pulmonary obstruction/ restrictive defects.Corticosteroids such as prednisone is thestandard treatment for chronic GVHD with otherdrugs such as MMF, CSA, tacrolimus andthalidomide being used singly or in combination.HSCT PROGRAM IN INDIA

In India the first HSCT was done in TMH,Mumbai in 1983 followed by transplants inCMCH Vellore. There are several other centerswhich have started a transplant program.Approximately 17 centres are running an HSCTprogram in India. Over 3300 transplant have beendone including nearly 2000 allo-HSCTs and 1300auto-HSCTs. Many more transplant centers areexpected to open all over India as there is a lot ofscope for this procedure considering the patientload of various hematological disordersTMHMumbai has done over 377 HSCT’s (of which 60%have been allo-HSCT) and are presentlyperforming approximately 30 HSCT’s every year.CMCH Vellore has done over 1002 HSCT’s and isyearly performing approximately 60 HSCT’s. Ofthese more than 227 HSCT’s have been forthalassemia major. AIIMS, New Delhi have donemore than 264 HSCT’s with a large series of auto-

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Dr. Sunil ParekhProfessor, haematology

Haematology Laboratory, Parekh House

Chairman, MDRI (Marrow Donor Registry Programme, India)

Member, International Committee -American Society of Hematology

Marrow Donor Registry India (MDRI)

Introduction

Allogeneic Bone Marrow Transplants (BMT)and Allogeneic Peripheral Blood Stem CellTransplants (PBSCT) have become the standardof care for several life threatening blooddisorders like leukemia (AML, CML, ALL, CLL), otherhematological malignancies (HD, NHL, MM, MDS),immunodeficiency diseases, aplastic anemia,thalassemia, etc. Successful transplants arelifesaving and can cure these patients.

At any time, all over the world, there are over3,000 people searching for a stem cell donor. Only30% of such patients will find a suitable donorwithin their family. The other 70% depend on theavailability of matched unrelated donors. If sucha donor can be quickly located, the transplant canbe done without any delay. Realising this need,several international marrow donor registrieshave been successfully established.

The existing international registries have anextreme paucity of matching donors for Indianpatients, since the HLA alleles in the Indianpopulation are genetically different from thoseof other populations in the world.

On April 11, 2009, thanks to the vision andguidance of Prof. John Goldman, Director, AnthonyNolan Registry, UK, we were able to host aconference in Mumbai. Medical directors of allthe major international registries voluntarilycame to Mumbai for this unique meeting alongwith representatives of the transplant centers inIndia. Together they planned a road map forestablishing an Indian donor registry.

Although facilities for Matched UnrelatedDonor (MUD) transplants are now available inIndia, there was no established Indian registryto help in finding a matched unrealated Indiandonor. The rare Indian who does find a matchingdonor from the international registries has toincur very heavy costs for importing the stem cells

from abroad ($ 30,000 – $ 40,000). With theintention of saving crucial search time and hugecosts of imported stem cells, we have set up ourIndian marrow donor registry in Mumbai. TheMDRI is a database of voluntary, unrelated stemcell donors. We have so far recruited 3500voluntary donors of which 3200 have alreadybeen HLA typed. The donors do not incur anyexpenditure since all the costs, including HLAtyping, are borne by the registry. We aim to haveover 1 million voluntary altruistic donors asrapidly as possible. The major difficulties ofsetting up such a registry include the high costsof HLA typing, recruiting well trained anddedicated staff and web based databaseinformation processing facilities.

Objectives

Activities

HLA TypingAt MDRI, HLA typing of the Class I ( HLA A,B)

and Class II (HLA DRB1) alleles are done atintermediate resolution (up to 2 digits) bymolecular biology techniques such as SequenceSpecific Oligonucliotide Probing (SSOP) andSequence Specific Primers (SSP).

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Although High resolution typing techniques(4 digits) are available, MDRI has currentlyadopted the intermediate typing techniques fortwo reasons:1) Intermediate typing is more economical than

the high resolution typing.2) Ease of screening for a matched donor is

possible with 2 digit typing. Once the donormatches at the first 2 digits these donors can befurther typed till 4 digits before processing themfurther for the final confirmation prior todonation for the patient awaitng a transplant.

Donor SelectionFor selection of an unrelated donor, HLA

typing of both donor and recipient must berepeated using fresh blood samples such thateach individual’s typing and identity can bereconfirmed. The final typing must be performedin the transplant center laboratory.

Advice on selecting donors for patients canbe provided by the MDRI. However, the finaldecision on donor suitability is always theresponsibility of the transplant center physician.

Donation ProcessOnce a donor has had all the essential blood

tests performed and the patient’s physician issatisfied that he has enough information to choosethe best donor, he is requested to confirm that he iswilling and committed for donating his stem cells.

Stem cells may be obtained from the bonemarrow (under general anesthesia) by aspirationfrom the hip bones. Anesthesia is essential toeliminate any pain during the procedure.Alternatively, the stem cells could be collectedfrom the peripheral blood using a cell separatormachine (Apheresis Technology).This procedureis known as PBSC harvesting. Usually, the donorwill receive about a month’s notice before beingscheduled for the actual donation of stem cells.

Apheresis :

Transplant Centers in India (Courtesy Prof.Mammen Chandy and Dr. Navin Khattry)

AcknowledgementMDRI acknowledges the inspiration and

financial help for this project from: Sir Ratan TataTrust, Tata Education And Development Trust, TataMemorial Hospital, ACTREC (Kharghar), SYNTEL Inc.,R-Tec Systems, The Rahejas, HDFC Ltd. and manyother supporters, volunteers and well-wishers.

A secure website (https://www.mdrindia.org) andsoftware program has been developed by M/s SyntelInc., the total cost of which has been generouslyborne by them. The server for this has been generouslydonated by M/s R. Tec Systems (I) Pvt. Ltd.

Two audio/video presentations (YouTubeVideos: Google <hitenge site:YouTube.com> “Hope ForLeukemia patients” and “Pledge Your marrow Today,Give Someone A Tomorrow “) have also beenlaunched for creating awarness through the country.

We humbly appeal to you to give us yourgenerous donations to enable us bear the huge costsof building this Registry which will benefit anunlimited number of patients in India and abroad.

All contributions are requested by cheque onlyin the name of “MARROW DONOR REGISTRY INDIA”

We request you to come forward and lend ahelping hand for this project for our nation.

