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Cholelithiasis and gastroesophageal reflux are both very common diseases that may occur simultaneously. Management of asymptomatic gallstones is still controversial. Because severe complications due to gallstones may occur incidental cholecystectomy during nonrelated abdominal surgery may be offered to patients with coexisting gallbladder disease. The aim of this study was to assess the clinical outcome of patients after laparoscopic fundoplication and incidental cholecystectomy for cholelithiasis compared with the outcome of patients after fundoplication alone. We conducted a retrospective chart review and prospective analysis using a questionnaire of the clinical outcome of patients who underwent laparoscopic fundoplication and incidental cholecystectomy from June 1991 to January 2000 in comparison with sex- and age-matched patients who had antireflux surgery alone. Sixty-seven (6.3%) of 1065 patients had a laparoscopic cholecystectomy at the time of laparoscopic antireflux surgery; 101 (75%) of 134 answered the questionnaire. The mean follow-up time was 4.6 years. Laparoscopic cholecystectomy did not influence surgical morbidity or mortality. Postoperative symptom score (1–10) did not show a statistically significant difference regarding bloating, diarrhea, abdominal pain, nausea, vomiting, biliary problems, jaundice, pancreatitis, dysphagia for liquids and solid, heartburn, regurgitation, and chest pain when the two groups were compared. We conclude that incidental cholecystectomy during laparoscopic antireflux surgery is safe and does not appear to influence the clinical outcome of the antireflux procedure.

ObjectiveThis study tested whether substrate concentrations or fatty acid storage proteins predict storage of endogenous lipids in visceral adipose tissue (VAT) and upper body subcutaneous adipose tissue (UBSQ) fat.MethodsThe day prior to surgery, 25 patients undergoing bariatric procedures received an infusion of autologous [1‐14C]triolein‐labeled very low‐density lipoprotein (VLDL) particles, and during surgery, they received a continuous [U‐13C]palmitate infusion/bolus [9,10‐3H]palmitate tracer. VAT and UBSQ fat were collected to measure VLDL‐triglyceride (TG) storage, direct free fatty acid (FFA) storage rates, CD36 content, lipoprotein lipase (LPL), acyl‐CoA synthetase, diacylglycerol acetyl‐transferase, and glycerol‐3‐phosphate acyltransferase activities.ResultsStorage of VLDL‐TG and FFA‐palmitate in UBSQ and VAT was not different. Plasma palmitate concentrations correlated with palmitate storage rates in UBSQ and VAT (r = 0.46, P = 0.02 and r = 0.46, P = 0.02, respectively). In VAT, VLDL‐TG storage was correlated with VLDL concentrations (r = 0.53, P < 0.009) and LPL (r = 0.42, P < 0.05). In UBSQ, VLDL‐TG storage was correlated with LPL (r = 0.42, P < 0.05). CD36, acyl‐CoA synthetase, glycerol‐3‐phosphate acyltransferase, and diacylglycerol acetyl‐transferase were not correlated with VLDL‐TG or palmitate storage.ConclusionsAdipose storage of VLDL‐TG is predicted by VLDL‐TG concentrations and LPL; FFA concentrations predict direct adipose tissue FFA storage rates.

