Abdel-Razik Ahmed, Mousa Nasser, Shabana Walaa, Refaey Mohamed, Elzehery Rasha, Elhelaly Rania, Zalata Khaled, Abdelsalam Mostafa, Eldeeb Ahmed A, Awad Mahmoud, Elgamal Ayman, Attia Ahmed, El-Wakeel Niveen, Eldars Waleed
Departments of Tropical Medicine.
Department of Tropical Medicine, Faculty of Medicine, Zagazig University, Zagazig City.
Eur J Gastroenterol Hepatol. 2018 Oct;30(10):1237-1246. doi: 10.1097/MEG.0000000000001232.
BACKGROUND/AIMS: The pathogenesis of nonalcoholic fatty liver disease (NAFLD) may include increased insulin resistance, upregulation of proinflammatory cytokines, lipopolysaccharide, and BMI. Rifaximin is a minimally absorbable antibiotic that might act against a broad spectrum of gut bacteria. This study aimed to investigate the effects of rifaximin on NAFLD.
Fifty participants with biopsy-proven nonalcoholic steatohepatitis (NASH) were registered in this multicentric, double-blind, randomized, placebo-controlled study. BMI, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase, lipid profile, serum endotoxin, homeostatic model assessment, toll-like receptor-4, interleukin-10 (IL-10), IL-6, tumor necrosis factor-α, and cytokeratin-18 (CK-18) levels were evaluated at baseline and at 1, 3, and 6 months of rifaximin therapy (1100 mg/day).
Patients were randomized into two groups (rifaximin group; n=25 and placebo group; n=25). After 6 months of rifaximin therapy, patients with NASH showed a significant reduction in homeostatic model assessment, alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase, endotoxin, toll-like receptor-4, IL-6, tumor necrosis factor-α, CK-18, and NAFLD-liver fat score (all P<0.05), but no changes in the lipid profile; moreover, there was a mild nonstatistically significant reduction of BMI. However, in the placebo group, there was no significant difference in these variables at baseline and after therapy.
Rifaximin therapy appears to be effective and safe in modifying NASH through reduction of serum endotoxin and improvement of insulin resistance, proinflammatory cytokines, CK-18, and NAFLD-liver fat score.
背景/目的：非酒精性脂肪性肝病（NAFLD）的发病机制可能包括胰岛素抵抗增加、促炎细胞因子、脂多糖上调以及体重指数（BMI）升高。利福昔明是一种极少被吸收的抗生素，可能对多种肠道细菌起作用。本研究旨在探讨利福昔明对NAFLD的影响。
五十名经活检证实为非酒精性脂肪性肝炎（NASH）的参与者被纳入这项多中心、双盲、随机、安慰剂对照研究。在基线以及利福昔明治疗（1100毫克/天）的第1、3和6个月时，评估BMI、丙氨酸转氨酶、天冬氨酸转氨酶、γ-谷氨酰转移酶、血脂谱、血清内毒素、稳态模型评估、Toll样受体4、白细胞介素-10（IL-10）、IL-6、肿瘤坏死因子-α和细胞角蛋白-18（CK-18）水平。
患者被随机分为两组（利福昔明组；n = 25和安慰剂组；n = 25）。利福昔明治疗6个月后，NASH患者的稳态模型评估、丙氨酸转氨酶、天冬氨酸转氨酶、γ-谷氨酰转移酶、内毒素、Toll样受体4、IL-6、肿瘤坏死因子-α、CK-18和NAFLD-肝脏脂肪评分均显著降低（均P < 0.05），但血脂谱无变化；此外，BMI有轻度但无统计学意义的降低。然而，在安慰剂组中，这些变量在基线和治疗后无显著差异。
利福昔明治疗似乎通过降低血清内毒素以及改善胰岛素抵抗、促炎细胞因子水平、CK-18和NAFLD-肝脏脂肪评分来有效且安全地改善NASH。
