acute viral hepatitis clinical presentation. dignosis. epedemology of viral hepatitis infection...
TRANSCRIPT
ACUTE VIRAL HEPATITIS
CLINICAL PRESENTATION.DIGNOSIS.EPEDEMOLOGY OF VIRAL
HEPATITIS INFECTION A,B,C IN KSA.
MANAGEMENT.
Viral Hepatitis - OverviewViral Hepatitis - Overview
AA BB CC DD EESource ofvirus
feces blood/blood-derived
body fluids
blood/blood-derived
body fluids
blood/blood-derived
body fluids
feces
Route oftransmission
fecal-oral percutaneouspermucosal
percutaneouspermucosal
percutaneouspermucosal
fecal-oral
Chronicinfection
no yes yes yes no
Prevention pre/post-exposure
immunization
pre/post-exposure
immunization
blood donorscreening;
risk behaviormodification
pre/post-exposure
immunization;risk behaviormodification
ensure safedrinkingwater
Type of HepatitisType of Hepatitis
Diagnosis of hepatitis
Patient history
Physical examination
Liver function tests
Serologic tests
Symptoms and Signs Pre-icteric phase
1. Anorexia2. Fatigue3. Nausea4. Vomiting5. Arthralgia6. Myalgia7. Headache8. Photophobia9. Pharangitis10. 11.
Icteric phase::1. Enlarged liver2. Tender upper quadrant3. Discomfort4. Splenomegaly (10-20%)5. General adenopathy
Post-icteric phase
Lab Findings
1. L FT increase >5-10 times of normal
2. Markers of hepatitis B or C or A might be positive
Case report.
30/9/13Ahamed ,50y.teacher,living in jazan. abdominal discomfort, nausea, lose of appetit,coloration of urine.
Exam. Marked jaundice.
Lab. result
30/9/13 :
ALT 1745 U/L(40)
AST 990 U/L (17-59)
BIL.9.5MG/DL (0.0-1.4)
PLT:267000(150000-400000)
Lab. result
28/10/113 :
ALT 185U/L(21-72)
AST 41 U/L (17-59)
ALKALINE PHOSPHATASE 247.0 U/L.
YGT 97,0U/L
BIL.1.4MG/DL (0.0-1.4)
ALB.3.6 g/l(3.5-5.0)
PT 14,8.6 (10-14)
PLT:88000(150000-400000)
Lab. result
22/2/12 :ALT 176 U/L(21-72)
AST 61 U/L (17-59)
ALKALINE PHOSPHATASE 47 U/L.
YGT 64U/L(15.0-73)
BIL.2.4MG/DL (0.0-1.4)
ALB.3.7 g/l(3.5-5.0)
PT
DD:
1. Infectious Mononucleosis
2. Drug Induced Hepatitis
3. Chronic Hepatitis.
4. Alcohol Hepatitis
5. Cholecystitis, Cholelithiasis
6-Auto-immun hepatitis
MARKERS OF VIRAL HEPATITIS
HBV MARKERS
HCV MARKERS
HAV MARKERS
Hepatitis B Markers
anti-HBc exposure (IgM = acute)
HBsAg infection (carrier)
anti-HBs immunity
HBeAg viral replication
anti-HBe seroconversion
HBV-DNA viral replication
Hepatitis C Markers
ANTI -HCV
PCR-RNA HCV
Hepatitis A Markers
HAV igM
HAV igG
Hepatitis E Markers
HEV igM
HEV igG
HEV RNA PCR
AUTOIMMUN HEPATITIS MARKERS
ANA
ANTI MITOCHONDRIAL AB
ANTI SMOOTH MUSCLES ABS.
AUTOIMMUN HEPATITIS MARKERS
ANA (1:1280)
ANTI MITOCHONDRIAL AB(1:400)
ANTI SMOOTH MUSCLES ABS.(1:400)
FINAL DIAGNOSIS
ACUTE AI HEPATITIS
MANAGMENT
INCIDENCE OF ACUTE HEPATITIS IN 5 HEPATOLOGY CLINICS IN KSA 2013
Causes of Hepatitis
HAV HBV HCV AIH DILI
KKUH 7 3 1 11 ?
NGH 10 5 2 8 8
AMC 1 0 0 3 3
KFH 1 2 0 3 ?
