family medicine 1 issue -22!01!2014

8/13/2019 Family Medicine 1 Issue -22!01!2014

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ContentsFirst Feature

Minimizing CVD risk in diabetic

patients by maintaining ABC:

A1c

, Blood pressure, and

Cholesterol ..........................................4

Guideline Updates

Management of dyslipidemia

and prevention of

atherosclerosis...................................9

Evidence

Are antihistamine-analgesic-

decongestant combinations

effective in reducing the

duration and alleviating the

symptoms of the common

cold in adults and children? ........13

Journal Scans......................15

Case in Question

A sporadic case of

meningoencephalomylitis

with malaria and Goldenhar

syndrome .........................................19

Earth Siege: Diseases thatimpact our WORLD

Diabetes mellitus and

Tuberculosis: Convergence

of two epidemics ............................22

Emeritus Editor

Prof. Dr. S. Arulrhaj, India

Editor

Dr. K.M. Abul Hassan, India

Editorial Board

Advisors

Dr. T.N. Ravisankar, Chennai

Dr. J.A. Jayalal, Chennai

Dr. Raman Kumar, Delhi

Dr. Punitha Rebacca, Chennai

Dr. K.Surya Rao, AP

National

Dr. Adrija Rahman Chattopadya, Bangaluru

Dr. Bahulesh Metha Mumbai

Dr. Satish Chug, Hariyana

Dr. Abbas Ali, UP.Dr. Akilesh Varma, Bilalpur

Dr. Hari Dass, Kerala

Dr. Panigrahi, Mumbai

Dr. Bahulesh Metha, Mumbai

Dr. Ravi Wankehedkar, Mumbai

Dr. Anilkumar Singh, Bihar

International

Prof. Dr. Riaz Qureshi Saudi Arabia

Prof. Dr. Pratap Prasad Kathmandu

Dr. Preethi Wijayaguna Wardane Srilanka

Dr. Antonetto Perera Srilanka

Dr. ALP Seneverethne Srilanka

Dr. Azizkhan Tank Pakistan

Dr. Noor Akthar Pakistan

Dr. Kanu Bala Bangladesh

Dr. Falahuzzaman Khan Bangladesh

Dr. Katherine Currow Australia

Dr. Sivashunmuganathan Malaysia

Dr. J.P. Tabon Malta

Dr. Ohneba Owusu Danso Ghana

Dr. Garth Manning CEO, WONCA

Executive-Editorial

Vishvanatha M

Shoukath Ali Kareem

Design & Layout

Ganesh KB

Gurumahesh MR `100 Per Copy

Vol. 3. Issue 1 | January 2014

Formerly The Family Practitioner of India


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The Family Doctor, The official Journal of IMA College of General Practitioners, is published by Medeka Health Pvt Ltd. #2, Jyothi Tower 1st floor, 1st

Cross, Kumaracot Layout, Highgrounds, Bangalore 560 001. Although great care has been taken in compiling and checking the information given in this

publication, the author/s, purchaser/s, sponsor/s, advertiser/s shall not be responsible or in any way liable for the present and or continued accuracy of the

information or for any errors, omissions or inaccuracies in this publication whether arising from negligence or otherwise howsoever, or for any consequencesarising there from. Opinions expressed do not necessarily reflect the views of the publisher, editor or the editorial board.

IMA College of General Practitioners - HQRS, Chennai, India.

IMA TN State Hqrs Building, Doctors Colony, Via Bharathi Nagar

First Main Road, Off. Mudichur Road, Tambaram, Chennai 600 045.

Tel: 044 29000325 | Email: [email protected] | Web: www.imacgpindia.com

IMA College of General Practitioners

Indian Medical Association College of General Practitioners (IMACGP) is the academic wing of Indian Medical Association

catering to the academic needs of Family Physicians of India and Asia.

Started in the year 1963 by Dr. P C Bhatla, IMA CGP was aimed at providing knowledge to General Practitioners awarding

Fellowship of the College of General Practitioners with definite syllabus and curriculum approved by the College of General

Practitioners. Changing times and the need for International exposure and recognition has made IMA CGP collaborate with

other Universities.

MRCGP (International) from Royal College of GPs London

Post Graduate Diploma in Emergency Medicine from George Washington University, USA

Diploma in Family Medicine & Diploma in Emergency Medicine from Vinayaka Missions University, Salem

Diploma and M.D (Family Medicine) from Colombo

Various diploma courses through St. Peters University, Chennai.

IMA CGP conducts an annual Conference - International Congress of Family Physicians, at State, Regional and National

levels with the best international faculty gracing the event.

IMA CGP organises an All India Young Doctor Convention every year with the objective to advocate young doctors to pursue

family medicine practice as their choice and not by chance.

An International Study tour every year refreshes the members as well as provides them with first-hand information of the

Family Doctor concept in other countries.

Reincarnation of THE FAMILY DOCTOR - the motto of IMA CGP is pursued with all vigour by the College.