Marrow Donor Registry IndiaTata Memorial HospitalDept.of Transfusion, 5th floor,Blood Bank Building, ParelMumbai 400 012Phone: +91-22-65152695, Cell: +91-9223586076Email: info@mdrindia.orgWebsite: https://www.mdrindia.org

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Milestones in Sickle cell disease• 1910 James Herrick notes “peculiar,

elongated sickle-shaped erythrocytes”in a patient with anemia.

• 1930s Lemuel Whitley Diggs suggests thatpain in sickle cell patients is due tosickle cells clogging up small bloodvessels.

• 1949 Linus Pauling discovers that sickle celldisease is caused by an abnormalhemoglobin.

• 1957 Vernon Ingram discovers that a changein one amino acid in hemoglobin Scauses sickling.

• 1970s Sickle cell anemia becomes the firsthuman disease to be explained at thelevel of a single nucleotide mutation:Using recombinant DNA technologytechniques, scientists find that thenucleotide change in the DNA for sicklehemoglobin results from an A to Tsubstitution. The civil rights movementcalls attention to racial inequality inhealth care. Charles Whittenestablishes the Sickle Cell DiseaseAssociation of America to improveresearch, education and health care forsickle cell patients.

• 1972 The Sickle Cell Anemia Control Actallocates government funding forscreening, research, and treatment .With these funds, the National Heart,Lung, and Blood Institute establishes theCooperative Study of Sickle Cell Disease.

• 1980 Robert P. Hebbel observes that sicklecells stick to the lining of blood vesselsand shows that this correlates withseverity of illness.

• 1983 The Prophylactic Penicillin Study (PROPS)finds that treatment of well sickle cellpatients with penicillin could preventdeath related to serious infections.

• 1995 The Multicenter Study of Hydroxyureaproves the usefulness of hydroxyurea

50 YEARS IN HEMATOLOGYResearch That Revolutionized Patient Care

Excerpted from ASH 2008 Edited by Dr Abhay A. Bhavein preventing complications in patientswith sickle cell disease.

• 1996 The Multicenter Bone MarrowTransplant Study demonstrates a curefor children with sickle cell disease.

• 1998 The Stroke Prevention in Sickle CellDisease clinical trials show thattranscranial Doppler ultrasonography,a method of analyzing blood flow in thebrain, is an effective screening tool.

• 2000 A published study by Lennette J. Benjamindemonstrates that a day hospital for thetreatment of pain improves quality of life& prevents hospitalizations.• Hemolysis (a breakdown of red blood

cells) results in free hemoglobin, whichdecreases the availability of nitricoxide (an important signalingmolecule), causing widespreadpathologic consequences, includingpulmonary hypertension. Furtherstudies determine that pulmonaryhypertension is common in sickle celldisease and a strong predictor of death.

• 2001 Gene therapy successfully cures asickle-cell mouse.

• 2005 Genetic methods are developed to predictcomplications of sickle cell disease.

• 2007 Techniques are developed in sickle-cellmice to convert normal cells into stem cellsto be used for gene therapy and transplant.

MILESTONES IN TRANSFUSION MEDICINE• 1818 The first successful human-to-human

blood transfusion in performed byJames Blundell.

• 1900 Karl Landsteiner develops the classifi-cation of blood into A, B, and C (laterchanged to O) groups.

• 1902 Alfred Decastello and Adriano Sturli addAB to the blood classification system.

• 1907 Ludvig Hektoen is the first to suggest thatdonors and patients should be screenedfor compatibility (now known as cross-matching).

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• 1912 Roger Lee shows that O blood can begiven to a person with any blood type(universal donor) and that a personwith AB blood can receive blood fromany blood group (universal recipient).

• 1939 Karl Landsteiner, Alex Wiener, PhilipLevine, and R.E. Stetson develop theRhesus (Rh) blood classification system.

• 1943 J.F. Loutit and Patrick L. Mollisondevelop a solution of acid citratedextrose, which allows greater volumesof blood to be transfused and makeslonger-term storage possible.

• 1950 Audrey Smith successfully freezes redblood cells using glycerol cryoprotectant.

• 1950 Carl Walter and W.P. Murphy Jr. developthe plastic bag for blood collection.

1958 Jean Dausset discovers the first humanleukocyte antigen (HLA) on the surfaceof blood cells, which determineswhether blood from one person mightbe successfully transfused into anotherindividual. Rose Payne and othersidentify other HLAs, key discoveries forunderstanding tissue compatibility.

• 1960 Alan Solomon and John L. Fahey developplasmapheresis, a procedure forseparating whole blood into plasmaand red blood cells.

1964 A method of concentrating clottingfactors from fresh frozen plasma isdiscovered by Judith Pool, allowingpatients with hemophilia to receivetransfusions outside of the hospital.

1968 Rh Immune Globulin, the first treatmentthat addresses the differences betweennegative and positive blood types,proves effective in preventing hemolyticdisease of the newborn. This condition,once a major cause of fetal death,occurs when an incompatibilitybetween the mother’s and the baby’sblood causes her antibodies to destroythe baby’s red blood cells.

• 1969 Scott Murphy and Frank Gardnerdevelop a method for storing plateletsat room temperature.

• 1971 The practice of testing donated bloodfoe hepatitis B begins.

• 1972 The use of apheresis, the process ofseparating out only plasma or onespecific type of blood cell from donatedblood, and then returning the remainingblood cells back to the donor, begins.

• Mid-1980s The practice of testing donatedblood for HIV begins.

• 1999 The use of nucleic acid amplificationtesting for active viruses in donatedblood begins.

• 2005 The FDA approves the first West Nilevirus blood test to screen blood donors.

MILESTONES IN THE TREATMENT OFPAEDIATRIC LEUKAEMIA

• 1948 Sidney Farber treats leukemia withaminopterin, which blocks folic acidand becomes the first agent to causeremission in children with ALL.

• 1950 George Hitchings and Gertrude Eliondevelop 6-mercaptopurine to block DNAmetabolism and kill rapidly growingleukemic cells.

• 1950s The first combination chemotherapyregimens are designed by Emil Frei, EmilFreireich, and James Holland.

