Contributing Factors to Postoperative Length of Stay in Laparoscopic Cholecystectomy

This study indicates that patients undergoing laparoscopic cholecystectomy have discernable characteristics that can contribute in a major way to postoperative length of stay

Heterogeneity of proliferative markers in pancreatic beta-cells of patients with severe hypoglycemia following Roux-en-Y gastric bypass

Severe postprandial hypoglycemia with neuroglycopenia is an increasingly recognized, debilitating complication of Roux-en-Y gastric bypass (RYGB) surgery. Increased secretion of insulin and incretin hormones is implicated in its pathogenesis. Histopathologic examination of pancreas has demonstrated increased islet size and/or nuclear diameter in post-RYGB patients who underwent pancreatectomy for severe refractory hypoglycemia with neuroglycopenia (RYGB + NG). We aimed to determine whether beta-cell proliferation or apoptosis is altered in RYGB + NG. We performed an observational study to analyze markers of proliferation, apoptosis, cell cycle, and transcription factor expression in pancreatic tissue from affected RYGB + NG patients (n = 12), normoglycemic patients undergoing pancreatic surgery for benign lesions (controls, n = 6), and individuals with hypoglycemia due to insulinoma (n = 52). Proliferative cell nuclear antigen (PCNA) expression was increased in insulin-positive cells in RYGB + NG patients (4.5-fold increase, p < 0.001 vs. controls) and correlated with beta-cell mass. Ki-67 immunoreactivity was low in both RYGB + NG and controls, but did not differ between groups. Phospho-histone H3 levels did not differ between RYGB + NG and controls. PCNA and Ki-67 were both significantly lower in both controls and RYGB + NG than insulinomas. Markers of apoptosis and cell cycle (M30, p27, and p21) did not differ between groups. PDX1 and menin exhibited similar expression patterns, while FOXO1 appeared to be more cytosolic in RYGB + NG. Markers of proliferation are heterogeneous in patients with severe post-RYGB hypoglycemia. Increased beta-cell proliferation in some individuals may contribute to increased beta-cell mass observed in severely affected patients548737747FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPJuvenile Diabetes Research Foundation; American Society of Metabolic and Bariatric Surgery; Graetz Foundation; Novo Nordisk Foundation; KG Jebsen Foundation; Novo Nordisk Foundation; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK