Pol J Pathol. 2020;71(1):38-45. doi: 10.5114/pjp.2020.95414.
Nonalcoholic fatty liver disease (NAFLD), a very common comorbidity of obesity, may progress from simple steatosis to nonalcoholic steatohepatitis and liver cirrhosis. The aim of this study was to determine whether mast cells (MCs) participate in the pathogenesis of liver fibrosis in patients with NAFLD. Liver specimens collected either from obese subjects or the control group were prepared for histological examination. The patients were divided into groups depending on inflammation and fibrosis grade, and the mean total number of mast cells/mm2 and those located only in portal areas/ fibrous septa or within lobules were calculated for each grade. Mast cells were detected by pina-cyanol erythrosinate staining. There was a strong positive correlation between the number of mast cells, especially those located within portal areas and fibrous septa, and the liver fibrosis grade (r = 0.736, p < 0.0001). No similar dependency between the number of mastocytes within lobules and liver fibrosis grade was identified. The results from this study suggest the involvement of mast cells from portal areas and fibrous septa in the pathogenesis of liver fibrosis in patients with NAFLD.
非酒精性脂肪性肝病（NAFLD）是肥胖症非常常见的合并症，可能从单纯性脂肪变性发展为非酒精性脂肪性肝炎和肝硬化。本研究的目的是确定肥大细胞（MCs）是否参与NAFLD患者肝纤维化的发病机制。收集肥胖受试者或对照组的肝脏标本用于组织学检查。根据炎症和纤维化分级将患者分组，并计算每个分级的肥大细胞/mm²的平均总数以及仅位于门区/纤维间隔或小叶内的肥大细胞数量。通过哌卡氰醇红藻酸盐染色检测肥大细胞。肥大细胞数量，尤其是位于门区和纤维间隔内的肥大细胞数量与肝纤维化分级之间存在强正相关（r = 0.736，p < 0.0001）。未发现小叶内肥大细胞数量与肝纤维化分级之间存在类似的相关性。本研究结果提示门区和纤维间隔的肥大细胞参与了NAFLD患者肝纤维化的发病机制。
