After successful pancreas transplantation, recipients with type I diabetes mellitus achieve a return to normal fasting plasma glucose levels, normal oral glucose tolerance tests, and normal levels of HbA,C (1-7). However, whether recipients undergo alterations in counterregulatory hormonal responses to glycopenia, or improvement in counterregulation of hypoglycemia, has not been determined. These are important considerations because type I diabetic patients commonly have defective glucagon and epinephrine responses to hypoglycemia and, consequently, deranged counterregulation of hypoglycemia with its attendant risks (8-13). Therefore, presence or absence of improvement in these responses are highly relevant factors in the evaluation of the overall benefits of pancreas transplantation. Moreover, since the transplanted pancreas is denervated and since islet alpha cell and pancreatic polypeptide cell function is neurally modulated, investigation of pancreas recipients offers a unique opportunity to assess regulation ofglucagon and pancreatic polypeptide secretion from the pancreas in humans in the setting of absent central nervous system input into the islet.To evaluate hormonal counterregulation of hypoglycemia in patients with type I diabetes mellitus who have received successful pancreas allografts, we have examined glucose, glucagon, pancreatic polypeptide, and catecholamine responses during insulin-induced hypoglycemia. We have also assessed glucagon and pancreatic polypeptide responsivity to direct stimulators of alpha and pancreatic polypeptide cells (arginine and secretin, respectively) to ascertain whether possible alterations in secretory responses in pancreas recipients are specific for hypoglycemic signaling or more general in nature. In this study, the responses of pancreas recipients were compared with responses of patients with similar durations of type I diabetes mellitus, who had not received pancreas transplantation, and to nondiabetic control subjects. MethodsSubjects. 38 type I diabetic recipients of pancreas allografts with iliac vessel anastomoses and with intact native pancreases who had been transplanted between 3 and 60 mo previously were studied (Table I). All recipients were normoglycemic, had normal hemoglobin A,C levels and mildly elevated serum creatinine levels, and none were receiving exogenous insulin or other medication for diabetes. Immunosuppression was achieved with the triple-drug regimen of azathioprine, cyclosporine, and prednisone (14). 54 patients with type I diabetes and with similar age, sex distribution, body-mass index, serum creatinine levels, and duration ofdiabetes, as well as 26 normal volunteers of similar age, sex distribution, and body-mass index, were studied to obtain control data. All subjects were admitted to the University

To evaluate the metabolic consequences of pancreas transplantation with systemic venous drainage on beta-cell function, we examined insulin and C-peptide responses to glucose and arginine in type I (insulin-dependent) diabetic pancreas recipients (n = 30), nondiabetic kidney recipients (n = 8), and nondiabetic control subjects (n = 28). Basal insulin levels were 66 +/- 5 pM in control subjects, 204 +/- 18 pM in pancreas recipients (P less than 0.0001 vs. control), and 77 +/- 17 pM in kidney recipients. Acute insulin responses to glucose were 416 +/- 44 pM in control subjects, 763 +/- 91 pM in pancreas recipients (P less than 0.01 vs. control), and 589 +/- 113 pM in kidney recipients (NS vs. control). Basal and stimulated insulin levels in two pancreas recipients with portal venous drainage were normal. Integrated acute C-peptide responses were not statistically different (25.3 +/- 4.3 nM/min in pancreas recipients, 34.2 +/- 5.5 nM/min in kidney recipients, and 23.7 +/- 2.1 nM/min in control subjects). Similar insulin and C-peptide results were obtained with arginine stimulation, and both basal and glucose-stimulated insulin-C-peptide ratios in pancreas recipients were significantly greater than in control subjects. We conclude that recipients of pancreas allografts with systemic venous drainage have elevated basal and stimulated insulin levels and that these alterations are primarily due to alterations of first-pass hepatic insulin clearance, although insulin resistance secondary to immunosuppressive therapy (including prednisone) probably plays a contributing role. To avoid hyperinsulinemia and its possible long-term adverse consequences, transplantation of pancreas allografts into sites with portal rather than systemic venous drainage should be considered.

To ascertain the consequences of pancreas transplantation with systemic venous drainage on glucose homeostasis and insulin secretion, glucose and insulin responses to intravenous glucose were compared in 10 recipients and 15 normal control subjects. There were no differences in fasting glucose levels or intravenous glucose disappearance rates. However, basal insulin levels and acute insulin responses to glucose were threefold greater in the recipients. It is not clear whether this consequence of hyperinsulinemia in the recipients is due to the abnormal circulatory drainage, the lack of autonomic input, or concurrent immunosuppressive drug therapy.

Purpose:To analyze the prevalence and resistance rates of bacterial agents causing urinary tract infections (UTIs) in Aseer, Saudi Arabia (2013–2016).Patients and Methods:This was a 4-year (2013–2016) retrospective study undertaken in Aseer Central Hospital, Saudi Arabia. A total of 49,779 urine and other UT specimens obtained from patients suspected of having a UTI were analyzed. Urine specimens were inoculated onto cystine lactose electrolyte deficient agar following standard procedures. Cultures showing significant bacteriuria were subjected to identification and sensitivity testing using VITEK 2 system. Data of patients and uropathogens were assembled, checked, and analyzed using SPSS software.Results:Culture positive samples were 49,779 (59.9% males, 40.1% females; P = 0.000). Year trend showed significant variations (P = 0.000) and the forecast trend line hypothesized a clear rise. Age groups 70–79 years were the most vulnerable group (22.3%). Gram-negative bacilli were 91.8% and the major species were Escherichia coli - 39.7%, Klebsiella pneumoniae - 15.8%; Pseudomonas aeruginosa - 13.8%, Proteus mirabilis - 10.6%, and Acinetobacter baumannii - 5%. Antimicrobials with high sensitivity rate were linezolid (99.1%), daptomycin (89.3%), vancomycin (86.7%), teicoplanin (85.5%), ertapenem (85.1%), fosfomycin (82.1%), and tigecycline (80.2%). High resistant rates to uropathogens were encountered with cephalothin (89.8%), nalidixic acid (86.7%), and ampicillin (81.9%).Conclusions:The majority of uropathogens were resistant to antibiotics commonly used in clinical practice. Linezolid, daptomycin, and vancomycin showed the lowest resistance to all uropathogens; this can be revised for empirical treatment of UTIs. Continuous surveillance of uropathogens and their susceptibility is important.