DAMMAM UN.
2 1 0 1 5
TOTAL 21 11 4 26 16
Complications
1.Chronic hepatitis cirrhosis- HCC
2.Fulmnant hepatitis
FULMINANT HEPATITIS
Definition: Hepatic Failure Within 8 Weeks Of Onset Of Illness.
Manifestation: Encephalopathy and Prolonged PT
Histopathology: Massive Hepatic Necrosis.
Hepatitis B - Clinical FeaturesHepatitis B - Clinical Features
• Incubation period: Average 60-90 daysRange 45-180 days
• Clinical illness (jaundice): <5 yrs, <10%5 yrs, 30%-50%
• Acute case-fatality rate: 0.5%-1%
• Chronic infection: <5 yrs, 30%-90%5 yrs, 2%-10%
• Premature mortality fromchronic liver disease: 15%-25%
Natural History
Gow, BMJ 2001
• Sexual
• Parenteral
• Perinatal
Hepatitis B Virus Modes of Transmission
Hepatitis B Virus Modes of Transmission
Concentration of Hepatitis B Virus in Various Body Fluids
Concentration of Hepatitis B Virus in Various Body Fluids
High ModerateLow/Not
Detectable
blood semen urineserum vaginal fluid feces
wound exudates saliva sweat
tearsbreastmilk
Possible transmission route of HBV in KSA
1-Horisontal transmission (person to person) is the main transmission route 2-Perintal transmission (positive HBSAG mothers) especially if they are HBEAG positive3- Heterosexual transmission 4-Illegal injection drug use 5- Contaminated equipment used for therapeutic injections and other health care related procedures6- Folk medicine practice 7-Blood and blood products transfusion without prior screening
HBV INFECTIONbefore and after
vaccination program
OVERALL PREVALENCE OF HBsAg AMONG SAUDIS IN THE 80’S ACCORDING TO REGIONS
5.5
8.99.6
8.3
0
2
4
6
8
10
Central (n=6649) South-western(n=7235)
Eastern(n=8300)
Total (n=32183)
Pos
itiv
ity
(%)
Al-Faleh. Annals of Saudi Medicine, 1988
PREVALENCE OF HBeAg AMONG HBsAg POSITIVE SAUDIS PREGNANT WOMEN (n = 20920)
3.7
5.4
0
1
2
3
4
5
6
% of HBsAg pos. % of HBeAg Pos.
Al-Faleh, Annals of Saudi Medicine, 1988
FREQUENCY OF HBeAg AMONG HBsAg POSITIVE SAUDI CHILDREN (n=307)
17.2
19.4
17.1
17.9
15.5
16
16.5
17
17.5
18
18.5
19
19.5
Perc
ent
1-3 years(93/16)
4-6 years(103/20)
7-10 years(111/19)
Total(307/55)
Al-Faleh et al. Journal of Infection, 1992
PREVENTION STRATEGIES OF MINISTRY OF HEALTH IN KSA
Introducing HBV vaccine in EPI program; and
Mandatory screening of blood donors and expatriates.
Vaccination of risk groups.
Health education especially among
medical personnel.