National President, IMA

Dr. K. Vijayakumar

Chief Patron, IMACGP

Prof. Dr. S. Arulrhaj

Secretary, General IMA

Dr. Narendra Saini

Dean,IMACGP

Dr. Pulla Rao

Secretary, IMACGP

Dr. K.M. Abul Hassan

IMA Past Secretary

Dr. T.N. Ravisankar

Joint Secretaries

Dr. A. Rajarajeswar

Dr. R. Anburajan

Dean Elect

Dr. Anil Panchnekear

Academic DirectorDr. J.A. JayalalDr. Akhilesh Verma

Dr. Avdhesh Kumar Gupta

Dr. Neeraj Kumar Gupta

Dr. P. Radha Krishna Murthy

Dr. Amrit Pal Singh

Dr. Amutha Karunanidhi

Dr. Kiranshankar Wasudeo Deoras

Dr. Piyush Kanti Roy

Dr. Satish Chandra Pandey

Governing Council Members:


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Editorial

Best Wishes

Prof. Dr. S. Arulrhaj

Chief Patron, Emeritus Editor, IMACGP

www.drarulrhaj.com | www. healthy-india.net

Dear Colleagues,

Warm Golden Jubilee Greeting from

IMA College of General Practitioners, India.

IMACGP was established in the year 1963. 2013 is the Golden Jubilee year. To commemorate this historic landmark,

the official publication of IMACGP, The Family Practioner of Indiahas been rechristined as The Family Doctorwith

professional touch in the exterior and interior.

The pilot copy of the first issue The Family Doctorwas launched on 19thSaturday, October 2013 at Hyderabad during the

Golden Jubilee Conference, GPCON and ICON 2013.

The ancestorial Family Doctor is the custodian of health of the citizen through his effective and compassionate primary care

and emergency primary care. In course of time with civilization, Family Doctor system is forgotten and tertiary care system

has come to the frontline. Though hitech health care has flourished well in India, Accessible, Affordable and Equitable

Health Carehas become a nightmare for Indian and citizen of many developing nations.

Governments and people have started evaluating the health care system in countries and finally landed at primary care can

only offer Affordable, Accessible and Equitable Health Careto all the citizen. The fulcrum of Universal Health Collage

(UHC) lies in primary care.

The key objective of IMACGP is to strengthen primary care in India by strengthening the knowledge and skills of general

practitioners through print, electronic, academic materials, courses and certification, so that they can offer efficient curative

and preventive health care to Indians.

In this direction The Family Doctorwill be a milestone to strengthen primary care in our vast nation.

I am thankful to the Editorial Board, National and International Advisors for synergizing their mind and pens to make the

journal highly purposeful and satisfying to the GPs.

Medeka Health Pvt Ltd. Bengaluru, our co-publisher needs appreciations for their efforts to fit into this Mission.

Waiting to receive your directions on the further issues of The Family Doctormoving towards its target.

Accessible, Affordable and EquitableHealth Care can only be through Primary care Physician.

Jai hind


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Minimizing CVDrisk in diabetic patients 5

A

B

C

CVD risk assessment

The risk of CVD increases with the onset

of type 2 diabetes.5The United Kingdom

Prospective Diabetes Study (UKPDS) has

identified various factors associated with

increased risk of CVD in patients with type 2diabetes. The factors are:6

m Hyperglycemia

m Dyslipidemia

m Hypertension

m Central obesity

m Cigarette smoking

Seon et al. suggested the following methods

to estimate CVD risk in type 2 diabetic

patients5:

UKPDS risk engine: To estimate the risk

of coronary heart disease and stroke for

10 years using the following risk factors

age, gender, race, current smoking

status, glycosylated hemoglobin (HbA1c),systolic blood pressure, total cholesterol,

HDL-C, and presence or absence of atrial

fibrillation.

Biochemical tests: To estimate blood

pressure, blood glucose, and blood

cholesterol levels.

Vascular examinations:

m Carotid intima-media thickness

(CIMT) for early detection of

atherosclerosis.

m Pulse wave velocity (PWV) and

augmentation index (AI) to assess

arterial stiffness.

m Flow-mediated dilation (FMD)

to assess early endothelial cell

dysfunction.

Treatment goals:The ABC of diabetes careRegulatory authorities like the American Diabetes Association

(ADA), the Joint National Committee (JNC) on Prevention,

Detection, Evaluation, and Treatment of High Blood Pressure,

and the National Cholesterol Education Program (NCEP) havesuggested that vascular complications in people with diabetes

can be reduced through control of glycemia, blood pressure,

and blood lipid levels, as well as through smoking cessation.7,8,9

Further, the National Diabetes Education Program (NDEP) has

promoted the concept of ABCs of diabetes care.1

A represents HbA1c Signifies the importance of blood glucose control in preventing

the complications of diabetes.10

Each 1% decrease in HbA1creduces the frequency of

microvascular complications by 3540%.10

The suggested target goal for glycosylated hemoglobin

(HbA1c) level: 50 mg/dL in women.7

The suggested target level for triglycerides:


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Minimizing CVDrisk in diabetic patients6

Inadequate control of CVD riskfactors: A major challenge

According to a National Health and

Nutrition Examination Survey (NHANES),less than 10% of people with type 2 diabetes

have the three major CVD risk factors undercontrol (Figure 1).11

Action plan: Interventions andrecommendations to reduceCVD risk

Lifestyle modification is the cornerstone

of treatment for reducing CV complicationsin people with diabetes. Optimal control of

blood glucose levels, lipid levels, and blood

pressure usually requires regular physicalactivity and a diet designed to reducesodium intake, alter lipid patterns, lower

blood glucose levels, and induce weight loss.If the patient displays inadequate response

to dietary modifications and exercise,drug therapy (Figure 2) may be able to

achieve target HbA1c, blood pressure, andcholesterol levels.1

Treatment of hyperglycemia with

medications like sulfonylureas,metformin, glitazones, acarbose,voglibose, and insulin has significant

effects.1

Lipid-lowering therapy (statins, fibrates)

should be considered in patients withdiabetes and dyslipidemia, specifically in

those with coronary artery disease.1

Thiazide diuretics provide effective

management of hypertension. Diabetes-

associated CVD can also be preventedor delayed by angiotensin convertingenzyme (ACE) inhibitors.1