• 1960s Criteria are established for thediagnosis of ALL. The phases of therapybecome recognized as important:remission induction, intensification,central nervous system therapy, andcontinuation (maintenance) therapy.New treatment drugs are introduced:vincristine, asparaginase, cytoxan,daunomycin, and cytosar.

• 1970s Donald Pinkel develops a “total therapy”approach to prevent a relapse of thecancer in patients’ central nervoussystems (leukemic meningitis).Supportive care, such as platelettransfusions and antibiotics, improvepatient outcomes.

• 1975 For the first time, ALL is classified intosubtypes for better treatment strategies.

• 1980s About 50 percent of ALL patients becomelong-term survivors in much of the U.S.

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and Western Europe. Cytogenetics (thestudy of chromosomes & cell division)emerges as a key tool predictingoutcome in ALL.

• 1998 Researchers begin individualizing thedosage of chemotherapy to increasesurvival rates in children with ALL.

MILESTONES IN THE TREATMENT OF CML• 1845 John Hughes Bennett and Rudolph

Virchow describe the first cases of CML.• 1960 Peter Nowell and David Hungerford

identify an abnormal chromosome inthe blood cells and bone marrow ofpatients with CML.

• 1973 Janet Rowley determines thatthe abnormal chromosome identifiedby Nowell and Hungerford results fromthe exchange of genetic materialbetween two chromosomes.

• 1982-1985 John Groffen, NoraHeisterkamp, Gerard Grosveld, E.Cannani, David Baltimore, and OwenWitte show that an abnormal gene andprotein called BCR-ABL is produced asa consequence of the chromosomerearrangement that characterizes CML.

• 1987 Nicholas Lydon and Alex Matter begin adrug discovery program to targetproteins such as BCR-ABL incollaboration with Brian Druker,Thomas Roberts, and Charles Stiles.

• 1993 Brian Druker’s laboratory shows thatSTI571 (Imatinib) is the best of thecompounds developed by NicholasLydon’s group at specifically targetingand killing CML cells.

• 1998 Brian Druker, Charles Sawyers, andMoshe Talpaz begin clinical trials ofImatinib.

• 2001 Imatinib is FDA-approved for patientswith CML.

2001 Charles Sawyers, Brian Druker, AndreasHochhaus, and Francois-Xavier Mahonreport that mutations of BCR-ABL arethe major mechanism of resistance toImatinib.

2006 Follow-up data show a 95 percent five-year survival for patients with CMLtreated with Imatinib.

• 2006, 2007 Dasatinib and nilotinib areFDA-approved for patients with Imatinibresistance.

MILESTONES IN THE TREATMENTOF HODGKINS LYMPHOMA

• 1832 Sir Thomas Hodgkin publishes “On SomeMorbid Appearances of the AbsorbentGlands and Spleen,” about a series ofsix patients with clinical findings thatwere different from tuberculosis,syphilis, and inflammation.

• 1865 Samuel Wilks reports on similar caseswith lymph node & splenic enlargementand names the disorder “Hodgkin’sdisease”. This invariably fatal illness istreated with herbs, surgery, and arsenic.

• 1900s German pathologist Carl Sternberg(1898) & American pathologist DorothyReed (1902) independently providedetailed accounts of the giant “Reed-Sternberg” cells, which are the microscopichallmarks of Hodgkin’s lymphoma.

• 1902-03W. Pusey and N. Senn note remarkableregressions of Hodgkin lymphoma uponexposure to X-rays.

• 1943 Temporary reduction in the size oflymph node is reported in six Hodgkinpatients treated with nitrogen mustardby Rene Gilbert and colleagues.

• 1950 Vera Peters reports excellent survivalrates on Hodgkin patients treated withradiotherapy to adjacent lymph nodesnot known to contain disease.

• 1962 Henry Kaplan introduces the linearaccelerator in the treatment of Hodgkinlymphoma at Stanford University. Curesare reported after wide-fieldradiotherapy treatment of localizedHodgkin lymphoma.

• 1964 Vincent DeVita Jr. and colleagues arethe first to demonstrate the cure ofadvanced-stage Hodgkin lymphoma inapproximately 50 percent of patientswith combination chemotherapy usingthe MOPP(mustard, vincristine, procar-bazine, prednisone) regimen.

• 1966 Robert J. Lukes and James J. Butlerdescribe the natural history of Hodgkin

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lymphoma related to histopathologicclassification. Saul Rosenberg andHenry Kaplan describe the orderlyprogression of Hodgkin lymphomaand Rosenberg reports on the stagingof the disease.

• 1975 Gianni Bonadonna reports on achemotherapy combination, ABVD(doxorubicin, bleomycin, v i n b l a s t i n e ,dacarbazine), which is effective afterfailure of MOPP. ABVD later becomes thestandard chemotherapy regimen forHodgkin lymphoma, curing more thantwo-thirds of patients with advancedor bulky disease.

1980s Adverse effects of MOPP, includingsecondary leukemia and sterility, arereported. Late effects of radiotherapyare observed in the form secondarycancers (particularly lung and breast)and cardiovascular disease.

Remissions are achieved with high-dose chemotherapy and autologoustransplantation in Hodgkin lymphomarecurrent after chemotherapy andradiation therapy. This approachbecomes the standard second-linetherapy for advanced disease.

• 1994 Ralf Kuppers plucks individual Reed-Sternberg cells from Hodgkin tissuesand establishes that they representmalignant B cells by gene rearrange-ment analyses.

• 1990s Randomized trials in North America andEurope combine limited field, lower-doseradiotherapy with a brief course of lesstoxic chemotherapy (e.g. ABVD), resultingin cure rates of 90 percent or greater inlimited-stage disease. Brief chemo-therapy (Stanford V) & radiotherapy areintroduced for advanced disease.

The German Hodgkin Study Groupreports superior survival with anintensive chemotherapy regimen,escalated BEACOPP (bleomycin,etoposide, doxorubicin, Cyclophos-phamide, vincristine, procarbazine,prednisone), in advanced Hodgkinlymphoma.

• 2000s Positron-emission-tomography scansearly in the treatment course predictthe outcome of treatment with ABVD,

suggesting that therapy could be morepersonalized, reserving radiotherapy &prolonged more intensive treatmentsfor a subset of patients.First successful treatments oflymphocyte-predominant Hodgkinlymphoma with a monoclonal antibody,rituximab, are reported by investigatorsin Germany and at Stanford University.