History of HBV infection control in KSA
Vaccination of All infants
At birth
Vaccination of all children
at school entry
vaccination of All risk groups
mandatory
Screening of all Expatriates coming
To work in KSA
1989 1990 -
until now 1990 -
until now1990
THE CURRENT EPI IN THE KINGDOM OF SAUDI ARABIA
1. At birth BCG + HB1
2. At 6 weeks DPT1 + OPV1 Hb2
3. At 3 months DPT2 + OPV2
4. At 5 months DPT3 + OPV3
5. At 5months Measles HB3
6. At 12 monthsMMR
7. At 18 months(DPT + OPV) Booster 1
8. At 4-6 years (DPT + OPV) Booster 2
COMPARISON OF PREVALENCE OF HBsAg AMONG SAUDI CHILDREN IN 1989 (n=4575) AND 1997 (n=5355) – ACCORDING TO AGE
9.68
0 0
6.54
0.16
7.24
0.3
5.06
0
6.35
0
7.57
0.2
6.51
0.82
7.2
0.93
5.81
2.31
0
66.71
0.310
2
4
6
8
10
Perc
enta
ge
1 2 3 4 5 6 7 8 9 10 11 12
Tota
l
(Age in years)
1989 1997Al Faleh, J Infect 1999
COMPARISON OF PREVALENCE OF HBsAg AMONG SAUDI CHILDREN IN 1989 (n=4575)
AND 1997 (n=5355) – ACCORDING TO REGION
8.63
0
3.48
0.52
2.87
0
5.83
0.83
5.71
0
10.29
1.52
7.59
0
8.83
0.77
5.22
0
9.04
0
12.67
0.47
3.14
0
3.73
0.3
7.53
0
6.71
0.31
-1
1
3
5
7
9
11
13
Per
cent
age
Riy
adh
Qas
sim
Hai
l
Mak
kah
Med
ina
Ase
er
Al-B
aha
Giz
an
Naj
ran
Al-J
ouf
Tab
ouk
Dam
mam
Jedd
ah Tai
f
Tot
al
1989 1997
Al Faleh, J Infect 1999
Prevalence Of HBsAg Among Saudi Population Before & After Vaccination over 18 y
6.70%
0%0.16%
0%0%
2%
4%
6%
8%
10%
1989 1992 1997 2007/8
After
Before
1-10yr4575
1-2yr637
1-12yr 3666
Agenumbers
16-18yr1365
Long Term Seroconversion Rate Over 18 Years (Anti-HBS)
95%
77%
60%
0%
20%
40%
60%
80%
100%
1992 1997 2007/8
*Al Faleh et al Annals of Saudi meds 1993 **Al Faleh et al Journal of infection 1999
***AlFaleh et al journal of infection2008
1-2yr637
1-12yr3666
16-18yr 1365
AgeN
*
***
**
Long-Term protection of HB- vaccine over 18 years ( anti-HBS>10IU/L)(n=1355)
93%(637)
65%(3666)
38%(1365)
0%
20%
40%
60%
80%
100%
1992 1997 2007/8
1-2yr5
1-8yr13
16-18yr3
AgeRegion
AL Faleh et al, J Infection 2008
CHANGING PATTERNS OF HBsAg POSITIVITY AMONG BLOOD DONORS IN MOH,CENTRAL
BLOOD BANK 1994-2005
4.4
3.25
1.5
00.5
11.5
22.5
33.5
44.5
1994n=9690
2000n=91695
2005n=177037
4.7
3
1.4
1.971.7
2 2.2
1 1 0.8 0.780.65
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
5
Po
sit
ivit
y %
PREVALENCE OF HBsAg POSITIVITY AMONG BLOOD DONORS IN KKUH FROM 1987 TO 2008
HCV INFECTION
Transmission of HCV Percutaneous
– Injecting drug use– Clotting factors before viral inactivation– Transfusion, transplant from infected donor – Therapeutic (contaminated equipment, unsafe
injection practices)– Occupational (needlestick)
Permucosal– Perinatal– Sexual
Features of Hepatitis C Virus InfectionFeatures of Hepatitis C Virus Infection
Incubation periodIncubation period Average 6Average 6--7 weeks7 weeksRange 2Range 2--26 weeks26 weeks
Acute illness (jaundice)Acute illness (jaundice) Mild (Mild (<<20%)20%)
Case fatality rateCase fatality rate LowLow
Chronic infectionChronic infection 75%75%--85%85%
Chronic hepatitisChronic hepatitis 70% (most asx)70% (most asx)
CirrhosisCirrhosis 10%10%--20%20%
Mortality from CLDMortality from CLD 1%1%--5%5%
*Reported in U.S.
Household Transmission of HCV
Rare but not absent
Could occur through percutaneous/mucosal exposures to blood– Theoretically through sharing of contaminated
personal articles (razors, toothbrushes)
– Contaminated equipment used for home therapies• Injections*• Folk remedies
Sexual Transmission of HCV
Occurs, but efficiency is low– Rare between long-term steady partners– Factors that facilitate transmission between
partners unknown (e.g., viral titer)
Accounts for 15-20% of acute and chronic infections in the United States– Sex is a common behavior – Large chronic reservoir provides multiple
opportunities for exposure to potentially infectious partners
* Reported in U.S.