Smoking cessation and aspiring therapyare also important factors in the reduction

of risk of CVDs.1

In addition, patient adherence and

acceptance are often challenging inpatients with type 2 diabetes mellitus and

are important aspects in the management

of the diease.2

Figure 2. Interventions to reduce cardiovascular events indiabetic patients

Diet, exercise, oral hypoglycemic agents, insulin

Diet, exercise, thiazide diuretics, ACE inhibitors, otherantihypertensive agents as needed to achive target BP levels

Diet, exercise, cholesterol lowering medications(statins, fibrates)

Physician counseling, smoking cessation programmes,medications

Diet, exercise, daily aspirin therapy, maintaince of bloodgluose and blood choesterol levels, -blockers for MI

Diet, exercise, medications, bariatric surgery(weight-loss surgery)

ACE: Angiotensin converting enzyme; BP: Blood pressure; MI: Myocardial infarction.

Hyperglycemia

Hypertension

Hyperlipidemia

Tobacco use/smoking

Vascular events

Obesity

ABC care reduces the risk of CVD: Evidencefrom landmark trials

A The UKPDS trial has demonstrated that with each 1% reduction

in mean HBA1clevel in diabetic patients was associated with a

risk reduction of:

21% for any diabetes-related endpoint (p


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Minimizing CVDrisk in diabetic patients 7

C Studies have shown that rigorous lipid

reduction therapy can reduce the risk for

CVD in people with diabetes. In addition,

it can cause significant reduction in the

incidence of stroke, myocardial infarction,

coronary artery disease, and CV mortality

(Figure 4).17-22

Take home message

Diabetes is associated with significant CV

morbidity and mortality. In order to prevent

CVD in type 2 diabetes patients, the control

of risk factors is important. The CVD risk can

be effectively minimized with ABC care: A1c,

blood pressure, and cholesterol. Daily aspirin

intake and lifestyle modifications are alsoimportant for CVD risk reduction.

Figure 3. Reduced CVD risk by lowering BP in people with diabetes

50

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20

30

40UKPDS

32

UKPDS44

UKPDS21

HOT51

CAPPP33

HOPE

DecreaseinCVevents(%)

37

CV: Cardiovascular; CVD: Cardiovascular disease; UKPDS: United Kingdom Prospective Diabetes Study; HOT:Hypertension Optimal Treatment; CAPPP: Captopril Prevention Project; HOPE: Heart Outcomes PreventionEvaluation.

CV: Cardiovascular; CARDS: Collaborative Atorvastatin Diabetes Study; HPS: Heart Protection Study; CARE:Cholesterol and Recurrent Events; LIPID: Long-term Intervention with Pravastatin in Ischemic Disease; VAHIT:

Veterans Affairs High-Density Lipoprotein Intervention Trial; FIELD: Fenofibrate Intervention and Event Loweringin Diabetes.

Pravasta

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emfibro

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ReductioninCVrisk(%)

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CARDS

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CARE

LIPID

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FIELD

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25

19

24

11

Figure 4. Lipid treatment in diabetes yields CV risk reduction

References1. Gavin JR 3rd, Peterson K, Warren-Boulton E. Reducing cardiovascular disease risk in patients with type 2 diabetes: A

message from the National Diabetes Education Program. Am Fam Physician. 2003;68(8):156974.

2. Baldwin MD. Assessing cardiovascular risk factors and selecting agents to successfully treat patients with type 2

diabetes mellitus. J Am Osteopath Assoc. 2011;111(7 Suppl 5):S212.

3. American Diabetes Association. Treatment of hypertension in adults with diabetes. Diabetes Care. 2002;25(1):S713.

4. Gomes MB, Giannella-Neto D, Faria M, et al. Estimating cardiovascular risk in patients with type 2 diabetes: A

national multicenter study in Brazil. Diabetol Metab Syndr. 2009;1(1):22.

5. Seon CS, Min KW, Lee SY, et al. Cardiovascular risk assessment with vascular function, carotid atherosclerosis and the

UKPDS risk engine in Korean patients with newly diagnosed type 2 diabetes. Diabetes Metab J. 2011;35(6):61927.

6. Turner RC, Millns H, Neil HA, et al. Risk factors for coronary artery disease in non-insulin dependent diabetesmellitus: United Kingdom Prospective Diabetes Study (UKPDS: 23) BMJ. 1998;316(7134):8238.

7. American Diabetes Association. Standards of medical care for patients withdiabetes mellitus. Diabetes Care. 2003;26(1):S33S50.

8. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the JointNational Committee on Prevention, Detection, Evaluation, and Treatmentof High Blood Pressure: The JNC 7 report. JAMA. 2003;289(19):256072.

9. National Cholesterol Education Program Expert Panel on Detection,Evaluation and Treatment of High Blood Cholesterol in Adults. Executivesummary of the Third Report of the National Cholesterol Education Program(NCEP) Expert Panel on Detection, Evaluation and Treatment of High BloodCholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285:248697.

