management of hepatits a
DESCRIPTION
MANAGEMENT OF HEPATITS A . Dr Rajdeep Singh Department of Gastroenterology Fortis Hospital Mohali. Human Hepatitis Viruses. Virus Genome Genome Envelope Family / genus size (kb). - PowerPoint PPT PresentationTRANSCRIPT
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MANAGEMENT OF
HEPATITS A
Dr Rajdeep SinghDepartment of Gastroenterology
Fortis Hospital Mohali
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Human Hepatitis VirusesVirus Genome Genome Envelope Family / genus
size (kb)
HAV RNA 7.5 - Picornaviridae hepatovirus
HBV DNA 3.2 + Hepadnaviridae
HCV RNA 9.6 + Flaviviridae hepacivirus
HDV RNA 1.7 + Unclassified (viroid), delta virus
HEV RNA 7.5 - Unclassified, togavirus and alpha virus-like
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Hepatitis A Virus
27 nm· Nucleic Acid: 7.5 kb ssRNA· Classification: Picornaviridae,
Hepatovirus· One serotype and multiple
genotypes· Nonenveloped, acid and heat stable· In vitro model: monkey and
human cell cultures· In vivo replication: in cytoplasm of
hepatocyte; human and other higher primates
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Hepatitis A TransmissionFecal-oral route0 Food handlers0 Travel to endemic areas
Close personal contact0 Household or sexual contact0 Daycare centers
Blood-borne (rare)0 Injecting drug users
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EPIDEMIOLOGY
Acute hepatitis A is a reportable infectious disease in the USDifferent epidemiological patterns seenIn developing countries where sanitary conditions are poor, most children are affected at an early ageMajority of pre school children in these countries had anti-HAV in serum reflecting previous subclinical infection
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In developed countries, there is low prevalence of HAV infection among children and young adultsUniversal HAV vaccination was adopted in 2005 in the US.
Zhou F, Shefer A, Weinbaum C, et al: Impact of hepatitis A vaccination on health care
utilization in the United States, 1996-2004. Vaccine 2007; 25:3581-7.(Ref 34.)
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EPIDEMIOLOGICAL SHIFT
Shift in the age of acquiring infection from childhood to older age groupsPeak age of seroprevalence is shifting from 1st decade of life to 2nd and 3rd decadesAn increase in symptomatic cases and severe clinical outcomes including fulminant hepatic failure
Indian J Med Res 128, December 2008, pp 699-704
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CASE 37 year male presents with low grade fever for 7 days associated with nausea, vomiting, retching, headache.
H/O passage of deep yellow urine, yellow eyes for 3 days and now fever has subsided. No h/o BT, surgery, jaundice in past.
On examination he is icteric, no stigmata of CLD, mild tender hepatomegaly, no splenomegaly.
Investigated found to have TSB 5mg% with direct 4%, SGOT 3675, SGPT 4698 and ALP 250, INR 1.2.
