Viral hepatitis

1. Dr.Vadivel Kumaran.S,MD.,DM
Consultant Medical Gastroenterologist &
Hepatologist
SUGAM CLINIC
&
GASTRO CARE
CENTRE,
ADAMBAKKAM

2. `
Find the MISSING million

4. WHAT IS VIRAL HEPATITIS?
 A systemic disease with primary inflammation of liver
by hepato-tropic viruses commonly & rarely by non-
hepatotropic viruses.
 Hepatotropic virus- Hepatitis-A,B(D) & C.
 Non-hepatotropic virus- HSV,EBV,CMV & Yellow fever.

6. MOST COMMON SYMPTOMS
 Fever (87%)
 Malaise (74%)
 Jaundice (62%)
 Additional prodromal symptoms fatigue, weakness,
anorexia, nausea, vomiting and abdominal pain.
 Less common symptoms headache, arthralgias, myalgias
and diarrhea.

8. HEPATITIS-A
 Acute hepatitis-A can have a prolonged or a relapsing course.
 5 clinical patterns:
(1)Asymptomatic without jaundice.
(2)Symptomatic with jaundice and self-limited after
approximately 8 weeks.
(3)Cholestatic, with jaundice lasting 10 weeks or more.
(4)Relapsing, with 2 or more bouts of acute HAV infection
occurring over a 6- to 10-week period; and
(5)FHF(Age>75yrs).

9.  Evanescent rash (14%)
Arthralgias (11%)
 Leukocytoclastic vasculitis, Glomerulonephritis,Arthritis
 Toxic epidermal necrolysis, fatal myocarditis, renal failure in
the absence of liver failure, optic neuritis, transverse myelitis,
polyneuritis and cholecystitis
 Thrombocytopenia, aplastic anemia and red-cell aplasia
Extrahepatic Manifestations
Hepatitis-A

10. VACCINATION

13. DETECTION
 HBsAg- First marker for detecting infection.
 HBsAg negative:
HBsAg gene-mutant HBV- anti-HBc.
“occult” hepatitis B- HBV DNA (<200 IU/mL)

14. Extrahepatic Manifestations
 Arthritis-Dermatitis
 PAN
 Nephrotic syndrome & Glomerulonephritis- Membranous &
MPGN
 Cryoglobulinemia

17. VACCINATION

18. Special polpulation
 HBeAg positive mothers- in the third trimester.
 Severe Acute Hepatitis-
HBeAg >3months, INR>1.5 & Jaundice >4weeks
 Cirrhosis
 HBV-HIV Coinfection- CD4 count less than 350/mm3-
lamivudine and tenofovir
 HBV-HCV Coinfection

19. Lenvervimab, a mAb against HBsAg,
can induce sustained HBsAg loss in a chronic hepatitis B
Kim J-H, et al. ILC 2019; PS-077
CONCLUSIONS Removal of HBsAg by Lenvervimab resulted in
restoration of HBV immune responses. Sustained HBsAg loss was achieved
by elimination of HBV+ hepatocytes.
Chronic
hepatitis
B:
Immune
balance
Immune
response
restored
Functio
nal cure
Chronic
hepatitis B
again:
Balance
restored
Lenvervimab
treatment
Immune
cells
HBs
Ag
Lenverv
imab

20. Hepatitis-C infection
 HCV successfully evades the host immune response in
50% to 90% of acutely infected persons.
 Chronic hepatitis C is the only chronic viral infection
that can be cured by antiviral therapy.

22. Extrahepatic Manifestations

23. Global real-world sofosbuvir/
velpatasvir as a simple regimen
BACKGROUND & AIMS
• The WHO has set a global goal to eliminate HCV as a public health
threat by 2030; pangenotypic regimens provide opportunities to simplify
treatment access
• SOF/VEL is a pangenotypic, panfibrotic, PI-free, single-duration, single-
tablet regimen
• Efficacy of SOF/VEL for 12 weeks without RBV was evaluated in an
integrated analysis of a heterogeneous real-world cohort of adults with
HCV, including with compensated cirrhosis (CC)
METHODS
• Data from 12 cohorts across North America, Canada and the EU
included*
• CC was determined and patients treated according to local standards
of care
• SVR was assessed ≥12 weeks after
end of treatment (SVR12)

24. HCV in CKD on HD
 SOFOSBUVIR 200mg on HD days + DACLATASVIR
60mg daily for 6-months.

27. HBV+HDV

29. Vaccination
 Recombinant truncated HEV capsid protein
 Truncated ORF2 protein
At 0, 1, and 6 months

31. EBV
 Triad of pharyngitis, fever, and lymphadenopathy
 Liver involvement is nearly universal
 Elevated levels of alkaline phosphatase
 Fulminant EBV hepatitis- immunosuppressive agents
& stem cell transplantation.
 Hemophagocytic lymphohistiocytosis (HLH)- fever,
hepatosplenomegaly, hepatic synthetic dysfunction,
cytopenias, and marked hyperferritinemia (>10,000
μg/L)

32. CMV
 Primary infection or reactivation of latent infection
 Granulomatous cholestatic CMV hepatitis & fatal
hepatic necrosis
 Papillary stenosis
 Organ transplant recipients- fibrosing cholestatic
hepatitis
 Ganciclovir & Val-gancyclovir.

33. HSV
 Mucocutaneous vesicular oral or genital lesions
 Most common in 3rd trimester.
 High-dose IV acyclovir- at least 10 mg/kg every 8
hours

34. UDCA
 Regulate the levels of hydrophobic bile acids-LCA & DCA
 Increases total bile acid pool size- lowers cytotoxicity
 UDCA capacity as an antioxidant
 UDCA increased the N-acetylcysteine content
 Stone dissolution:(0.7 mm per month)
70% for stones less than 5 mm
49% for stones smaller than 10 mm
29% for stones larger than 10 mm