10. Abbate SL. Expanded ABCs of diabetes. Clinical Diabetes. 2003;21(3):128133.

11. Saydah SH, Fradkin J, Cowie CC. Poor control of risk factors for vasculardisease among adults with previously diagnosed diabetes. JAMA.2004;291(3):33542.

12. Stratton IM, Adler AI, Neil HA, et al. Association of glycaemia withmacrovascular and microvascular complications of type 2 diabetes (UKPDS35): Prospective observational study. BMJ. 2000;321(7258):40512.

13. UK Prospective Diabetes Study Group. Tight blood pressure control andrisk of macrovascular and microvascular complications in type 2 diabetes:UKPDS 38. BMJ. 1998;317(7160):70313.

14. Hansson L, Zanchetti A, Carruthers SG, et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension:Principal results of the Hypertension Optimal Treatment (HOT) randomisedtrial. HOT Study Group. Lancet. 1998;351(9118):175562.

15. Niskanen L, Hedner T, Hansson L, et al. Reduced cardiovascular morbidityand mortality in hypertensive diabetic patients on first-line therapy withan ACE inhibitor compared with a diuretic/beta-blocker-based treatmentregimen: A subanalysis of the Captopril Prevention Project. Diabetes Care.2001;24(12):20916.

16. Gerstein HC. Diabetes and the HOPE study: Implications for macrovascularand microvascular disease. Int J Clin Pract Suppl. 2001;(117):812.

17. Colhoun HM, Betteridge DJ, Durrington PN, et al. Primary prevention

of cardiovascular disease with atorvastatin in type 2 diabetes in theCollaborative Atorvastatin Diabetes Study (CARDS): Multicentrerandomised placebo-controlled trial. Lancet. 2004;364:68596.

18. Collins R, Armitage J, Parish S, et al. MRC/BHF Heart Protection Studyof cholesterol-lowering with simvastatin in 5963 people with diabetes: Arandomised placebo-controlled trial. Lancet. 2003 Jun 14;361(9374):200516.

19. Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronaryevents after myocardial infarction in patients with average cholesterol levels.N Engl J Med. 1996;335(14):10019.

20. Prevention of cardiovascular events and death with pravastatin in patientswith coronary heart disease and a broad range of initial cholesterol levels.The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID)Study Group. N Engl J Med. 1998;339(19):134957.

21. Rubins HB, Robins SJ, Collins D, et al. Gemfibrozil for the secondaryprevention of coronary heart disease in men with low levels of high-densitylipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein CholesterolIntervention Trial Study Group. N Engl J Med. 1999;341(6):4108.

22. Akauola H, Alford F, Barter P, et al. Effects of long-term fenofibrate therapy

on cardiovascular events in 9795 people with type 2 diabetes mellitus (theFIELD study): Randomised controlled trial. Lancet. 2005;366:184961.


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AACEGuidelines 9

AACE Guidelines: Management

of dyslipidemia and prevention

of atherosclerosis

Dyslipidemia is a major risk factor for

coronary artery disease (CAD) and

ischemic stroke. Evidence suggests

that insulin resistance is an important risk

factor for peripheral vascular disease,

stroke, and CAD (Evidence level 3). It is well

known that an increased serum level of low

density lipoprotein (LDL) is a major cause of

atherosclerosis and coronary heart disease

(CHD). Other serum lipoproteins such as

triglyceride (TG)-rich lipoproteins, very low-

density lipoproteins (VLDL), chylomicrons,

and high density lipoproteins (HDL) also

play a vital role in the pathophysiology

of atherosclerosis.1LDL, VLDL remnants,

chylomicron remnants, small dense LDL(sdLDL), lipoprotein-A [Lp(a)], and oxidized

LDL are pro-atherogenic lipoproteins,

whereas HDL is an anti-atherogenic

lipoprotein.2

The American Association of Clinical

Endocrinologists (AACE) Medical Guidelines

for Clinical Practice provide a practical

guide for the diagnosis and treatment

of dyslipidemia and prevention ofatherosclerosis.3

Treatment recommendations inpatients with dyslipidemia andCAD risk

Treatment goals by AACE

Lipid goals for all patients should be

personalized by levels of the risk. The AACE

recommended treatment goals for major

lipid parameters in patients at risk for CAD

are given below.3

TC


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AACEGuidelines0

Patients at high-risk, healthy, and

functional older (Grade A; BEL 1).3

Combination therapy is

recommended when

The cholesterol level is markedly

increased and monotherapy does not

achieve the therapeutic goal (Grade A;

BEL 1).

Mixed dyslipidemia is present

(Grade C; BEL 3).

Niacin or fibrates in combination with

statins may be appropriate options for

many patients with hypertriglyceridemia

and associated low HDL-C (Grade B;

BEL 2)

The risk of dosage-related adverse

effects has to be reduced (Grade D;

BEL 4).3

The AACE recommends combination

therapy with cholesterol absorption

inhibitors and statins to improve the

beneficial effects of statins on TGs and

HDL-C.3

Diabetic dyslipidemia

Type 2 diabetes is also associated with

atherogenic dyslipidemias (an interrelated

group of lipoprotein abnormalities that

lead to the development of CHD), and

hence patients with type 2 diabetes have

a significantly increased risk of developing

cardiovascular disease. Once clinicalcardiovascular disease develops, these

patients have a poorer prognosis than

normoglycemic patients. The combination

of increased TG levels and decreased HDL-C

levels, which constitutes the most common

dyslipidemic pattern in type 2 diabetes,

is known as diabetic dyslipidemia.

