. More than a dozen other miscellaneous agents have been investigated in small, Selleckchem LY294002 proof-of-concept studies and their detailed evaluation is beyond the scope of this guideline. Recommendations 23. UDCA is not recommended for the treatment of NAFLD or NASH. (Strength – 1, Quality – B) 24. It is premature to recommend omega-3 fatty acids for the specific treatment of NAFLD or NASH but they may be considered as the first

line agents to treat hypertriglyceridemia in patients with NAFLD. (Strength – 1, Quality – B) As the majority of patients undergoing bariatric surgery have associated fatty liver disease, there has been an interest in foregut bariatric surgery as a potential treatment option for NASH. There are no RCTs that evaluated any type of foregut bariatric surgical procedure to specifically treat NAFLD or NASH. However, there are several retrospective and prospective cohort studies that compared liver histology in the severely obese individuals before and after bariatric surgery. Unfortunately, in the majority of these studies, post-bypass liver biopsies

were performed at varying intervals and only in selected patients undergoing surgical procedures such as hernia repair or adhesiolysis. One exception is the study by Mathurin et al.,143 that prospectively correlated clinical and metabolic data with liver histology click here before and 1 and 5 years after bariatric surgery in 381 adult patients with severe obesity. Gastric band, bilio-intestinal bypass, and gastric bypass were done in 56%, 23%, and 21%, respectively. Compared to baseline, there was a significant improvement in

the prevalence and severity of steatosis and ballooning at 1 and 5 years following bariatric surgery. In patients with probable or definite NASH at baseline 上海皓元医药股份有限公司 (n=99), there was a significant improvement in steatosis, ballooning, and NAS and resolution of probable or definite NASH at 1 and 5 years following bariatric surgery. Most histological benefits were evident at 1 year with no differences in liver histology between 1 and 5 years following bariatric surgery. Intriguingly, a minor but statistically significant increase in mean fibrosis score was noted at 5 years after the bariatric surgery (from 0.27± 0.55 at baseline to 0.36 ± 0.59, P=0.001). Despite this increase, at 5 years 96% of patients exhibited fibrosis score ≤ F1 and 0.5% had F3, indicating there is no clinically significant worsening in fibrosis that can be attributed directly to the procedure. In the important subgroup of patients with probable or definite NASH at baseline, there was no worsening of fibrosis at 1 and 5 years, compared to baseline liver biopsy. As no patient in the study had F3 or F4 at baseline, the effect of bariatric surgery in those with advanced fibrosis and cirrhosis could not be evaluated. Two meta-analyses144, 145 evaluated the effect of bariatric surgery on the liver histology in patients with NAFLD.