Inhibition of inducible nitric oxide synthase reduces bacterial translocation in a rat model of acute pancreatitis.

INTRODUCTION: Translocation of bacteria from the gut into pancreatic necrosis is an important factor in the development of septic complications and mortality in acute pancreatitis. S-methylisothiourea (SMT) is an inducible nitric oxide synthase inhibitor that has been shown to decrease bacteria] translocation in sepsis and thermal injury. AIM: To investigate whether SMT could affect bacterial translocation in acute necrotizing pancreatitis. METHODOLOGY: Forty-five Sprague-Dawley rats were studied. Acute pancreatitis was induced in Group I and Group II by injection of taurocholate and trypsin into the common biliopancreatic duct. Group III underwent laparotomy with the manipulation (but not cannulation) of the pancreas and received saline injection. Group I rats received normal saline as a placebo, and Group II rats received SMT after surgery for 2 days. At 48 hours, blood was drawn for serum amylase determinations. Bacterial translocation to mesenteric lymph nodes and distant sites (pancreas, liver, and peritoneum) were examined. A point scoring system of histologic features was used to evaluate the severity of pancreatitis. RESULTS: Plasma amylase levels and pancreatic histologic score were significantly reduced in Group II rats given SMT compared with those in Group I rats given saline (p < 0.01, p < 0.05, respectively). All Group I rats had bacterial translocation to mesenteric lymph nodes compared with 7 of 12 rats in Group II (p < 0.05). There was no difference in bacterial translocation to distant organs between the two groups, although rates tended to be lower in Group II compared with Group I (p > 0.05). Bacterial counts in the pancreas were significantly reduced in Group II rats compared with those in Group I rats (p < 0.05). CONCLUSION: Treatment with SMT appears to have ameliorated the course of acute pancreatitis; however, mortality was not affected.

Accessory suprarenal gland: report of a case.

The suprarenal glands are normally located at the superomedial aspect of the kidneys. Accessory cortical masses are seen in approximately half of the newborn but usually disappear later. Several cases with accessory cortical tissues located near the main suprarenal glands have been reported but their usual locations have been rarely described. Here we report a case with accessory cortical tissue located on the right in the retrocrural space with compression symptoms. Such a lesion may be confused with lymphadenopathy radiologically.

Insulin resistance in non-alcoholic steatohepatitis.

BACKGROUND: Non-alcoholic steatohepatitis is a chronic liver disease that is capable of progressing to end-stage liver disease, but generally has a benign course. Obesity, non-insulin-dependent diabetes mellitus and hyperlipidaemia are the most common associations of the disease. AIMS: To investigate the insulin resistance in patients with non-alcoholic steatohepatitis who have no other causes of insulin resistance such as obesity, diabetes mellitus, and hyperlipidaemia. PATIENTS: Thirteen patients (7 male, 6 female) with non-alcoholic steatohepatitis and 12 (6 male, 6 female) healthy volunteers. METHODS: All patients and healthy volunteers were submitted to biochemical tests and hyperinsulinaemic euglycaemic insulin clamp technique. RESULTS: Basal insulin levels and C-peptide levels were significantly higher in non-alcoholic steatohepatitis group than in controls (p<0.001 and p<0.001, respectively). Hyperinsulinaemic euglycaemic insulin clamp technique revealed lower glucose utilization in the non-alcoholic steatohepatitis group and the difference was statistically significant (p<0.001). CONCLUSIONS: Our study revealed marked hyperinsulinaemia and insulin resistance in patients with non-alcoholic steatohepatitis. Hyperinsulinaemia and insulin resistance may contribute to pathogenesis of nonalcoholic steatohepatitis.

Detection of Helicobacter pylori colonization in dental plaques and tongue scrapings of patients with chronic gastritis.

OBJECTIVE: It has been suggested that the oral cavity and dental plaque might be a reservoir for Helicobacter pylori (Hp). In this study, our aims were to detect the prevalence of Hp colonization in dental plaque and tongue scrapings of patients with chronic gastritis and to investigate the effect of systemic treatment upon this colonization and eradication of Hp from gastric mucosa. METHOD AND MATERIALS: Eighty-one patients (49 men, 32 women) were included in the study. Dental plaque and tongue scraping specimens were obtained and assessed with Campylobacter-like organism (CLO) test, prior to endoscopic examination. By endoscopy, 2 antral and 1 corpus biopsy samples were taken for histologic examination, and 1 antral biopsy sample was taken for CLO test examination. RESULTS: Chronic gastritis was diagnosed in 63 (77.7%) of 81 patients. Dental plaque samples of 64 (79%) patients and tongue scraping samples of 48 (59.2%) patients were urease positive. Of the 63 patients with chronic gastritis, dental plaque and tongue scrapings were urease positive in 52 (83%) and 37 (59%) patients, respectively. After 14 days of triple drug therapy (omeprazole, clarithromycin, and amoxicillin), Hp was eradicated from the gastric mucosa of almost all of the patients, whereas no changes were detected in dental plaque and tongue scrapings by CLO test examination. CONCLUSION: Helicobacter pylori colonization, which seemed to be high in dental plaque and on the tongue, might play an important role in the pathogenesis of the reinfection process. In order to eradicate Hp from both the oral cavity and the gastric mucosa, studies should be performed to assess the effects of plaque control procedures in addition to present treatment modalities.

CA-125; a new marker for diagnosis and follow-up of patients with tuberculous peritonitis.

BACKGROUND: Most malignancies with peritoneal infiltration, especially ovarian cancers and chronic liver diseases associated with ascites give rise to high serum CA-125 levels. Tuberculous peritonitis is another cause for high serum CA-125 levels. AIM: To investigate the relation between serum CA-125 level and response to treatment in tuberculous peritonitis patients. PATIENTS: Ten patients with tuberculous peritonitis were enrolled in the study. METHOD: Definite diagnosis of tuberculous peritonitis was made by acid-fast smears, specific culture, and polymerase chain reaction. Serum CA-125 levels were measured before and at the fourth month of treatment. RESULTS: Before antituberculous treatment, serum CA-125 levels of all patients were very high (mean+/-SD: 475. 80+/-106. 19 U/ml) and comparable with those of patients with ovarian cancers. At the end of the fourth month of treatment, serum CA-125 levels in all patients decreased to within normal limits (<35 U/ml)(20.80:+/-5.18 U/ml) in parallel with the clinical improvement. The differences in CA125 levels before and after treatment were statistically significant (p<0.001). CONCLUSIONS: Results of our study suggest that serum CA-125 levels in patients with tuberculous peritonitis are as high as ovarian cancers associated with peritoneal infiltration. By the end of the fourth month of antituberculous therapy, serum CA-125 levels have returned to normal. We, therefore, suggest that serum CA-125 can be used to evaluate the efficacy of therapy in tuberculous peritonitis.