Nosocomial Transmission of HCV
Recognized primarily in context of outbreaks Contaminated equipment
– hemodialysis*– endoscopy
Unsafe injection practices– plasmapheresis,* phlebotomy– multiple dose medication vials– therapeutic injections
Natural history
Marcellin, J Hepat 1999
1989 1997 2008
No. of children
Positive(%) No. of
childrenPositive
(%)No. of
studentsPositive(%)
449639*
)0.87%(5350
2**)0.04%( 1357
)5(30.22%
Diagnostic test only by
1st-generation EIA kit .
Diagnostic test by3rd-generation EIA
kit and confirmatory test by RIBA kit.
Diagnostic test byPCR for anti- HCV
Positive cases.
Overall prevalence rate of HCV infection in KSA among children and adolescent during the last
18 yrs.
* ALFaleh et al. Hepatology 1991** ALFaleh Ann Saudi Med. 2003
Prevalence of HCV Positivity Among Different Saudi population
Type of patient number Prevalence(%)
Children from 1-18y 3854 0.1
Pregnant women 3127 0.7
Hemodialysis patients 29054 55.8
Drug addicts 9137 14
Shobokshi et al , SMJ 2003
Prevention Of HCV Transmission
Avoiding shared use of Razors or brushes and any item that pierces the skin.
Strict adherence of the universal precautions in health facilities.
Educating and training of HCW’s to the proper use of standard precautions
Folk medicine?!
HAV INFECTION
COMPARISON OF PREVALENCE OF ANTI-HAV AMONG SAUDI CHILDREN IN 1989 (n=4375) AND 1997 (n=5255) –
ACCORDING TO AGE
23.7
13.4
34.8
17.6
41.6
20.3
43.9
23.4
48.5
24
54.1
26.7
59.8
28
59.7
30.6
63.5
33.1
72.6
34.5
26.4
48.850.5
24.9
0
10
20
30
40
50
60
70
80
Per
cent
age
1 3 5 7 9 11 Total
(Age in years)
1989 1997
Al-Faleh et al. Saudi Med. J, 1999
COMPARISON OF PREVALENCE OF ANTI-HAV AMONG SAUDI CHILDREN IN 1989 (n=4375) AND
1997 (n=5255) – ACCORDING TO REGION
39
16.1
62.7
31.6
56
20.4
55
20.1
59.5
28.2
44.5
19
43.6
25.4
81.682.279.1
51.3
64.4
47.9
76
45.638.4
18.2
51.1
17.5 19
9.6
50.5
24.9
1112131415161718191
Per
cent
age
Riy
ad
h
Qa
ssim
Ha
il
Ma
kka
h
Me
din
a
Ase
er
Al-
Ba
ha
Giz
an
Na
jra
n
Al-
Jou
f
Ta
bo
uk
Da
mm
am
Jed
da
h
Ta
if
To
tal
1989 1997
PREVALENCE OF ANTI-HAV IN SAUDI CHILDREN IN 1997 ACCORDING TO SEX
25.7524
0
5
10
15
20
25
30
Per
cent
Male (n=2642) Female (n=2713)
No. of children = 5355
PREVALENCE OF ANTI-HAV IN SAUDI CHILDREN IN 1997 ACCORDING TO LOCATION
20.98
33.04
0
5
10
15
20
25
30
35
Per
cent
Urban (n=3635) Rural (n=1715)
No. of children = 5255
AGE SPECIFIC PREVALENCE OF ANTI-HAV IN SAUDIS FROM RIYADH, CENTRAL REGION
Age(Years)
1986 1994P
No. Positive/ No. Tested %
No. Positive/ No. Tested %
1 – 9 103/194 53.0 81/210 38.6 3.4 x 10.3
10 – 19 164/193 85.0 110/180 61.1 1 x 10.4
20 – 30 182/200 91.0 188/240 78.3 3 x 10.4
Total 449/587 76.5 379/630 60.2 1 x 10.4
Arif et al. Saudi J Gastroenterology, 1995
Changing pattern of Hepatitis A prevalence within the Saudi population over 18 yrs
53
24.318.1
0
10
20
30
40
50
60
1989 1999 2008
Age Region
1-10 YRS 13
1-12 yrs 13
16-18 yrs 3
*
** ***
*AlRashed R. Ann SM 1997** AlFaleh et al SMJ 1999*** AlFaleh et al WJG 2008
THANK YOU