MILESTONES IN HAEMOPHILIA

• 1950s The use of fresh frozen plasma, whichoften required hospitalization, is themainstay of treatment for hemophilia.

• 1964 Judith Pool discovers a simple way tomake cryoprecipitates (cold insolubleprecipitates that contain factor VIII) orthe treatment of hemophilia.

• 1970s The availability of lyophilized (dried)factor VIII or factor IX concentratesallows home infusion therapy tobecome a common treatment practice.

• 1973 The Hemophilia Act of 1973 allows federallyfunded comprehensive hemophiliatreatment centers to be established.

1982 Using gene sequencing techniques,researchers clone factor IX.

• 1984 Using gene sequencing techniques,researchers clone factor VIII.HIV, thevirus that causes AIDS, is discovered.

• 1980s The hepatitis viruses and HIV threatenthe worldwide blood supply. To combatthis, manufacturers of plasma-derivedclotting factor concentrates attempt to killthe viruses with dry heat, solvent-detergent treatment, & pasteurization.Screening methods for these viruses, suchas the ELISA test, are also developed.

• 1990s After only a few years of successfulclinical trials, recombinant humanfactor products become licensed andare available to hemophilia patients.

• 2000s Recent advances include a betterunderstanding of the cause, detection,& elimination of inhibitor antibodiesfound in many hemophilia patients.

MILESTONES IN THE DEVELOPMENT OFANTICOAGULANTS

Heparin• 1916 Heparin is discovered in dog liver by a

team from The Johns Hopkins Universityin Baltimore. MD.

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• 1930s Scientists purify heparin and produceenough pure material for clinical use.

• 1932 A U.S. clinical scientist shows thatheparin requires a plasma factor (nowknown as antithrombin or AT) for itsanticoagulant action.

1970s The mechanism of the interactionbetween heparin and AT is explainedby scientists from Harvard Universityand from the University of Uppsala.

Warfarin• 1920s Cattle in the northern U.S. and Canada are

dying from a bleeding disease caused bya substance in moldy sweet clover.

• 1930s A Danish scientist discovers thatdietary vitamin K is necessary to preventbleeding.

• 1939 Researchers at the University ofWisconsin identify the substance inmoldy clover as dicumarol. Over nextseveral years, warfarin, a relatedcompound, is made in this laboratory.

• 1941 Dicumarol is first given to patients atthe Mayo clinic.

• 1950s Clinical studies with warfarin beginin the U.S., and the drug is approvedor clinical use in 1954.

• 1970s The mechanism of action of vitamin Kis explained by scientists who discoverthat warfarin’s anticoagulant effect iscaused by interference with the actionof vitamin K

Low-Molecular-Weight Heparin (LMWH)• 1970s Researchers begin work on LMWH.• 1980s The first clinical studies of LMWH are

performed in the mid- 1980s and showthat LMWH is effective for preventingvenous thrombosis in high-riskpatients.

• 1990s LMWH can now be administered safelyin an out-of-hospital setting.

Fondaparinux• 1979 Scientists determine the structure of the

high-affinity binding site on heparinand soon after demonstrate that thishigh-affinity site is a pentasaccharide(five-sugar unit) with a unique structure.

• 1980s The pentasaccharide is synthesized,and, over the ensuring two decades, thesynthetic compound is developed intoa drug for clinical use.

• 2000s Multicenter clinical trials show thatfondaparinux is an effectiveantithrombotic drug.

Aspirin• 1899 Aspirin is introduced for pain and fever

control by a German scientist and ispatented in 1900.

• 1960s Scientists demonstrate that aspirinimpairs platelet aggregation andprevents arterial thrombosis inexperimental animals.

• 1975 Aspirin’s mechanism of action isdetermined by scientists fromWashington University in St. Louis.

• 1978 The first randomized trial showing thebeneficial effects of aspirin is reportedby a Canadian group who show thataspirin reduces the risk of stroke inpatients with minor strokes. Soon after,several clinical trials demonstrate thataspirin is effective in treating heartattacks and stroke.

ADP-Receptor Antagonists

• 1980s Theirreversible platelet ADP antagonistticlopidine is developed & later shownto be effective in stroke patients in 1989.

• 1990s Clopidogrel, an analogue of Ticlopidine,is developed and shown to be effectiveclinically.

• 2001 The combination of clopidogrel andaspirin proves to be effective in patientswith acute coronary syndrome.

GP IIb/IIIa-Receptor Antagonists• 1970s/1980s The glycoprotein IIb/IIIa (GP

IIb/IIIa) receptor is found to mediateplatelet aggregation by binding tosoluble adhesive proteins.

• 1990s Monoclonal antibodies to block the GPIIb/IIIa receptor are developed & showpromise as an antithrombotic treatment.

• Soon after, a region of the monoclonal antibodyc7E3 Fab (abciximab, ReoProTM) is found to beeffective in patients with coronary stents;several studies then identify a pivotal role thatthe blockage of GP IIb/IIIa has in themanagement of acute coronary syndromes.Small intravenous GPIIb/IIIa antagonists arethen developed and shown to be effective.

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Proposal:Organizing a State level Seminar on the topic of‘Industrial Disaster Management-Role of Doctors’.

This would be a joint venture of IndianMedical Association (Maharashshtra StateBranch), Department of Industrial Safety andHealth (Govt. of Maharashtra) and IndianOccupational Health Association (MaharashtraState Branch)

Preamble:We are into the 21st Century in real earnest

and the Industrial Revolution has gatheredrenewed speed in newer directions. Hence it is achallenging task for the medical profession tokeep pace with the revolution in the IndustrialWorld vis-à-vis the occupational health hazardsand especially the preparedness in case ofIndustrial Mishaps and Disasters.

In case of any small mishap, or a disaster,in the Industrial establishment the affected work-force has to be ultimately treated by the medicalprofessionals. At present it has been variouslyobserved that in spite of protocols being in placethe medical fraternity largely remains ignorantof these protocols and hence morbidity andmortality remain on the higher side.

Similarly another area where muchimprovement is desirable is the ‘Coordination’between the Industries, Government Authoritiesand the Medical Professionals so as to dispensetimely and proper medical care in case ofindustrial mishaps or Disasters.

Objective:We need to plan and put in place a system

whereby we can ensure better COORDINATION andPREPAREDNESS to dispense better medicaltreatment to the affected people in case ofIndustrial Mishap or Disaster.

