Fracchia M, Secreto P, Tabone M, Zaffino C, Pera A, Galatola G
Gastroenterology Unit, Ospedale Mauriziano Umberto I, Torino, Italy.
Eur J Gastroenterol Hepatol. 2000 Apr;12(4):463-8. doi: 10.1097/00042737-200012040-00016.
Interferon-gamma may have immunopathogenic importance in primary biliary cirrhosis, stimulating aberrant expression on biliary epithelium of class II major histocompatibility molecules and inter-cellular adhesion molecule-1. Liver transcripts for interferon-gamma are found in primary biliary cirrhosis. Its serum level is increased in pretransplantation stages and decreases after transplantation.
(1) To verify whether serum interferon-gamma levels are increased in non-cirrhotic stages of primary biliary cirrhosis. (2) To evaluate the effect of ursodeoxycholic acid and prednisone alone and in combination on serum levels of interferon-gamma and soluble inter-cellular adhesion molecule-1.
Nine non-cirrhotic, anicteric patients with primary biliary cirrhosis (patient test group), 14 healthy, negative controls and 14 positive controls, with chronic hepatitis related to hepatitis C virus were studied in basal condition. Primary biliary cirrhosis patients were treated with ursodeoxycholic acid, prednisone and the association of the two drugs for three 4-week periods, each period separated by a 4-week wash-out. Interferon-gamma and soluble inter-cellular adhesion molecule-1 were measured in serum by commercially available immuno-enzymatic kits.
Median interferon-gamma levels were increased in patients with primary biliary cirrhosis compared with healthy controls (44 vs 19 pg/ml; P < 0.01) but similar to those in chronic hepatitis patients (47 pg/ml). Serum soluble inter-cellular adhesion molecule-1 was significantly reduced by ursodeoxycholic acid, and an even greater reduction was obtained on addition of prednisone. No treatment affected interferon-gamma levels.
Serum interferon-gamma is increased in noncirrhotic patients with primary biliary cirrhosis, but this is not disease-specific. Neither ursodeoxycholic acid, nor prednisone, nor the combination of the two drugs influenced this immunological pathway of primary biliary cirrhosis.
干扰素-γ在原发性胆汁性肝硬化中可能具有免疫致病重要性，可刺激II类主要组织相容性分子和细胞间黏附分子-1在胆管上皮细胞上异常表达。在原发性胆汁性肝硬化中可发现干扰素-γ的肝脏转录本。其血清水平在移植前阶段升高，移植后降低。
（1）验证原发性胆汁性肝硬化非肝硬化阶段血清干扰素-γ水平是否升高。（2）评估单独及联合使用熊去氧胆酸和泼尼松对血清干扰素-γ水平及可溶性细胞间黏附分子-1的影响。
对9例非肝硬化、无黄疸的原发性胆汁性肝硬化患者（患者试验组）、14例健康阴性对照者和14例丙型肝炎病毒相关性慢性肝炎阳性对照者进行基础状态研究。原发性胆汁性肝硬化患者接受熊去氧胆酸、泼尼松及两种药物联合治疗，为期3个4周疗程，每个疗程间隔4周洗脱期。采用市售免疫酶试剂盒检测血清中的干扰素-γ和可溶性细胞间黏附分子-1。
与健康对照者相比，原发性胆汁性肝硬化患者的干扰素-γ水平中位数升高（44 vs 19 pg/ml；P<0.01），但与慢性肝炎患者相似（47 pg/ml）。熊去氧胆酸可显著降低血清可溶性细胞间黏附分子-1水平，加用泼尼松后降低幅度更大。没有治疗影响干扰素-γ水平。
原发性胆汁性肝硬化非肝硬化患者血清干扰素-γ升高，但这并非疾病特异性表现。熊去氧胆酸、泼尼松及两种药物联合使用均未影响原发性胆汁性肝硬化的这一免疫途径。
