The Center for Non-Infectious Liver Disease, Institute of Alcoholic liver Disease, The Fifth Medical Center of Chinese PLA General Hospital, Beijing, 100039, China.
Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Alcohol Alcohol. 2021 Oct 29;56(6):669-677. doi: 10.1093/alcalc/agab017.
Alcohol-associated liver disease represents a spectrum of histopathological changes from steatosis to advanced fibrosis and cirrhosis. The major goals of this retrospective study were to characterize the histologic features in patients with excessive alcohol use who presented with an abnormal hepatic panel and/or abnormal radiographic imaging and did not meet the clinical diagnosis of alcoholic hepatitis or cirrhosis.
We performed a retrospective study to describe hepatic histology of 62 and 83 excessive drinkers with normal and abnormal serum aspartate transaminase, respectively. The types of inflammatory cells in the liver were characterized by immunohistochemistry for CD4, CD8, CD20, CD68 and myeloperoxidase.
Among 62 patients with aspartate aminotransferase (AST) ≤ 50 U/L, 37% had histological evidence of steatosis. Of these, we found evidence of hepatocyte ballooning (21%), lobular inflammation (50%), portal inflammation (52%) and fibrosis (14%). For those with AST > 50 U/L, the presence of hepatic steatosis, lobular inflammation and portal inflammation was observed in 29, 60 and 69% of patients, respectively. Fibrosis was found in 33%, four with bridging fibrosis, and one with cirrhosis. We observed the aggregation of CD68+ macrophages, rather than normally distributed with minimal neutrophilic infiltration. Lobular and portal lymphocytic infiltrations are primarily CD8+ T cells.
Abnormal hepatic histopathology occurs in excessive drinkers with normal transaminase activity. Future studies to determine the diagnostic modalities to detect such abnormalities and to better understand its clinical implications and long-term outcome are needed.
酒精相关性肝病代表了一系列从脂肪变性到晚期纤维化和肝硬化的组织病理学变化。本回顾性研究的主要目的是描述那些大量饮酒但不符合酒精性肝炎或肝硬化临床诊断标准、肝酶谱和/或影像学异常的患者的组织学特征。
我们进行了一项回顾性研究，描述了血清天门冬氨酸转氨酶（AST）正常和异常的 62 例和 83 例过量饮酒者的肝脏组织学。通过 CD4、CD8、CD20、CD68 和髓过氧化物酶的免疫组化来描述肝脏中的炎症细胞类型。
在 AST 水平≤50 U/L 的 62 例患者中，有 37%的患者存在组织学脂肪变性证据。其中，我们发现肝细胞气球样变（21%）、肝小叶炎症（50%）、门脉炎症（52%）和纤维化（14%）的证据。对于 AST＞50 U/L 的患者，分别有 29%、60%和 69%的患者存在肝脂肪变性、肝小叶炎症和门脉炎症。纤维化见于 33%的患者，其中 4 例为桥接纤维化，1 例为肝硬化。我们观察到 CD68+巨噬细胞的聚集，而不是正常分布和最小程度的中性粒细胞浸润。小叶和门脉淋巴细胞浸润主要是 CD8+T 细胞。
在 AST 活性正常的大量饮酒者中存在异常的肝脏组织病理学改变。需要进一步研究以确定检测这些异常的诊断方法，并更好地了解其临床意义和长期预后。