Proposal:The Beginning:

With the abovementioned objective in ourview we propose to begin with an ‘OrientationSeminar’ to be organized in Mumbai, tentativelyon 24th October, 2010 (Sunday) between 9.00 A.M.to 4.00 P.M.

Industrial Disaster Management—Role of DoctorsThe invitees for this seminar would be leaders

from Industry, Maharashtra Government’s SeniorOfficials from the Departments of Industry,Industrial Safety & Health, Public Health and Labour.

The participants shall be the MedicalProfessionals, from all over the State ofMaharashtra, who are the members of IndianMedical Association and Indian OccupationalHealth Association.

Similarly Medical Professionals from variousGovt.Hospitals, Govt. District Hospitals & PrimaryHealth Centers in the vicinity of Industrial zonesand all Corporate Hospitals should necessarilybe the participants at this Seminar.

After this ‘Beginning’ we propose a further‘Action Plan’ to achieve our goals.

ACTION PLAN:1) Bringing out an informative ‘Souvenir’ which

would be a concise ‘Ready-Reckoner’ for allthe stakeholders.

2) Organizing Industrial Disaster ManagementWorkshops at Regional levels.

3) Preparing a ‘Text Book’ with all the latest dataconcerning the Industrial Health and DisasterManagement.

4) Formation of ‘Coordination Committees’ atevery industrial Zone level. The DISH Officials,Govt. Medical Officers, DistrictAdministration, MIDC Officials, DistrictAdministration Officials, IOHA MemberDoctors and IMA Member Doctors from thatarea would constitute these Committees.

5) The Indian Medical Association MaharashtraState (IMA MS) shall be honoured to be the leadorganization in this innovative programme.

6) We can achieve the targets by cooperative andconstructive effort over a period of two to threeyears.

7) Implementation of this proposal would be apath-breaking avenue in the sphere of ‘Public-Private-Partnership’ for the benefit of publicat large.

Dr. Sanjiv Sharangpani

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DR. SHIVKUMAR UTTUREM.S.,F.I.C.S.(USA)

President, IMA, Mumbai BranchHon. Treasurer IMA, Maharashtra State

Member of Central Working Committee (H.Q.)Member of Maharashtra Medical Council

Hon. Prof. of Surgery Grant Medical College (J.J. Hospital)Hon. Surgeon & Unit Head Saint George’s Hospital

Hon. Surgeon Shushrusha HospitalHon. Surgeon S. L. Raheja (A Fortis Associate) Hospital

Super session of MCI- The Path ahead.How justified is the governments action

The Government of India promulgated anordinance on 15th May 2010 to supersede theMedical Council of India and replace it with asix member panel which will be in charge for thenext one year. The MCI was established in 1934under the Indian Medical Council Act 1933. thiswas an Act of Parliament brought about toregulate medical education and practice andbrought into existence to give an AutonomousStatus to this body so as to keep it away frompolitical influence.

The supercession of the MCI has to beevaluated in the context of the fact that theGovernment of India is finalizing a draft Bill“National Council for Human Resources in Health”(NCHRH). The NCHRH is to be set up as anoverarching regulatory body with dual purposeof reforming the current regulatory frameworkand enhancing the supply of skilled personnel inthe health sector. On enactment of the proposedBill the existing legislations governing MCI, DCI,Pharmacy Council of India Indian NursingCouncil and Rehabilitation Council of India areexpected to be repealed. A task force was formedto deliberate upon the structure and function ofthe proposed National Council on HumanResources in Health. The task force has proposedto establish a compact council of professionalswith only five members who are selected andappointed on the recommendation of a selection

committee comprising of Cabinet Secretary,Principal Secretary to P.M, Health Secretary G.O.Iand 2 Technical Experts from Search Committeecomprising of Health Secretary and TechnicalExperts from Health, Education, SocialDevelopment and Public Administration. In effectthe members of NCHRH shall be exclusivelynominated by the Politicians and theirBureaucrats. We the members of MedicalFraternity shall loose our democratic right ofelecting Members who shall be responsible forthe standards of Health and Medical Educationin future. In effect the Government is keen to takecontrol of MCI and bring it under the ambit ofHRD and Ministry of Health. This is not the firsttime that the Govt. has made such a move. In 2005the then Union Minister Dr. Abumani Ramadosstried unsuccessfully to bring in a legislation todissolve MCI and set up another council underthe Health Ministry. The bill was referred to thestanding committee of the Parliament of Ministryof Health and Family Welfare and an exhaustivereport thereof has not only unanimously observedthat the Bill was prejudicial to the autonomy ofMedical Council of India but also been said to bean attempt by the Govt. to centralize the powerswith itself and reduce down a Body of Expertscreated for a distinct purpose by a Parliamentaryenactment into a Department working under theGovt. of India.

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The Govt. might have had emergentreasons for super session of the offices of thePresident and Vice President of M.C.I. But werethey justified in dissolving the entire body thuscasting aspersions on the conduct of all thecouncil members and all medical professionalsin general. Has there been a precedence ofdissolving the whole State or Central Govt. if theChief Minister or Prime Minister is suspected offraud? Was the whole Securities and ExchangeBoard of India (SEBI) dissolved when a majorracket was unearthed? Are all the members of aMinistry (including Bureaucrats) summarilysacked if the concerned Minister is involved in ascam? Then why is the Govt. forming the NCHRHwhich will effectively take away the independenceof a medical regulatory body and place all thepowers in the hands of Politicians and Bureaucrats?

A perusal of the existing provisions of theIndian Medical Council Act 1956 wouldcategorically show that the Govt. of India hassubstantial and reasonable control on the affairsof the Medical Council of India.

• Section 32 states that the Govt. of India issingularly empowered to frame rules andnotify them which are binding to the MCI.

• Section 33 requires MCI to take prior approvalof the Govt. of India before notification of anyRegulations.

• The Govt. directly and in consultation withState governments nominates 38 members onthe MCI, representatives of Universitiesnumber 83 and only 20 members are electedby the registered medical graduates.

• Central Govt. directly controls the postgraduate medical education committee of MCIby nominating six out of nine members to thiscommittee.

• No person shall establish a medical collegeor no medical college shall open a new orhigher course of study (postgraduate course)except with the prior permission of the CentralGovt. obtained in accordance with theprovisions of the MCI Act.