Individuals with diabetic dyslipidemia tend

to have atherogenic sdLDL cholesterol

particles, whether or not LDL-C levels are

Table 1. Pharmacotherapy for dyslipidemia

Drug class Recommendedstarting daily dosage

Dosage range

Statins

Lovastatin 20 mg 1080 mg

Pravastatin 40 mg 1080 mg

Simvastatin 2040 mg 580 mga

Fluvastatin 40 mg 2080 mg

Atorvastatin 1020 mg 1080 mg

Rosuvastatin 10 mg 540 mg

Pitavastatin 2 mg 24 mg

FibratesFenofibrate 48145 mg 48145 mg

Gemfibrozil 1200 mg 1200 mg

Fenofibric acid 45135 mg 45135 mg

Niacin

Immediate-release 250 mg 2503000 mg

Extended-release 500 mg 50 mg, 02000 mg

Bile acid sequestrants

Cholestyramine 816 g 424 g

Colestipol 2 g 216 g

Colesevelam 3.8 g 3.84.5 g

Cholesterol absorption inhibitors

Ezetimibe 10 mg 10 mgCombination therapies (single-pill)

Ezetimibe/simvastatin 10/20 mg 10/10 to 10/80 mg

Extended-release niacin/simvastatin 500/20 mg 500/20 to 1000/20 mgaSimvastatin (80 mg)-not approved for therapy unless patient has been on treatment for more than 1 year withoutmyopathy.

TG


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AACEGuidelines 11

elevated.4Among LDL particles, sdLDL are more susceptible to

oxidation, and have longer residence time and higher affinity to

the extracellular matrix. Delayed clearance of TG-rich lipoproteins

results in the formation of sdLDL, which is associated with insulin

resistance and postprandial hyperlipidemia.2

Treatment goals by AACE

The AACE recommended treatment LDL goals for diabetic

patients are3

Diabetes alone


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15/28

Antihistamine-analgesic-decongestants for cold 13

Several over-the-counter (OTC) preparations

comprising of antihistamines, decongestants,

and/or analgesics are being widely used in

the treatment of the common cold. However,

the efficacy of these preparations has beenquestioned by conflicting clinical evidence. These

unclear and conflicting results urged a group of

Belgian researchers to evaluate the efficacy of

these combinations in reducing the duration and

alleviating the symptoms of the common cold in

adults and children.

In this study, data was procured from the

Cochrane Central Register of Controlled Trials

(CENTRAL, The Cochrane Library 2011, Issue 4),

which contains the Cochrane Acute RespiratoryInfections Groups Specialized Register, OLD

MEDLINE (1953 to 1965), MEDLINE (1966 to

November Week 3, 2011), and EMBASE (1990

to December 2011). Only those randomized

controlled trials which had evaluated the

efficacy of antihistamine-decongestant-analgesic

combinations in comparison to placebo and other

active treatments (excluding antibiotics) were

included. The trials were categorized according

to the active ingredients studied. Two review

authors independently extracted and summarized

EVIDENCEEBM for cliniciansAre antihistamine-analgesic-

decongestant combinations

effective in reducing the duration

and alleviating the symptoms ofthe common cold in adults and

children?

Evidence for ancient medicinal

remedies found in 5,100-year-oldEgyptian wine jarsA selection of wine jars from Scorpion Is tomb atAbydos, laid out on the desert sand. (Photographcourtesy of German Institute of Archaeology,Cairo.)

For further details, visit http://www.pennmuseum.org/press-releases/658-5100-year-old-chemical-evidence-for-ancient-medicinal-remedies-discovered-in-ancient-egyptian-wine-jars.html

Dr. B. Sundara Rajan, MS DLOSenior ENT ConsultantBeent Hospital19, Devadoss Street

Vedachala Nagar

Chengalpattu - 603 001Tamil Nadu, India


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Antihistamine-analgesic-decongestants for cold4

data on general recovery, nasal obstruction, rhinorrhea, sneezing, cough, and

side effects. A total of 27 trials (n=5117) were considered. Of these, 14 trials

evaluated antihistamine-decongestant combinations, 2 studied antihistamine-

analgesic combinations, 6 studied analgesic-decongestant combinations, and 5

studied antihistamine-analgesic-decongestant combinations. Active ingredients

were used in 6 trials, whereas placebo was used in 21 trials. In most of the trials,

there were large differences in design, participants, interventions, and outcomes,and moreover, pooling was possible only for a limited number of studies and

outcomes.

Based on the clinical results obtained for various combinations (Table 1),

the authors of the study concluded that antihistamine-analgesic-decongestant

combinations have some general benefits in adults and older children (but not

in young children). However, these benefits must be weighed against the risk of

adverse effects.

Table 1. Results of various clinical trialsFormulation(No. of trials)

Observation Clinical findings Adverse effects

Antihistamine-decongestant (12)

Eight trials reported on globaleffectiveness, of which only 6could be pooled (Active treatment:n=309; Placebo: n=312).

OR of treatment failure was 0.27.

NNTB was 4.

