Mechanisms of liver cell damage in acute hepatitis B

✍ Scribed by B. J. Mohite; S. Rath; Vineeta Bal; S. A. Kamat; S. N. Marathe; A. J. Zuckerman; Dr. R. S. Kamat

• Publisher: John Wiley and Sons
• Year: 1987
• Tongue: English
• Weight: 519 KB
• Volume: 22
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.1890220302

✦ Synopsis

Markers of hepatitis B viral infection and the evolution of immune response to these were compared with serum alanine aminotransferase (ALT) levels in adult male and non-pregnant and pregnant female patients with acute hepatitis B from the time of onset of disease to the seventh week. In the adult male and nonpregnant female patients, the peak ALT levels of about 360 IU/litre, seen at the time of onset, gradually declined during the course of the disease. Significantly, even in the seventh week, the median ALT level was abnormal (80 IU/litre). In contrast. the disease was mild in pregnant patients and the ALT levels declined rapidly, returning to normal by the third week. Markers associated with HBV replication, i.e., serum HBV-DNA and HBeAg, declined early in the course of the disease in both groups. The anti-HBc-IgM and anti-HBe responses were well evolved early in the course of the disease in both groups. HBsAg was present in the serum in large amounts (1-1.5 x 104 AU/100 p l ) early in the course of the disease and remained so up to the seventh week. Even the pregnant patients who had recovered clinically by the fourth week continued to have HBsAg in their sera in large amounts in spite of normal ALT levels. LMI and LTT responses t o HBsAg, which were practically absent in the first week, gradually increased to a peak during the fourth week and remained elevated up to the seventh week in adult male and non-pregnant female patients. In contrast, LMI response to HBsAg was absent in pregnant patients with acute hepatitis B even up to the fourth week. Thus, continued liver cell necrosis after the fourth week, as indicated by raised ALT levels. may be associated with T cell responses to HBsAg.