Hence it is amply clear that the Central Govt.has adequate and active representation withinthe MCI and is party to all decisions taken by theexecutive committee. Hence it can be safelydeduced that the Govt. was privy to all theshenanigans of the president and the vicepresident during their tenure. The million dollarquestion in the mind of every medicalprofessional is that if the Govt. could not controlthe wrong doings of the MCI in spite ofoverwhelming representation in the Council, thenwhat is the guarantee that a body exclusivelynominated by the Politicians and Bureaucratswill be functioning in an unbiased, transparentand accountable way? How are we to believe thatthe Council which owes its very existence toPoliticians and Bureaucrats will in futuremaintain and coordinate the standards ofMedical education throughout India. Will thisnominated Council grant recognition to medicaleducation institutions in a transparent mannerespecially when we are aware that all PrivateMedical Colleges are directly or indirectlycontrolled by Politicians? We, the medicalfraternity appose the Govt. move to destroy theautonomous status of the Council and protest theannexation of our democratic right to electmembers to this regulatory body. The Councilwhich is a body representing the collective voiceof the medical practitioners all over India shouldnot be reduced to being a mouth piece of theCentral Govt. The Council should be insulated fromPolitical interference and should be publiclyaccountable for the discharge of its functions.

Hope better sense prevails and the Govt. takesinto confidence all the recognized MedicalAssociations and bodies before it formulates anydefinitive plans to repeal the Medical Council ofIndia. If any new Council is formed, there shouldbe adequate representation [more than 50%] ofelected members on this council. It would be moreprudent to make amendments to the existing MCIACT to make the council more accountable andtransparent in its functions. This would definitelyenhance the diminishing prestige of our nobleprofession.

DR. SHIVKUMAR UTTURE

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INDIAN MEDICAL ASSOCIATIONIMA Nagpur

MONTHLY REPORT FORMAT

Name of the Local Branch Indian Medical Association, IMA House, NorthAmbazari Road, NAGPUR – 440 010

Name of the State Branch Indian Medical AssociationIMA MaharashtraBranchMUMBAI

Branch Email ID (Correspondence) ima_nagpur@yahoo.com

Membership Strength(1st April 2009 to 31st March 2010) 2020

Pl. attached details on separate sheet -1. Topics for CMEName of Speaker -2. Community Related Projects done 1st July 2010 - Health Check-up Camp at Panchawati

Vruddha Ashram for inmates. Break fast and sweetswere distributed.4th July 2010Blood Donation Campat Sadar. 130people donated the blood.10th July 2010 Inauguration of “Road Safety Abhiyan”by Hon’ble Mr. R.R. Patil, Home Minister, MaharashtraGovt.

a) Any Combined District / Zonal / State National meets Sponsored by your Branch —b) Details of Participation in any State / National IMA events by your branch —c) Govt. Health Programmes Implemented by your branch during this month. —d) Observation of any international / 1stJuly 2010Doctors Day Celebration Dr.B.J. Subhedar, National Designed days, weeks & Renowned physician was the Chief Guest. Dr. Kishor month by your branch Taori, was the Guest of Honour.

6th July 2010 Conference on Zoonosis withCommonwealth Association for Health & disabilityon the eve of “World Zoonosis Day” ICMR SponsoredNational Symposium.

e) Any Immunization activity by your branch - 3. Social / Cultural — 4. Any legal members concern issues and solution by your branch — 5. Any other - 5th July 2010Meeting on R.N.T.C.P. along with Nagpur

Municipal Corporation’s Members. - 8th July 2010Rally on “Exorbitant Hike in Water Bill” along withJanakrosh.

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IMA Mumbai West BranchACTIVITIES REPORT

HIGHLIGHTS OF BRANCH ACTIVITIES FROM 1ST JUNE 2010 TO 10TH AUGUST 2010· We conducted regular Weekly Tuesdays’ & Thursdays’ CME programmes.· We organized following seminars :

a) A seminar in “CONTROVERSIES AND INTERPRETATION IN ONCOLOGY” was held on SUNDAY, 20TH JUNE2010 in our branch premises. THIS HAS BEEN THE FIRST MMC ACCREDITED CME OF OUR BRANCH.

b) MEDICINE UPDATE on the occasion of DOCTOR’S DAY CELEBRATIONS. It was held on the SUNDAY,04TH JULY 2010.

c) The prestigious GYNAECON 2010 on held on SUNDAY, 25TH JULY 2010 from 09.00 am to 04.00pm. This programme also received 2 (two) hours of MMC Accreditation.This was the 5th consecutive successful joint programme by IMA Mumbai West with IMA – CGPSub Faculty of our branch and Association of Fellow Gynaecologists (AFG) and was wellappreciated by all the delegates.

d) Cardiology Seminar – INDIA AT HEART was organized on SUNDAY, 01ST AUGUST 2010. Thisprogramme also received 1 (one) hour of MMC Accreditation.

On the occasion of Doctor’s Day our branch had organised an excellent programme onSUNDAY, 4TH OF JULY 2010.The following dignitaries were felicitated :

Medicines Sans Frontiers (MSF), a Nobel Peace Prize(1999) winning international organization whichprovides medical aid to strife torn and calamity torncommunities around the world, was first to befelicitated. Dr. Shobha Varthaman who is anAnaesthetist and who gave her services in the wartorn communities, along with Ms Farah Mantoo.Drs. D. R. Dadhich (Neuro-Radiology), Rajan Badwe(Breast Cancer), (Mrs.) Rama Vaidya (ReproductiveEndocrinology), Ashok Johari (Pediatric Orthopedics)and Shrikant Gokhale (Family Practice) were felicitatedby Chief Guest Hon. Minister Suresh Shetty, PresidentDr. Bal M. Inamdar, Guest of Honor IMA-MS-President,Dr. Bakulesh S. Mehta, Trustee Dr. Anil Suchak, IPP Dr.Jayesh Lele, Hon. Secretary Dr. Ashok Balsekar.Last but not the least, Chief Guest of the day, Hon.Cabinet Minister for Public Health and Family Welfare,Environment, Protocol and Additional Charge of Sportsand Youth Welfare, Government of Maharashtra, -Hon. Mr. Suresh Shetty was felicitated with a shawland shreephal. In his speech, he gave us an insightinto the thinking of Govt. of Maharashtra andinformed us about some of the initiatives to bundertaken by his ministry and the government. Hegave USM in a nutshell, his vision of health caresystem, in the days to come.