About 66% of the participantsin the active treatment groupshowed favorable responsecompared to 41% in theplacebo group.

Antihistamine-decongestant hadmore adverse effects comparedto placebo; however, this wasinsignificant.

About 19% and 13% of the patientstreated with antihistamine-decongestant and placeboexperienced 1 or more adverseeffects, respectively.

Antihistamine-analgesic (3)

Two trials reported on globaleffectiveness, data from 1 studywas presented (n=290 on activetreatment, n=292 ascorbic acid).

OR of treatment failure was 0.33.

NNTB was 6.67.

After 6 days of treatment,43% were cured in the controlgroup and 70% in the activetreatment group.

The second study alsoshowed an effect in favor ofactive treatment.

About 12% and 10% of the patientstreated with antihistamine-analgesicand placebo experienced 1 or moreadverse effects, respectively.

Analgesic-decongestant (6)

One trial reported on globaleffectiveness

Analgesic-decongestantwas beneficial in 73% of thepatients, whereas paracetamolwas beneficial only in 52% ofthe patients.

Analgesic-decongestantcombinations had significantly moreadverse effects than control.

NNTH was 14.

None of the other 2 combinationscaused significantly more adverseeffects.

Antihistamine-analgesic-decongestant (5)

Four trials reported on globaleffectiveness, of which, 2 trialscould be pooled

Global effectiveness was 52% and34% with active treatment andplacebo, respectively

OR of treatment failure was 0.47

NNTB was 5.6

The 2 trials did not reportany benefits, and another2 studies did not show anyeffects. Two studies withantihistamine-decongestant(113 children) could not bepooled.

Active treatment did not showany significant effect.

In 1 study, incidence of adverseeffects was more with activetreatment compared to placebo(2% vs. 4%).

Two other trials reported nodifferences between treatmentgroups but numbers were notreported.

NNTB: Number needed to treat for an additional beneficial outcome; OR: Odds ratio; NNTH: Number needed to treat for an additional harmful outcome.

ReferenceDe Sutter AI, van Driel ML, Kumar AA, et al. Oral antihistamine-decongestant-analgesic combinations for the common cold.

Cochrane Database Syst Rev. 2012;2:CD004976.


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Impact of a fixed-dose combination strategy

on adherence and risk factors in patients with

or at high risk of CVD

Fixed-dose combinations (FDCs) of drugs for the treatment of

blood pressure (BP), cholesterol, and platelet control significantly

improve long-term adherence in patients with or at high risk

of cardiovascular disease (CVD) when compared to usual care,

suggests the investigators of the UMPIRE trial. Majority of the

patients with CVD fail to adhere to long-term therapy. Previously

published studies have evaluated the short-term effects of FDCs in

comparison to placebo or no treatment. Thus, the objective of the

UMPIRE trial was to assess whether treatment with FDC comprising

of aspirin, statin, and two antihypertensive drugs improves long-

term adherence (defined as self-reported use of antiplatelets,

statins, and 2 antihypertensives) and changes in systolic bloodpressure (SBP) and low-density lipoprotein cholesterol (LDL-C) from

baseline. In this randomized, open-label, blinded-end-point trial,

participants with established CVD or at risk of CVD (n=2004)

were randomly treated with either of the following FDC-based

strategies (1:1):

75 mg aspirin, 40 mg simvastatin, 10 mg lisinopril, and 50 mg

atenolol (n=1002) (or)

75 mg aspirin, 40 mg simvastatin, 10 mg lisinopril, and 12.5 mg

hydrochlorothiazide

Usual care (n=1002)

Antiplatelets, statins, and 2 antihypertensives were used in

1233 participants. At baseline, the mean BP was 137/78 mmHg

and LDL-C was 91.5 mg/dL. After a median follow-up of 15

months, medication adherence was significantly high with FDC

when compared to usual care (86% vs. 65%; p


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Journal scans6

Impact of esomeprazole on sleep disturbancesin patients with GERD

Sleep disturbance is usually seen in patients with gastro-

oesophageal reflux disease (GERD); however, there is no muchdata to support the same in patients already receiving drugtherapy for GERD. A cluster-randomized, open-label studyassessed the sleep problem through a questionnaire-basedtest (PASS test) and evaluated the efficacy of esomeprazolein improving sleep disturbances in patients with GERD. In thisprimary carebased study, subjects were divided into two groups:Intervention group and control group. Patients who failed in thePASS test continued with the control group (current treatment) or

switched to the intervention group (esomeprazole 20 or 40 mg/dayfor 4 weeks). At the end of the treatment, study outcomes wereassessed based on sleep questions, which were extracted from theQuality of Life in Reflux and Dyspepsia (QOLRAD) questionnaire.

The PASS questionnaire was used to evaluate the presence orabsence of sleep disturbances.

Overall 1388 patients with evaluable data were included in the4-week analysis. About 825 patients experienced GERD-relatedsleep disturbance at baseline. A greater number of patients in

the control group reported continued sleep disturbances whencompared to the intervention group (Figure 1). Furthermore,patients in the intervention group showed improvement in QOLRADscores associated with sleep when compared to patients in thecontrol group. Researchers concluded that a PASS strategy aids in

recognising sleep disturbance in patients with GERD in primary careand may be helpful in modifying acid-suppressive therapy.

