Abstract: PUB112
Acute Hepatitis B Virus (HBV) Infection with Very High Viral Load of HBV Cleared Spontaneously in a Patient on Hemodialysis
Session Information
Category: Dialysis
- 801 Dialysis: Hemodialysis and Frequent Dialysis
Author
- Bashir, Nihal, SEHA Kidney Care, Al Ain, Abu Dhabi, United Arab Emirates
Group or Team Name
- Seha Kidney Care Al Ain Group.
Introduction
During the natural history of chronic hepatitis B virus (HBV) infection, the loss of serum hepatitis B e antigen (HBeAg) and the development of anti-HBe antibodies (HBeAg seroconversion) mark a transition from the immune-active phase of disease to the inactive carrier state.
Case Description
26 year old male patient, presented to the emergency room with history of fever, abdomnial pain and distension and hisotry of dialysis started 3 months prior to his presentation. The patient had small kindeys bilaterally on Ultrasound below 7 cms. The patient had high inflamatory markers, he was treated for klebseilla pneumoniae bactremia with improvment. HIs hepatitis screening showed hepatitis B surface antigen positive, hepatitis Be antigen and antibody are positive, Hepatitis B core Antibody IgM positive, HBV quantitative PCR showed 84,390,000 copies/ml. Hepatitis D and E were negative. Liver function test is showed in the figure below. Five months later, his HBV PCR was not detected, his HBV surface antigen is negative, Hepatitis B surface antibody titer 17.95 milli IU/ml, Hepatitis Be antigen negatie and his Hepatits Be antibody remained positive.
Discussion
In acute HBV infection, hepatitis B surface antigen (HBsAg) becomes detectable in the serum after an incubation period of 4 to 10 weeks, followed shortly by the appearance of antibody against the hepatitis B core antigen, which is predominantly of the IgM isotope in the early phase. Levels of HBV DNA are generally very high, frequently in the range of 200 million IU/mL to 200 billion IU/mL (109–1012 copies/mL). Circulating HBeAg can be detected in most patients with acute HBV infection, and these patients can readily transmit the infection. Aminotransferase levels do not increase until after viral infection is well established because time is required for specific cytotoxic T lymphocyte responses to develop against virally infected hepatocytes.