de Caestecker J S
Glenfield Hospital, Leicester, UK.
Eur J Gastroenterol Hepatol. 1997 Feb;9(2):145-7. doi: 10.1097/00042737-199702000-00007.
In primary biliary cirrhosis (PBC), liver damage results from both immune- and bile acid-mediated mechanisms. Therapies directed against the former have been either ineffective or toxic, while bile salt therapy is well tolerated but of uncertain long-term benefit. Because of slow disease progression, there is a need for surrogate markers of long-term efficacy. Candidates include markers of immune activation, such as soluble intercellular adhesion molecule-1 (sICAM-1) which shows promise in this respect. Using this marker, evidence has been presented to suggest an additive effect of the combination of ursodeoxycholic acid (UDCA) with azathioprine and prednisone in a short-term trial in PBC.
在原发性胆汁性肝硬化(PBC)中,肝脏损伤是由免疫介导和胆汁酸介导的机制共同导致的。针对前者的治疗方法要么无效,要么有毒性,而胆汁盐治疗耐受性良好,但长期益处尚不确定。由于疾病进展缓慢,需要有长期疗效的替代标志物。候选标志物包括免疫激活标志物,如可溶性细胞间黏附分子-1(sICAM-1),它在这方面显示出前景。使用该标志物,在一项针对PBC的短期试验中,已有证据表明熊去氧胆酸(UDCA)与硫唑嘌呤和泼尼松联合使用具有相加效应。