We evaluated keratin 7 (K7) hepatocellular expression in 92 patients with common types of acute and chronic cholestatic diseases caused by bile duct obstruction/destruction or parenchymal lesions [acute hepatitis (n=20), mixed/pure cholestasis (n=16), primary biliary cholangitis-PBC (n=35), primary sclerosing cholangitis-PSC (n=10), vanishing bile duct syndrome (n=3), complete large bile duct obstruction due to space-occupying lesions (n=8)]. K7 immunohistochemical hepatocellular expression and ductular reaction (DR) were semi-quantitatively assessed. Results were correlated with liver enzyme serum levels, cholestasis type, histological features, hepatocellular Ki67 labelling index (LI) and HepPar1 expression. Hepatocellular K7 expression was detected in 87% (81/92) cases and in all cholestatic disease types with lowest incidence in pure/mixed cholestasis and highest in incomplete bile duct obstruction (iBDO), reaching 100% in PSC. K7-positive hepatocytes had low Ki67 LI (0-5%) retaining HepPar1 expression, irrespective of disease type. PSC cases had high K7 hepatocellular expression even with intact bile ducts, a feature that may aid differential diagnosis of cholestatic syndromes. K7 hepatocellular expression significantly correlated with cholestasis type, bile duct loss and fibrosis stage. It was higher in milder acute cholestatic hepatitis showing inverse correlation with hepatocyte proliferation and serum transaminase levels. In iBDO, younger age independently correlated with high K7 expression, while serum GGT levels showed a nearly significant correlation. Correlation with DR findings implied that K7-positive hepatocytes may result through metaplasia. In conclusion, K7 hepatocellular expression is a sensitive though non-specific marker of cholestasis. It may represent a cytoprotective reaction of resting hepatocytes in cholestasis of longer duration especially in younger patients.

我们评估了 92 例常见类型的由胆管阻塞/破坏或实质病变引起的急性和慢性胆汁淤积疾病 [急性肝炎 ( n =20)、混合/纯胆汁淤积 ( n =16)、原发性胆汁性胆管炎-PBC（n = 35），原发性硬化性胆管炎-PSC（n = 10），胆管消失综合征（n = 3），占位性病变导致的完全大胆管梗阻（n=8)]。对 K7 免疫组化肝细胞表达和导管反应 (DR) 进行半定量评估。结果与肝酶血清水平、胆汁淤积类型、组织学特征、肝细胞Ki67标记指数（LI）和HepPar1表达相关。在 87% (81/92) 的病例和所有胆汁淤积疾病类型中检测到肝细胞 K7 表达，其中纯/混合胆汁淤积的发病率最低，胆管不完全梗阻 (iBDO) 的发病率最高，在 PSC 中达到 100%。K7 阳性肝细胞具有低 Ki67 LI (0-5%)，保留 HepPar1 表达，与疾病类型无关。即使胆管完整，PSC 病例也具有高 K7 肝细胞表达，这一特征可能有助于胆汁淤积综合征的鉴别诊断。K7肝细胞表达与胆汁淤积类型显着相关，胆管丢失和纤维化阶段。它在较轻的急性胆汁淤积性肝炎中较高，与肝细胞增殖和血清转氨酶水平呈负相关。在 iBDO 中，年轻与高 K7 表达独立相关，而血清 GGT 水平显示出几乎显着的相关性。与 DR 发现的相关性暗示 K7 阳性肝细胞可能通过化生产生。总之，K7 肝细胞表达是胆汁淤积的敏感但非特异性标志物。它可能代表静息肝细胞在较长时间的胆汁淤积中的细胞保护反应，尤其是在年轻患者中。年龄较小与高 K7 表达独立相关，而血清 GGT 水平显示出几乎显着的相关性。与 DR 发现的相关性暗示 K7 阳性肝细胞可能通过化生产生。总之，K7 肝细胞表达是胆汁淤积的敏感但非特异性标志物。它可能代表静息肝细胞在较长时间的胆汁淤积中的细胞保护反应，尤其是在年轻患者中。年龄较小与高 K7 表达独立相关，而血清 GGT 水平显示出几乎显着的相关性。与 DR 发现的相关性暗示 K7 阳性肝细胞可能通过化生产生。总之，K7 肝细胞表达是胆汁淤积的敏感但非特异性标志物。它可能代表静息肝细胞在较长时间的胆汁淤积中的细胞保护反应，尤其是在年轻患者中。