Department of Gastroenterology and Hepatology, Kochi Medical School, Nankoku, Kochi, Japan.
Hepatol Res. 2007 Oct;37 Suppl 3:S515-7. doi: 10.1111/j.1872-034X.2007.00232.x.
Recent studies of the effectiveness of ursodeoxycholic acid (UDCA) therapy in patients with primary biliary cirrhosis (PBC) reported that UDCA therapy did not necessarily stop the progression of liver fibrosis in all patients, even those with early stage PBC. Thus, there is a need for more effective treatments that could prevent asymptomatic PBC from progressing to the icteric stage. Bezafibrate is effective in approximately two-thirds of non-icteric patients who have not shown a complete response to UDCA. Serum bilirubin, aspartate aminotransferase and gamma-guanosine 5'-triphosphate levelswere significantly lower in patients who responded to additional bezafibrate on univariate analysis. The putative mechanism by which bezafibrate acts in cholestasis is by increasing phospholipid output into bile, which forms micelles with the hydrophobic bile acid that reduces its toxicity.
最近的研究表明,熊去氧胆酸(UDCA)疗法对原发性胆汁性肝硬化(PBC)患者的疗效并不一定能阻止所有患者的肝纤维化进展,即使是早期 PBC 患者。因此,需要更有效的治疗方法来预防无症状 PBC 进展为黄疸期。贝特类药物对大约三分之二的非黄疸患者有效,这些患者对 UDCA 没有完全反应。在单变量分析中,对额外贝特类药物有反应的患者的血清胆红素、天冬氨酸转氨酶和γ-鸟苷 5'-三磷酸水平显著降低。贝特类药物在胆汁淤积中的作用机制可能是通过增加磷脂向胆汁中的输出,与疏水性胆汁酸形成胶束,从而降低其毒性。