60

20

40

50

55

22.5

Control group

Continuedsleep

disturbance(%)

Intervention group

10

30

0

Figure 1. Continued sleep disturbance is high in the control group whencompared to the intervention group

High glucose level increasesrisk of dementia in individualswith or without diabetes

Diabetes is a risk factor for dementia.

However, it is not known whether patients

without diabetes are also at high risk forthe development of dementia. A team of

US researchers examined the association

between glucose levels and the risk of

dementia in subjects without dementia

(n=2067). Out of 2067 subjects, 232

participants had diabetes. During the study

period, 35,264 clinical measurements for

glucose levels and 10,208 measurements for

glycated hemoglobin levels were performed

to assess the relationship between glucose

levels and the risk of dementia. The

Cox regression model stratified patients

according to diabetes status and adjusted

for age, sex, study cohort, educational level,

level of exercise, blood pressure, status with

respect to coronary and cerebrovascular

diseases, atrial fibrillation, smoking, and

treatment for hypertension. Based on the

below clinical findings, the study researchersopined that higher glucose levels increase

the risk of dementia irrespective of the

presence or absence of diabetes mellitus.

Clinical findings

After a median follow-up period of 6.8

years, dementia was observed in 74

subjects with diabetes and 450 subjects

without diabetes.

The risk of dementia significantly (p=0.01)

increased with increase in average

glucose levels in the preceding 5 years in

subjects without diabetes.

The risk of dementia significantly (p=0.02)

increased with increase in average

glucose levels among participants with

diabetes.

Crane PK, Walker R, Hubbard RA, et al. Glucose levels andrisk of dementia. N Engl J Med. 2013;369(6):5408.

Moayyedi P, Hunt R, Armstrong D, et al. The impact of intensifying acid suppression on sleepdisturbance related to gastro-oesophageal reflux disease in primary care. Aliment Pharmacol Ther.2013;37(7):7307.

Avian H7N9 is a communicable virus

An epidemiological investigation study assessed the

transmissibility of novel avian influenza H7N9 virus. The study

also aimed to determine its efficiency of transmission. The

study included 2 patients (father and his daughter), their close


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Case in Question 19

A27-year-old male was hospitalized in anunconscious state after he was referred fromanother private hospital. The patient had convulsions

the previous day, abdominal distension and decreased

urine output since 2 days, and high grade intermittent

fever and headache since 10 days.

Parameters Findings

Pulse 110 beats/min

Blood pressure 140/80 mmHg

Temperature 103oF

Respiratory rate 38 breaths/min

Cyanosis None

Clubbing None

Icterus None

Lymphadenopathy None

Pallor and edema None

Eye Right eye: Dermoid cyst, corneal ulcer, and haziness,F=not able to see (Figure 1) , Left eye: Dermoid cystF=Normal (Figure 2), EOM=Fixed, Pupil=Normal size notreacting to light

Ear Preauricular skin tags on both sides (Figure 3)

DTR +

Central nervous system Patient was unconscious disoriented

Planter

Neck rigidity +

Respiratory system Bilateral crept

SpO2 80%

Pelvic abdomen Distention +

Cardiovascular system S1, S2 sounds were normal. No murmur

EOM: Extra ocular movement; DTR: Deep tendon reflex; SpO 2: Saturation of peripheral oxygen.

A sporadic case ofmeningoencephalomylitis with malaria

and Goldenhar syndromeDr. Amol Supe,DNB Medicine

Dr. S. Arulrhaj,MD, FRCP, (Glasg)Chairman & Head Acute Medicine,Sundaram Arulrhaj Hospitals145/5B, Jeyaraj Road, Tuticorin - 628 002Tamil Nadu, India

Examination

in

C

AS

E

Questio

n


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Case in Question20

Investigations Findings

Hemoglobin 12 g/dL

Total count 8300

Differential count Neutrophils 60%, Lymphocytes 35%, Eosinophils 5%

Platelets 2.8 Lakhs/L

Blood sugar 142 mg/dL

Blood urea 36 mg/dL

Serum creatinine 1.1 mg/dL

Serum bilirubin Direct bilirubin: 0.9 mg/dL, Indirect bilirubin: 0.5 mg/dL, Total bilirubin: 0.4 mg/dLSerum protein Protein total: 7.3 g/dL, Albumin: 4 g/dL, Globulin: 3.2 g/dL

Serum alkaline phosphate 120 IU/L

SGOT 28 U/L

SGPT 11 IU/L

Electrolyte Sodium: 136 mEq/L, Potassium: 4.6 mEq/L, Chloride: 95 mEq/L,

Serum calcium 8.5 mg/dL

Widal/MP/Dengue/ Chikungunya Negative

Blood / Urine culture Negative

HIV/ VDRL Negative

Chest X-ray Prominent bronchial marking

ECG Normal

USG abdomen Borderline hepatomegaly

ADA 1.4 (Positive)

MP for Plasmodium falciparum(ICT method)

Positive

EEG Normal

CSF analysis Cell Count: 36 (p-20% L= 80%), Sugar: 79 mg/dL, Protein: 78 mg/dL, Globulin: Positive,Chloride: 120 mEq/L

CSF malaria Negative

CSF C&S Negative

CSF cytology No immature cell

CT brain Cerebral edema (Figure 4)

MRI brain Mild prominence left ventricle, mild enhancement of leptomeningis seen in temporoparietalregion, suggestive of meningitis (Figure 5)

