Kaji K, Nakanuma Y, Sasaki M, Unoura M, Kobayashi K, Nonomura A
Department of Pathology (II), Kanazawa University School of Medicine, Japan.
Hum Pathol. 1995 Oct;26(10):1080-5. doi: 10.1016/0046-8177(95)90269-4.
We have recently noted a hitherto undescribed hepatic hemosiderosis confined to endothelial cells of the portal tract in chronic viral hepatitis. In this study, this lesion was surveyed in 156 liver biopsy specimens from patients with chronic hepatitis C and in 21 liver biopsy specimens from patients with chronic hepatitis B. As controls, we examined 110 liver biopsy specimens from patients with primary biliary cirrhosis (PBC), 36 from patients with alcoholic liver injury, nine from patients with autoimmune hepatitis (AIH), and five from patients with primary hemochromatosis. Hemosiderin deposition was found in the endothelial cells of venous vessels in portal tracts regardless of the presence or degree of hemosiderin deposition in hepatic parenchyma. This phenomenon was observed in 65 of 156 cases (42%) of chronic hepatitis C and in eight of 21 (38%) cases of chronic hepatitis B. In controls, this lesion was frequent in AIH (78%), but infrequent in PBC (8.1%) and alcoholic liver injury (11%). The incidence of this lesion showed significant differences between chronic hepatitis C, B, and AIH, and between PBC and alcoholic liver injury. There was a positive correlation between the progression of disease and the incidence of this feature in chronic viral hepatitis; the incidence was 18.3% and 11.1% in milder chronic hepatitis C and B, respectively, and 61.2% and 58.3%, respectively, in more severe cases. However, this correlation was not evident in either PBC or alcoholic liver injury. This hemosiderin deposition was positively correlated with the degree of piecemeal necrosis in chronic hepatitis C, and to a lesser degree, the positive correlation was shown in chronic hepatitis B. These findings suggest that the progression of chronic hepatitis and the piecemeal necrosis in chronic hepatitis C and B, followed by the release of hepatocellular iron to portal and periportal areas, are directly or indirectly responsible for endothelial hemosiderosis. Further studies focusing on this peculiar phenomenon in relation to choice of therapy and evaluation of chronicity of viral hepatitis are encouraged.
我们最近注意到一种迄今未被描述的肝铁沉积症，局限于慢性病毒性肝炎门静脉区的内皮细胞。在本研究中，对156例慢性丙型肝炎患者的肝活检标本和21例慢性乙型肝炎患者的肝活检标本进行了该病变的调查。作为对照，我们检查了110例原发性胆汁性肝硬化（PBC）患者的肝活检标本、36例酒精性肝损伤患者的标本、9例自身免疫性肝炎（AIH）患者的标本以及5例原发性血色素沉着症患者的标本。无论肝实质中铁沉积的有无或程度如何，在门静脉区静脉血管的内皮细胞中均发现有含铁血黄素沉积。这种现象在156例慢性丙型肝炎患者中的65例（42%）以及21例慢性乙型肝炎患者中的8例（38%）中观察到。在对照组中，这种病变在AIH中较为常见（78%），但在PBC（8.1%）和酒精性肝损伤（11%）中较少见。该病变的发生率在慢性丙型肝炎、乙型肝炎和AIH之间，以及PBC和酒精性肝损伤之间存在显著差异。在慢性病毒性肝炎中，疾病进展与该特征的发生率呈正相关；在较轻的慢性丙型肝炎和乙型肝炎中，发生率分别为18.3%和11.1%，在更严重的病例中分别为61.2%和58.3%。然而，这种相关性在PBC或酒精性肝损伤中均不明显。这种含铁血黄素沉积与慢性丙型肝炎中的碎片状坏死程度呈正相关，在慢性乙型肝炎中也有较弱程度的正相关。这些发现表明，慢性肝炎的进展以及慢性丙型肝炎和乙型肝炎中的碎片状坏死，随后肝细胞铁释放到门静脉和门静脉周围区域，直接或间接导致了内皮细胞铁沉积症。鼓励针对这一特殊现象进行进一步研究，以探讨其与治疗选择和病毒性肝炎慢性化评估的关系。
