BACKGROUND: Vascularized pancreas transplantation (PTx) for type I diabetes mellitus results in euglycemia at the expense of chronic immunosuppression, hyperinsulinemia, and dyslipidemia. However, the effect of PTx on native biliary lithogenesis remains unknown. METHODS: To address this issue, we retrospectively studied 72 consecutive pancreas transplant recipients and compared them with patients both with (n = 35) and without (n = 52) diabetes mellitus undergoing kidney transplantation alone (KTA). All patients underwent pretransplantation abdominal ultrasonography, which was repeated at 6- to 12-month intervals after transplantation. PTx recipients were managed with quadruple immunosuppression with OKT3 induction. Kidney transplant recipients received cyclosporine and prednisone. RESULTS: Seventeen (30.4%) of 56 evaluable PTx recipients had gallstones at a mean interval of 13 months (range, 5 to 24) after PTx. Eleven patients underwent open cholecystectomy (with one surgical exploration of common bile duct for choledocholithiasis), three underwent laparoscopic cholecystectomy, and the other three are being managed expectantly. Gallstone analysis revealed predominantly cholesterol stones. The incidence of cholelithiasis in kidney transplant recipients with and without diabetes mellitus was 27.3% and 12.2%, respectively (p = 0.04). CONCLUSIONS: Pancreas transplant and kidney transplant recipients with diabetes are predisposed to the development of gallstones compared with recipients without diabetes. An interaction between diabetes mellitus-induced gallbladder dysmotility and cyclosporine-induced cholestasis may be a possible mechanism. We recommend serial ultrasonographic examinations in pancreas transplant and kidney transplant recipients, and cholecystectomy in pancreas transplant recipients with cholelithiasis should be considered.
BACKGROUND: Vascularized pancreas transplantation (PTx) for type I diabetes mellitus results in euglycemia at the expense of chronic immunosuppression, hyperinsulinemia, and dyslipidemia. However, the effect of PTx on native biliary lithogenesis remains unknown. METHODS: To address this issue, we retrospectively studied 72 consecutive pancreas transplant recipients and compared them with patients both with (n = 35) and without (n = 52) diabetes mellitus undergoing kidney transplantation alone (KTA). All patients underwent pretransplantation abdominal ultrasonography, which was repeated at 6- to 12-month intervals after transplantation. PTx recipients were managed with quadruple immunosuppression with OKT3 induction. Kidney transplant recipients received cyclosporine and prednisone. RESULTS: Seventeen (30.4%) of 56 evaluable PTx recipients had gallstones at a mean interval of 13 months (range, 5 to 24) after PTx. Eleven patients underwent open cholecystectomy (with one surgical exploration of common bile duct for choledocholithiasis), three underwent laparoscopic cholecystectomy, and the other three are being managed expectantly. Gallstone analysis revealed predominantly cholesterol stones. The incidence of cholelithiasis in kidney transplant recipients with and without diabetes mellitus was 27.3% and 12.2%, respectively (p = 0.04). CONCLUSIONS: Pancreas transplant and kidney transplant recipients with diabetes are predisposed to the development of gallstones compared with recipients without diabetes. An interaction between diabetes mellitus-induced gallbladder dysmotility and cyclosporine-induced cholestasis may be a possible mechanism. We recommend serial ultrasonographic examinations in pancreas transplant and kidney transplant recipients, and cholecystectomy in pancreas transplant recipients with cholelithiasis should be considered.