ESR: Erythrocyte sedimentation rate; SGOT: Serum glutamic oxaloacetic transaminase; SGPT: Serum glutamic pyruvate transaminase; MP: Malarial parasite; HIV: Humanimmunodeficiency virus; VDRL: Venereal Disease Research Laboratory; CSF: Cerebrospinal fluid; MRI: Magnetic resonance imaging; ICT: Immunochromatographic test; ADA:Adenosine deaminase test; EEG: Electroencephalography; CT: Computed tomography

What would be your provisional diagnosis?

a) Meningoencephalitis

b) Congenital abnormality

Further investigations

Figure 1. Right eye with dermoid cystand corneal ulcer

Figure 2. Left eye with dermoid cyst Figure 3. Preauricular skin tags


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Diabetes and TuberculosisDiabe an Tu e o

Introduction

Globally, tuberculosis (TB)represents a major source ofmorbidity and mortality.1Diabetes isanother disease that is increasing inprevalence worldwide and is certainto be one of the most challenginghealth problems in the 21stcentury,especially in developing countries.2

The association between TB anddiabetes mellitus and their synergisticrole in causing human disease is

EarthSiegeSiege

Diseases that impact our WORLD

Dr. A. Rajasekaran, MD, DTCDChest PhysicianDeputy Director of Medical Services (TB)ErodeTamil Nadu, India

well known.3Numerous studieshave reported that the prevalenceof diabetes is high among patientswith TB when compared to thegeneral population.4Diabetes notonly increases the risk of TB butalso increases the risk of treatmentfailure, death and relapses of TB,suggests Baker and colleagues.1The Tuberculosis-Diabetes StudyGroup from India suggests that earlyscreening for diabetes in patients withTB provides opportunities for better

management of the comorbidity.5

TB FACTS

More than 9 million people areaffected by TB every year.

Over 1.5 million die from TB everyyear; the majority of the deathsoccur in the developing world.

One in three people in the worldare infected with latent TB.

People infected with latent TBhave a lifelong risk of developingand falling sick with active TB.6

DIABETES FACTS

About 350 million people areaffected by diabetes.

India is the diabetes capital ofthe world with 41 million Indians

having diabetes; every fifthdiabetic in the world is an Indian.

It is predicted that the globaldiabetes prevalence will increase

by 50% by the year 2030.

The prevalence of diabetes is

similar in both high- and low-income countries.

Over 80% of diabetes deaths

occur in low and middle incomecountries.6,7

Links between TB and

diabetes: An interesting

fact

The risk of developing active TB

is a 2-step process: initial exposureto Mycobacterium tuberculosisanddisease progression. 3

22


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Case in Question24

eye vision. Goldenhar syndrome

was first reported by Goldenhar

in the year 1952.4This

syndrome is characterized by

the maldevelopment of the first

and second branchial arches,ocular dermoids, and vertebral

anomalies. All three signs have

a variable presentation and are

considered part of a spectrum

of auriculo-vertebral anomalies.

Thus, Goldenhar syndrome

is also known as oculo-

auriculovertebral syndrome.

The exact cause for Goldenhar

syndrome is unknown. Its

occurrence is sporadic in nature

but many familial cases have

also been identified.5Ocular

manifestations, ear anomalies,

and vertebral defects are

the major clinical features of

Goldenhar syndrome. Ocular

and ear manifestations include

reduced visual acuity and

preauricular tags and/or pits. In

the present case, preauricular

skin tags and dermoid cystswere observed. Surgical

interventions such as the

removal of epibulbar dermoids,

repair of cleft lip/palate,

combined surgical-orthodontic

approach for dental occlusion,

and distraction osteogenesis are

methods that are employed in

the management of Goldenhar

syndrome.6

The immunochromatographic

(ICT) test for Plasmodium

falciparumwas positive,

and hence the patient was

diagnosed to have malaria

also and was treated with

antimalarial drugs accordingly.

At the time of discharge, the

patient was stable without any

complications.

References

1. Mucaj S, Dreshaj S, Kabashi S, et al.Tuberculous meningoencephalitis. MedArh. 2010;64(3):18990.

2. Nozaki H, Koto A, Amano T, et al. Clinicalfeatures of 10 cases of tuberculousmeningitis--with special reference topatients delay and doctors delay. Kekkaku.1996;71(3):23944.

3. Byrd T, Zinser P. Tuberculosis meningitis.Curr Treat Options Neurol. 2001;3(5):427432.

4. Maan MA, Saeed G, Akhtar SJ, et al.Goldenhar syndrome: Case reports withreview of literature. Journal of PakistanAssociation of Dermatologists. 2008;18:5355.

5. Anderson PJ, David DJ. Spinal anomalies inGoldenhar syndrome. Cleft Palate CraniofacJ. 2005;42(5):47780.

6. Chen H. Goldenhar syndrome. In: Atlas ofGenetic Counseling and Diagnosis. 2nd ed.USA: Springer; 2012.

Continued from page 21

A meta-analysis shows that depression is associated with low concentrations of zinc inperipheral blood. Biol Psychiatry. 2013;74:872-878.

Slow Eating Might Help Curb Calories. Study found some people consume more when mealsare rushed. J Acad Nutri Diet Jan, 2, 2014,

Statin medication use in postmenopausal women is associated with an increased risk fordiabetes mellitus. Arch Intern Med. 2012 Jan 23;172(2):144-52.

Highlights


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