DR SACHIN VERMAMD( MEDICINE),FICM,FCCS

CONSULTANT INTERNAL MEDICINE & CRITICAL CARE

IVY HOSPITAL MOHALI

Hepatitis D

Introduction

Recognized in 1977 – co existent with HBV infection

A defective RNA virus than need hepadnavirus(HBV) to replicate

1980 – noticed the dependency of HDV to HBV (need HBsAg to as virion coat)

Associated with most severe form of acute and chronic HBsAg +

Epidemiology of Hepatitis D

Spread worldwide Highest in Russia, Romania, Southern Italy,

Mediterranean countries, Africa, South America Low in China, Taiwan, India Latest trends

New foci in Okinawa, certain area of China, India, Albania

Decreasing trend in Mediterranean

Prevalence in region

New Delhi : 8.1% in 1996[Irshad M et al. Eur J Gastroenterol Hepatol 1996; 8: 995-99816]

New Delhi: 10.6% in 2005[Chakraborty P et al. Indian J

Med Res2005; 122: 254-25715]

Chandigarh :14.2%[Singh et al. J Viral Hepat 1995; 2: 151-15417].

Ludhiana:10% in HBsAg-positive patients[Ghuman et al. Indian J Med Sci 1995; 49: 227-23023].

Mode of Transmission

Spread Percutaneous and sexually and through body

fluid/blood Potentially infectious in whole phase

People at risk HBV carrier, HBV unvaccinated person

IVDU Unprotected sex Exposed to unscreen blood, body fluid People receiving blood, blood product

Hepatitis D Features

IP – 5 to 64 days

Super-infection* or co-infection with HBV

CLINICAL FEATURES :

In acute CO-Infection jaundice ,fatigue, abdominal pain, loss of

appetite , nausea, vomiting ,joint pain, dark (tea colored) urine

In super-infection

CLD and HCC.

DIAGNOSIS

Following HBV-HDV co-infection both IgM anti-HDV during the acute illness and IgG anti-HDV during convalescence are detectable

Following HBV-HDV super infection, chronic HDV infection with detectable HDAg usually occurs. Both IgM anti-HDV and IgG anti-HDV remain detectable.

DIAGNOSIS

Anti LKM3 antibodies

Serologic Course

Serologic Course

Prevention

HBV-HDV CoinfectionPre or postexposure prophylaxis to prevent

HBV infection.

HBV-HDV SuperinfectionEducation to reduce risk behaviors among

persons with chronic HBV infection

TREATMENT:

1. Acute HDV infection a) Supportive care

2. Chronic HDV infection 1. interferon-alfa 2. liver transplant

a-interferon 2b 9 mu sc tiw, Rx > 12 months

21-50% lose HDV RNA and have improved histology

Relapse occurs in almost all patients stopping treatment

Can stop treatment if HBV Surface Ag disappears (rare)

Thank you