HEMOSIDERIN DEPOSITION IN PORTAL ENDOTHELIAL-CELLS - A NOVEL HEPATIC HEMOSIDEROSIS FREQUENT IN CHRONIC VIRAL HEPATITIS-B AND HEPATITIS-C

We have recently noted a hitherto undescribed hepatic hemosiderosis co nfined to endothelial cells of the portal tract in chronic viral hepat itis. In this study, this lesion was surveyed in 156 liver biopsy spec imens from patients with chronic hepatitis C and in 21 liver biopsy sp ecimens from patients with chronic hepatitis B. As controls, we examin ed 110 liver biopsy specimens from patients with primary biliary cirrh osis (PBC), 36 from patients with alcoholic liver injury, nine from pa tients with autoimmune hepatitis (AIH), and five from patients with pr imary hemochromatosis. Hemosiderin deposition was found in the endothe lial cells of venous vessels in portal tracts regardless of the presen ce or degree of hemosiderin deposition in hepatic parenchyma. This phe nomenon was observed in 65 of 156 cases (42%) of chronic hepatitis C a nd in eight of 21 (38%) cases of chronic hepatitis B. In controls, thi s lesion was frequent in AIH (78%), but infrequent in PBC (8.1%) and a lcoholic liver injury (11%). The incidence of this lesion showed signi ficant differences between chronic hepatitis: C, B, and AIH, and betwe en PBC and alcoholic liver injury. There was a positive correlation be tween the progression of disease and the incidence of this feature in chronic viral hepatitis; the incidence was 18.3% and 11.1% in milder c hronic hepatitis C and B, respectively, and 61.2% and 58.3%, respectiv ely, in more severe cases. However, this correlation was not evident i n either PBC or alcoholic liver injury. This hemosiderin deposition wa s positively correlated with the degree of piecemeal necrosis in chron ic hepatitis C, and to a lesser degree, the positive correlation was s hown in chronic hepatitis B. These findings suggest that the progressi on of chronic hepatitis and the piecemeal necrosis in chronic hepatiti s C and B, followed by the release of hepatocellular iron to portal an d periportal areas, are directly or indirectly responsible for endothe lial hemosiderosis. Further studies focusing on this peculiar phenomen on in relation to choice of therapy and evaluation of chronicity of vi ral hepatitis are encouraged. Copyright (C) 1995 by W.B. Saunders Comp any