Nonalcoholic Fatty Liver Disease and Bariatric Surgery

Sindu Stephen; Ancha Baranova; Zobair M Younossi

Disclosures

Expert Rev Gastroenterol Hepatol. 2012;6(2):163-171. 

In This Article

Effects of Bariatric Surgery on NAFLD

Hepatic steatosis is seen in the majority of patients undergoing bariatric surgery. Despite this, there is a lack of large randomized controlled trials evaluating the benefits of bariatric surgery in NAFLD. Clinical implications of rapid weight loss due to early types of bariatric surgery concerned investigators, especially in light of the reports of hepatic failure associated with jejunoileal bypass. A case of hepatic failure following biliopancreatic diversion was also reported in 1992. After the loss of 83% of weight over 10 months, a patient developed acute cholestasis, hepatic failure and death.[55] These reports raised concerns, especially for patients with cirrhosis or decreased hepatic reserve.

It is important to note that any intervention leading to a rapid weight loss of greater than 1.6 kg per week could potentially increase the risk for portal fibrosis. For example, very low calorie diets have been shown to cause transient spikes in levels of liver enzymes, portal inflammation and fibrosis. It is likely that the pivotal role in liver disease exacerbation is caused by the rapid depletion of hepatic fat and an increase in visceral free fatty acids promoting a proinflammatory state.[56,57]

On the other hand, modern types of bariatric procedures do not promote exacerbation of liver symptoms. Dixon et al. evaluated the effect of weight loss following LAGB in 60 severely obese individuals with NAFLD, half of which had baseline NASH.[58] Repeat biopsies were performed after 29.5 ± 10 months. Improvements in biochemical liver tests, as well as inflammation and fibrosis, were noted (p < 0.001). Only six of the repeat biopsies revealed persistent NASH. In LAGB-induced weight loss, aminotransferase levels, especially γ-glutamyl transpeptidase levels, were predictive of liver histology improvement.[58] In 2007, Furuya et al. evaluated NAFLD histology in 18 obese patients undergoing RYGB.[59] All patients underwent baseline biopsy at time of surgery, as well as a repeat percutaneous liver biopsy at 2 years postsurgery. At baseline, 33% of patients had steatosis and 67% had NASH. Cirrhosis was seen in 5.5% of patients with NASH. After a mean bariatric weight loss of 60%, steatosis disappeared in 84% and fibrosis disappeared in 75% of the patients. Hepatocellular ballooning feature improved in 50%. Interestingly, liver biochemical variables were found within normal limits in 92.3% of patients at initial biopsy with no difference seen 2 years later.[59] Mathurin et al. performed a 5-year prospective study to evaluate NASH and fibrosis in 381 severely obese patients undergoing bariatric surgery.[60] A decrease in steatosis from 37.4 to 16% and reduction in the ballooning score from 0.2 to 0.1 was noted. Over 5 years, the percentage of patients with probable or definite NASH decreased significantly from 27.4 to 14.2%. Of note, 1 year after LAGB, the mean fibrosis score increased significantly (0.14–0.38; p < 0.0001).[60] It is unclear if worsening of fibrosis is related to a more severe natural history and worse baseline NAFLD score rather than to the procedure itself.[60] Weiner performed a second biopsy on 116 NAFLD patients who had initial liver biopsy during bariatric surgery.[4] On the first biopsy, grade 3 NAFLD was seen in 65.5% of patients and grade 4 disease was seen in 28.9%. The second biopsy after 18.6 ± 8.3 months revealed complete regression of NAFLD in 82.8%, while a complete regression of necroinflammatory activity was seen in 93.1%. Ten of the 12 patients with fibrosis also had complete remission.[4] Bell et al. reported significant improvement of the grade and stage of liver disease in 20 NAFLD patients biopsied at 15 months after bariatric surgery.[61] Additionally, surgical weight loss resulted in a decrease in hepatic malondialdehyde adduct staining that is reflective of the lipid peroxydation and CYP2E1 protein content, while CYP3A4/5 protein content was unchanged.[61] Moschen et al. showed that the weight loss after LAGB surgery drives the adipocytokine milieu towards a more anti-inflammatory state both systemically and in the liver.[62] In particular, a significant increase in serum adiponectin levels was observed at biopsies collected after the LAGB, whereas both leptin and PBEF/Nampt/visfatin levels decreased. Interestingly, resistin serum levels increased after 6 months but fell below baseline values after 12 months.[62] Other studies of patients with NAFLD bariatric surgery are summarized in Table 1. Most of the studies of NAFLD patients undergoing bariatric procedures consistently revealed an improvement in steatosis, while the results describing the effects of the procedure on hepatic fibrosis have been conflicting. Overall, surgical procedures with a large malabsorptive component seem to be well tolerated and beneficial, although mild worsening of liver disease may be seen with rapid weight loss.

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