Abstract
INTRODUCTION: Nonalcoholic fatty liver disease (NAFLD) is an epidemic in the obese population. Bariatric surgery is known to reverse multiple metabolic complications of obesity such as diabetes, dyslipidemia, and NAFLD, but the timing of liver changes has not been well described. MATERIALS AND METHODS: This was an IRB-approved, two-institutional prospective study. Bariatric patients received MRIs at baseline and after a pre-operative liquid diet. Liver biopsies were performed during surgery and if NAFLD positive, the patients received MRIs at 1, 3, and 6 months. Liver volumes and proton-density fat fraction (PDFF) were calculated from offline MRI images. Primary outcomes were changes in weight, body mass index (BMI), percent excess weight loss (EWL%), liver volume, and PDFF. Resolution of steatosis, as defined as PDFF < 6.4% based on previously published cutoffs, was assessed. Secondarily, outcomes were compared between patients who underwent laparoscopic sleeve gastrectomy (LSG) versus laparoscopic Roux-en-Y gastric bypass (LRYGB). RESULTS: From October 2010 to June 2015, 124 patients were recruited. 49 patients (39.5%) completed all five scans. EWL% at 6 months was 55.6 ± 19.0%. BMI decreased from 45.3 ± 5.9 to 34.4 ± 5.1 kg/m(2) and mean liver volume decreased from 2464.6 ± 619.4 to 1874.3 ± 387.8 cm(3) with a volume change of 21.4 ± 11.4%. PDFF decreased from 16.6 ± 7.8 to 4.4 ± 3.4%. At 6 months, 83.7% patients had resolution of steatosis. Liver volume plateaued at 1 month, but PDFF and BMI continued to decrease. There were no statistically significant differences in liver volume or PDFF reduction from baseline to 6 months between the LSG versus LRYGB subgroups. CONCLUSION: Patients with NAFLD undergoing bariatric surgery can expect significant decreases in liver volume and hepatic steatosis at 6 months, with 83.7% of patients achieving resolution of steatosis. Liver volume reduction plateaus 1-month post-bariatric surgery, but PDFF continues to decrease. LSG and LRYGB did not differ in efficacy for inducing regression of hepatosteatosis.