USG abdomen shows hypoechoic mild hepatomegaly with diffuse thickening of GB wall, no free fluid or spleenomegaly
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DIAGNOSTIC APPROACH ACUTE HEPATITIS IgM Anti HEV HbsAg, Anti HCV
Anti HEV + Anti HEV - Anti HEV - HbsAg ,Anti HCV neg HbsAg +, Anti HCV - HbsAg, Anti HCV - IgM Anti HBc + IgM Anti HAV +
Acute hepatitis E Acute hepatitis B Acute hepatitis A
Anti HDV+
Hepatitis D co infection
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DIAGNOSTIC APPROACH ACUTE HEPATITIS IgM Anti HAV, HEV - HbsAg, Anti HCV –
IgM Anti HBc
IgM Anti HBc + IgM Anti HBc -
Acute hepatitis B Work up for other causes of hepatitis- drugs, Wilsons, CMV, HSV, EBV
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Spectrum of sporadic acute viral hepatitis in India
Saigal Nundy Subrat
Hepatitis E 29% 45% 38%
Hepatitis B 23% 12.5% 7.3%
Hepatitis A 12% 33% 17.5%
Hepatitis C 0 0.8% 2.8%
Saigal et al , Indian Jr of Gastroenterology, 2007
Nundy et al, Medical Jr of armed forces, 2009 Subrat et al, Hepatobiliary Pancreat Dis Int,
2007
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Spectrum of acute hepatitis in India
Viral hepatitis 64%Drug induced 10%Ischemic 2%Acute fatty liver pregnancy 0.7%Cryptogenic 23%
Siagal S et al, Indian Journal of Gastroenterology , 2007
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Typical Serologic Course of Acute Hepatitis A Virus Infection
FecalHAV
ALT
IgM anti-HAV
Months after exposure
Symptoms
0 1 2 3 4 5 6 12 24
Total anti-HAV
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Clinical Variants of Hepatitis A Infection
Asymptomatic (anicteric) disease0 Children under 6 years of age, > 90%0 Children from 6-14 years old, 40-50%
Symptomatic (icteric) disease0 Adults and children over 14, 70-80%
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Clinical Patterns of HAV Infection
Cholestatic hepatitis
Relapsing hepatitis
Fulminant hepatic failure
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CHOLESTASIS
Can extend upto 8 weeksCorticosteroids have been used No conclusive evidence
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EXTRAHEPATIC MANIFESTATIONS
Evanescent rash 14%Arthralgias 11%
Leukocytoclastic vasculitisGlomerulonephritisArthritis
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RELAPSING HEPATITS A
10% of patients with acute hepatitis AShedding of HAV in stool documented during the relapse phase BenignInfection ultimately resolvesNo increase in mortality Treatment is symptomatic
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SYMPTOMATIC TREATMENT
No specific antiviral drug availableMost patients do not require hospital careRestricted physical activity High calorie diet is desirableAvoid hepatotoxic drugsSimple hygienic precautions
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MYTHSStrict bed rest
No fatty foods
No yellow foods
Sugarcane juice
Liv - 52
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HEPATITS A VACCINE
Licensed for use after 12 months of ageOnly high risk populations targeted for immunizationHAVRIX by SmithKlineVAQTA by MerckDerived from HAV grown in cell culture
Centers for Disease Control and Prevention: Prevention of hepatitis A thorough active or passive immunization. MMWR 2006; 55(No. RR07):1-23.(Ref 25.)
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HEPATITIS A VACCINE
Safe & immunogenic Long lasting immunity ~ 20 years
In age 1-18 yrs0.5 ml ( 720 ELU ) at 0, 6-12 months
In age >18 yrs1ml (1440 ELU ) at 0, 6-12 months
Centers for Disease Control and Prevention: Prevention of hepatitis A thorough active or passive immunization. MMWR 2006; 55(No. RR07):1-23.(Ref 25.)
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Post Exposure Prophylaxis
Single dose HAV vaccine within 2 weeks of exposure Long term immunity
Immunoglobulin was preferred earlier Immediate & short term protection
Centers of Disease Control and Prevention: Prevention of hepatitis A after exposure to hepatitis A virus and in international travelers. MMWR 2007; 56:1080-4.(Ref 54.)
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TWINRIXCombined formulation of HAV & HBV vaccinesApproved by FDA for persons 18 yrs or older0,1,6 schedule
At 1 year HAV seroconversion 100% HBV seroconversion 96.4 – 100%
FDA approval for a combined hepatitis A and B vaccine. MMWR 2001; 50:806.(Ref 60.)
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IAP RECOMMENDATIONS FOR USE
HAV Vaccine may be offered to all healthy children with special emphasis in risk groups
IAP Guide book on Immunization 2011
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RISK GROUPS
Patients with chronic liver diseaseCarriers of Hepatitis B and CCongenital or acquired immunodeficiencyTransplant recipientsAdolescents seronegative for HAV and leaving for boarding schoolsTravelers to high endemic areas for HAVHousehold contacts of patients with acute Hepatitis A within 10 days.
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TAKE HOME POINTS
In India, most individuals acquire natural infection in childhoodHAV infection tends to be more symptomatic in adultsHAV infection is a self limiting illnessNo specific antiviral drug is availableHAV vaccine provides long lasting immunity to individuals at risk
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THANK YOU