Liver histology in patients with HBsAg negative anti-HBc and anti-HCV positive chronic hepatitis

✍ Scribed by Evangelista Sagnelli; Giuseppe Pasquale; Nicola Coppola; Cecilia Marrocco; Ferdinando Scarano; Michele Imparato; Caterina Sagnelli; Carlo Scolastico; Felice Piccinino

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 71 KB
• Volume: 75
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.20260

✦ Synopsis

Abstract

The liver histology of 68 consecutive anti‐HCV/HCV‐RNA positive chronic hepatitis patients who were HBsAg/anti‐HBs negative, anti‐HBc positive (Case bC group) was compared with that of 68 anti‐HCV/HCV‐RNA positive chronic hepatitis patients who were HBsAg/anti‐HBc negative (control C group). The patients were pair‐matched by age (±5 years), sex, and risk factors for the acquisition of parenteral infection. Case bC group showed a significantly higher mean fibrosis score (2.3 ± 1.1) than control C group (1.5 ± 1.1, P < 0.001) and more histological evidence of cirrhosis (22% vs. 7.3%, P < 0.05). In addition, the patients in Case bC group showed more severe inflammation of the portal tracts (3.5 ± 0.8 vs. 3.0 ± 1.1, P < 0.005) and there was a higher prevalence of patients with rhomboid‐shaped hepatocytes (26.4% vs. 2.7%, P < 0.005), acidophilic bodies (33.8% vs. 1.4%, P < 0.0001), sinusoidal inflammation (29.4% vs. 10.3%, P < 0.01), lymphoid follicles in the portal tracts (72% vs. 44.1%, P < 0.05), Kupffer cell proliferation (29.4% vs. 11.8%, P < 0.05), bile duct damage (44.1% vs. 10.3%, P < 0.0001), and ductular proliferation (30.9% vs. 2.7%, P < 0.001) than in control C group. No difference in these histological features was observed between HBV‐DNA negative and positive patients in Case bC group. The data suggest that anti‐HBc positive patients with HCV chronic infection have a significantly higher degree of liver fibrosis, and that hepatocellular apoptosis, bile duct damage, and ductular proliferation correlate with the presence of this antibody in the serum. J. Med. Virol. 75:222–226, 2005. © 2004 Wiley‐Liss, Inc.