DR SACHIN VERMA MD( 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: ] New Delhi: 10.6% in 2005[ Chakraborty P et al. Indian J Med Res2005; 122: ] Chandigarh :14.2%[ Singh et al. J Viral Hepat 1995; 2: ]. Ludhiana:10% in HBsAg-positive patients [Ghuman et al. Indian J Med Sci 1995; 49: ].

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

Prevention HBV-HDV Coinfection Pre or postexposure prophylaxis to prevent HBV infection. HBV-HDV Superinfection Education 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)

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