Doctor’s Day - President Dr. Inamdarinteracting with Hon. Minister Suresh Shetty

IMA-MS, President Dr. B. S. Mehta felicitatingHon. Mr. Suresh Shetty

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• Cultural Sub Committee had organised aCrossword Competition for members & after thefelicitation programme an entertainment Musicalprogramme was presented by TachycardiaOrchestra Group – “SAAWAN AYO RE” on theoccasion of “Doctor’s Day Programme”.

• Addition of 06 new life members.• On the occasion of Doctor’s Day our branch

carried out Sapling Plantation Programme.We highly appreciate and thank M/s. NicholasPiramal for kind courtesy of supplying us thesapling pot and seeds of sapling.1. IMA has been opposing the following 3

bills : Bachelor of Rural Health Care; 2)Clinical Establishment Bill & 3) MCIDissolution

• Medical Education Sub Committee hadorganised a1. First ever – “Educational Programme For

Post Graduate Students/ Residents” onSATURDAY, 03RD JULY 2010.

2. Second Educational Programme forResident was held on SATURDAY, 24TH JULY2010, in Auditorium of Nanavati Hospital.The theme of this programme was “LiverResection and Transplantation”.

• Medical Education Sub Committee had• Medical Welfare Sub Committee had

organised a movie – OUTBREAK – 01.08.2010.• Additional General Body Meeting was held on

08.08.2010.• An orientation workshop on “CONTRACEPTIVE

UPDATES AND SAFE ABORTION TECHNIQUES”was held on the occasion of WORLDPOPULATION DAY on SUNDAY, 11TH JULY 2010

from 09.00 am onwards. It was a joint programme of IMA MUMBAI WEST-CGP SubFaculty and IMA MS-CGP Sub Faculty.

• Following Public Health & Welfare SubCommittee were arranged1. Health checkup camp for the Staff of Ramky

Foundation – 29.05.2010;2. Awareness lecture on “How To Quit

Smoking” on the occasion of “No TobaccoDay” on 31st May 2010;

3. A blood pressure & blood sugar checkupcamp – 06.06.2010;

4. Blood Donation Drive was arranged on theoccasion of “Doctor’s Day” on 04.07.2010.

• Information, Education & Communication SubCommittee had organised health awarenessprogramme:1. Tuberculosis – 03.07.2010;2. ANC Care, PNC Care, Breast Feeding &

Immunization – 12.07.2010;3. Awareness of HIV and AIDS – 29.07.2010.

• Women’s Wing Sub Committee organiseda) Demonstration of preparing Italian and

Thai recopies held on Friday, 06.07.2010b) A unique orientation workshop for Children

on Road Safety – “Be a Safe Pedestrian” –07.08.2010

• Future Programmes : • Flag Hoisting programme on Independence

Day 15.08.2010;• Self Defense Technique - 21.08.2010• Seminar on Diabetes – 22.08.2010;• Neurocon – 29.08.2010;• Teacher’s Day - 05.09.2010;• Jungle trail - 19.09.2010.

Lighting the lamp on the occasionof World Population Day

President Dr. Inamdar inaugural addressat Gynaecon 2010

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The managing committee of IMA MumbaiBranch has unanimously sent the nominationform of Dr. Sunita Kshirsagar for the post of VicePresident IMA Maharashtra State for the year2010-2011.

1st July 2010 - On the occasion of Doctor’sDay a Blood Donation Drive was organized atDadar railway station in association with IMAMaharashtra State, and State Blood Council. Wehad collected 112 bottles of blood.

4th July 2010 - Monsoon Marathon wasorganized in the morning from 7.00 a.m. onwardsat Race Course, Mahalaxmi. Marathon was forabout 4 kms. In spite of heavy rains about 60members and their family members took part inthe marathon. The members were given T-shirtsand other attractive gifts.

4th July 2010 – On the occasion of Doctors’Day we had arranged a grand function in theevening at IMA House from 6.30 p.m. onwards.We felicitated distinguished doctors like Dr. Aspi

I.M.A Mumbai Branch report for MAHIMA from1st July 2010 to 12TH August 2010

DR. RAJENDRA H. TRIVEDI

Golwalla, Dr. Indira Hinduja, Dr. Gopinath Shenoyand Dr. M. J. Shah. Dr. Vijay C. Panjabi was awardedDr. H. M. Shah Life Time Achievement Award. Dr.Aspi Golwalla delivered a talk on “Believe it or not– unique cases” and Dr. Gopinath Shenoyelaborated on “Why it is difficult to loose a caseof Medical Negligence today”. The programme wasfollowed by fellowship and dinner. More than 150members attended the function.

8th July 2010, Womens’ Wing Chairperson Dr.Sunita Kshirsagar and Co-chairperson Dr. PrabhaShinde had organized an excellent programme onthe occasion of World Anemia Day at IMA House.A Lecture on Anemia was delivered by Dr.AparnaPrabhu and healthy recipe competition wasorganized from 2.30 p.m. to 5.00 p.m. About 60recipes were displayed by about 44 participants.Dietician Madam Sneha, from Hinduja MadamKavita from Raheja Hospital, Dr. Sujata Pol, Ast.Prof. for P.S.M. from Sion Hospital were judges forthe competition, Six prizes were given by ourPresident Dr. Shivkumar Utture. Three prizes forIMA members and three prizes for Guest Memberswere awarded.

11th July 2010, On the occasion of WorldPopulation Day, we had arranged a district levelworkshop on “Contraceptive Updates & SafeAbortion Techniques” in collaboration with IMAHQ, IMA Maharashtra State and Ministry of Health& Family Welfare (Govt. of India) at IMA House. Dr.Vipin Checker and Dr. Arun Moray were thespeakers. About 45 members attended the seminar.Members were given certificates of participation.

15th July 2010, As per the directive of IMA HQ,IMA Mumbai Branch had organized a Dharna on15th July 2010 to oppose 1) Bachelor of Rural HealthCare (BRHC) Course 2) Clinical Establishment Billand 3) Dissolution of MCI. About 40 members tookpart in the Dharna held at Haji Ali. We also sentpress release on the occasion which was coveredby Indian Express on the next day edition.

