Mukai M, Bohgaki T, Notoya A, Kohno M, Tateno M, Kobayashi S
Division of Clinical Immunology and Hematology, Department of Medicine,Sapporo City General Hospital, Chuo-ku, Sapporo, Japan.
Lupus. 2000;9(1):74-7. doi: 10.1177/096120330000900115.
We report on a 23-year-old Japanese female with a 13-year history of systemic lupus erythematosus (SLE), and two episodes of deterioration followed by treatment with high dose prednisolone. Although she had been recently treated with prednisolone (12.5 mg daily), her liver function became worse in July 1998. Results of a liver biopsy revealed multi-focal hepatic cell death in a severe fatty liver, without any inflammatory cell invasion. The biopsy also showed a positive TUNEL (Tdt-catalysed DNA nick end labelling) reaction indicating apoptosis. Her liver function recovered rapidly following steroid pulse therapy. Serum soluble Fas ligand (sFasL) was found to be elevated to a concentration of 0.395 ng/ml at the time of liver damage, but was less than 0.03 ng/ml before liver damage and after prednisolone treatment. The liver damage in this case appeared to be involved with apoptosis induced by sFasL. Although hepatitis associated with SLE is rare, apoptosis directly related to elevated sFasL levels might cause this complication.
我们报告了一名23岁的日本女性，她有13年的系统性红斑狼疮（SLE）病史，曾有两次病情恶化，随后接受大剂量泼尼松龙治疗。尽管她最近一直在服用泼尼松龙（每日12.5毫克），但在1998年7月她的肝功能恶化。肝脏活检结果显示，在严重脂肪肝中存在多灶性肝细胞死亡，无任何炎性细胞浸润。活检还显示TUNEL（末端脱氧核苷酸转移酶介导的缺口末端标记）反应阳性，表明存在细胞凋亡。经类固醇脉冲治疗后，她的肝功能迅速恢复。在肝损伤时，血清可溶性Fas配体（sFasL）浓度升高至0.395纳克/毫升，但在肝损伤前及泼尼松龙治疗后低于0.03纳克/毫升。该病例中的肝损伤似乎与sFasL诱导的细胞凋亡有关。尽管与SLE相关的肝炎很少见，但与sFasL水平升高直接相关的细胞凋亡可能导致这种并发症。