AbstractObjectiveNonalcoholic fatty liver disease can lead to hepatic inflammation/damage. Understanding the physiological mechanisms that contribute to excess hepatic lipid accumulation may help identify effective treatments.DesignWe recruited 25 nondiabetic patients with severe obesity scheduled for bariatric surgery. To evaluate liver export of triglyceride fatty acids, we measured very-low-density lipoprotein (VLDL)–triglyceride secretion rates the day prior to surgery using an infusion of autologous [1-14C]triolein-labeled VLDL particles. Ketone body response to fasting and intrahepatic long-chain acylcarnitine concentrations were used as indices of hepatic fatty acid oxidation. We measured intraoperative hepatic uptake rates of plasma free fatty acids using a continuous infusion of [U-13C]palmitate, combined with a bolus dose of [9,10-3H]palmitate and carefully timed liver biopsies. Total intrahepatic lipids were measured in liver biopsy samples to determine fatty liver status. The hepatic concentrations and enrichment from [U-13C]palmitate in diacylglycerols, sphingolipids, and acyl-carnitines were measured using liquid chromatography/tandem mass spectrometry.ResultsAmong study participants with fatty liver disease, intrahepatic lipid was negatively correlated with VLDL-triglyceride secretion rates (r = −0.92, P = 0.01) but unrelated to hepatic free fatty acid uptake or indices of hepatic fatty acid oxidation. VLDL-triglyceride secretion rates were positively correlated with hepatic concentrations of saturated diacylglycerol (r = 0.46, P = 0.02) and sphingosine-1-phosphate (r = 0.44, P = 0.03).ConclusionWe conclude that in nondiabetic humans with severe obesity, excess intrahepatic lipid is associated with limited export of triglyceride in VLDL particles rather than increased uptake of systemic free fatty acids.

AbstractBackground and AimsLiver‐related clinical consequences of non‐alcoholic fatty liver disease (NAFLD) are seen only in the minority of patients with advanced fibrosis. The aim of our study was to generate insight into a potential endocrine basis of steatohepatitis with advanced fibrosis in NAFLD.MethodsBiopsy and blood samples were prospectively collected from patients with medically complicated obesity. Patients were categorized, according to liver histology, into: (i) normal, (ii) simple steatosis (SS), (iii) non‐alcoholic steatohepatitis (NASH) with fibrosis stage (FS) 0–1 and (iv) NASH with FS ≥ 2. A broad panel of potential biomarkers included DHEA‐S, growth hormone (GH), homeostasis model assessment‐insulin resistance (HOMA‐IR), leptin, resistin, adiponectin and cytokeratin 18 (CK‐18) fragments.ResultsWe studied 160 patients (mean BMI 46.8 ± 8.2 kg/m2). Liver biopsies demonstrated normal histology in 10%, SS in 45%, NASH with FS 0–1 in 37.5% and NASH with FS ≥ 2 in 7.5%. C‐reactive protein, IL‐6, GH, CK‐18, adiponectin, HOMA‐IR and quantitative insulin sensitivity check index (QUICKI) were significantly associated with NASH in univariate analysis, but overall predictivity of these parameters was low (AUC ROC = 0.62–0.68). In contrast, all patients with NASH with FS ≥ 2 had insulin resistance, as measured by QUICKI, and GH levels <0.45 ng/ml and all but one patient with NASH FS 2–3 had low DHEA levels (<123 μg/dl).ConclusionsLow serum levels of GH and DHEA are very common in patients with NASH with more advanced fibrosis. Other biomarkers, including CK‐18 fragment levels, have predictivity characteristics that would be of low clinical utility for distinguishing patients with normal histology or SS from those with NASH. These findings demonstrate an endocrine profile associated with advanced fibrosis.

Background and PurposeEarly physical functional changes after gastric bypass surgery (GBS) are unclear, and the relationship between these changes and health-related quality of life (HR-QOL) has not been reported. We measured distances from a 6-minute walk test (6MWT) and scores on the 36-Item Short-Form Health Survey (SF-36) before and after GBS.Subjects and MethodsTwenty-five people undergoing GBS completed the SF-36 and 6MWT presurgically and at the 3-month and 6-month follow-up visits. Ratings of perceived exertion (RPE) were measured during 6MWTs.ResultsPresurgical walking distance (X̅±SD; 414.1±103.7 m) was 55%±14% of normative values. Distances increased significantly at 3 months (505.2±98.0 m) and at 6 months (551.5±101.2 m). Final RPEs decreased significantly, and HR-QOL improved significantly. Both physical and mental health components of the SF-36 improved significantly. Distance was inversely correlated with body mass throughout the study and positively correlated with the SF-36 Physical Component Summary change from 3 to 6 months.Discussion and ConclusionsImproved functional capacity was associated with enhanced HR-QOL. At 6 months, walking distances remained 75% of those for age-matched peers who had normal weight.