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18th July 2010, CME on Psychiatry wasorganized at IMA House, Haji Ali. The topicsdiscussed were Anxiety & Depression in ElderlyPatients, Advances in Migraine Management andNewer perspective in Sleep Disorders. About 90members attended the CME programme.

25th July 2010, CME on Monsoon illnesseswas organized at Bombay Hospital. Dr. AkhileshSharma, Dr. Amita Nene and Dr. P. G. Samdanigave talks on Tips and Management of monsoonillnesses in adults, Chest Diseases duringmonsoon and Tips and Management of illnessesin children

31st July 2010, CME on “Trends and Advancesin Stroke Management” was organised at RahejaHospital.

2nd August 2010, EMERGENCY Meeting withDr. Sanjay Oak, Dean KEM Hospital and Dr. Ambe,Chief Executive Health officer of BMC, to discussthe steps to be taken to control Malaria in thecity at IMA house HAJI ALI. Dr. Ambe discussedNational Drug Policy on Malaria (2010) sent byMinistry of Health and Family Welfare,Government of India. More than 50 membersattended the meeting organized on short notice.

7th and 8th August 2010 outstation CME inGoa was organized. 36 couples attended the CME.DR HARESH MEHTA delivered lecture on FUTUREINNOVATIONS IN CARDIOLOGY .

15th August 2010, Flag Hoisting ceremonywill be held at IMA Lawns at 9.00 a.m.

21st August 2010, meeting of office bearersof IMA M.S. will be organized at IMA MumbaiBranch. A cultural programme is arranged in theevening for our esteemed guests.

22nd August 2010, 2nd State Executive meetingof IMA M.S. will be organized at IMA MumbaiBranch from 9.30 a.m. onwards.

29thAugust 2010, “PEDICON”-Pediatricsconference will be conducted from 9am onwardsat IMA Mumbai branch.

IMA PUNE BRANCH REPORTOur Dr. Nitu Mandke building Pune Branch is ready for occupation. We have following

facilitites as followes:

1) On the first floor A/C Auditorium of about 200 capacity.

2) On the second floor a hall for 150 person with movable chairs & optional A/c

3) On the third floor a Board Room for deliberation for about 35 persons.

4) On the fifth floor three well furnished A/C Guest- rooms and a Community Hall forabout 50 persons.

5) On the 6th floor Terrance Garden lounge for Receptions etc.

Tel No: (020)-24464771/24430042/32318771Email :- imapune@vsnl.com

Contact Secretary for reservation

Sd/- Sd/-

Dr. Sharad Agarkhedkar Dr. Arun Halbe / DR. Ganesh DatarPresident, IMA Pune Secretary, IMA Pune

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IMA MS SOCIAL SECURITY SCHEMEHON. SECRETARY’S REPORT

Date: 16 / 08 / 2010- The Scheme was launched on 1st October 1990.- The Effective membership as on 09th June 2010 - 5350 +Total No. of death since 1990 – 137 (Barring 1 member, nominees of all are paid the death benefit) Inthe year 2010-11 No. of deaths 05 till today & the nominees of each of 05 expired members is paid‘. 3, 65,700/-. Within few days of getting information of the death.

Young members, do not over look the security of family, thinking we are too young to die.Mishaps & deaths can occur any time unpredictably.

The younger – you join the less you pay – the more you accrue benefit for your members.Request to members of the scheme :-- Please keep the IMA MS SSS certificate in secured place with all FFC receipts.- Please keep your nominee informed of your membership of the scheme & how to act in case of Unfortunate death to get the death claim amount.- Please note – FFC – 2010 have been received from 4000 members, about 800 members have yet to pay. Pleasenote they have to make the payment Rs. 1800 FFC + Rs. 100/- Late fee = Rs. 1900/- before 31st July 2010. Noexcuse of notice not received will be entertained.

We have sorted out about 250 members forms, where in the IMA Life Membership No. is not found. We havesent the notices to all the members requesting them to provide the IMA life membership proof. If they are not IMALife members, they will have to enroll immediately and intimate us through their local branch. In case of IMA LifeMembership is not traced, their name will be deleted and till the same is not produced the nominee will not beconsidered beneficiary in the scheme.Request to the President / Hon. Secretary of each Local Branch. :-1) Please help us to get the Life Membership status of the demanded members urgently. If they are not

registered as life member get them enrolled immediately and inform us. In case of their being non IMA lifemember, in case of death their nominees will not be considered the beneficiary.

2) Please incorporate the above matters in your news bulletins / correspondence to members.3) On death of any member inform & inquire with IMA MS Office, whether he / she was member of IMA

MS SSS, if yes, please help in expediting the process of sending death claim benefit to the nominee.4) Advise members to send proper amount as mentioned above along with filled in form with Xerox

of age proof & IMA Life Membership certificate in case of new membership. We will be sendingyou the list of non payers, please motivate them to pay immediately.

5) IMA MS SSS recognizes the Best Working of Local Branches for propagation of the SSS. Please enrolllarger no. & receive award for your Branch.

6) FFC 2010:- The final reminder by registered A.D. post is already sent to 200+ members whose FFC2010 is not yet received. They are supposed to send ‘ 2100/- latest on 30th September 2010. Nonreceipt on 1st October 2010 will lead to deletion of membership without any further notice. We willbe contacting the respective local branch Hon. Secretary & IMA MS SSS Managing CommitteeMembers informing the list of non payers. Please help us to get their payments by the earliest.

7) Please note change of payment schedules.

From 1st April 2009Age Group Admission Fee Advance FFC Annual Subs. 2 yrs. Total

Up to 30 years Complete Rs. 1000/- Rs. 1000/- Rs. 200/- Rs. 2200/-30 yrs. Complete to 40 yrs. Rs. 2000/- Rs. 1000/- Rs. 200/- Rs. 3200/-40 yrs. Complete to 50 yrs. Rs. 3000/- Rs. 1000/- Rs. 200/- Rs. 4200/-50 yrs. Complete to 55 yrs. Rs. 4000/- Rs. 1000/- Rs. 200/- Rs. 5200/-55 yrs. Complete to 60 yrs. Rs. 5000/- Rs 1000/- Rs. 200/- Rs. 6200/-

Dr. Shrikant H. KothariHon. Secretary, IMA MS Social Security Scheme.(For printing in August 10 issue of MAHIMA – Please do not change text).