Postinfantile giant-cell hepatitis associated with ulcerative colitis and autoimmune hepatitis.

Postinfantile giant cell hepatitis (PGCH) is rare. It is characterized by the presence of multinucleated giant cells in liver biopsy, and although it has been associated with several etiological agents, in many cases its etiology remains unclear. The case is presented herein of an adult woman with PGCH in the setting of ulcerative colitis and autoimmune hepatitis. The presence of autoimmune hepatitis in the patient is consistent and supports the autoimmune pathogenesis of PGCH in a subgroup of patients. Furthermore, this finding, along with others, suggests that PGCH may be included in the list of hepatic complications of inflammatory bowel disease.

Bax and Bcl-2 protein expression in gastric precancerous lesions: immunohistochemical study.

BACKGROUND AND AIMS: Bcl-2 protein prolongs cell survival in the face of classical apoptotic stimuli, and is considered to be a suppressor of apoptosis. Bax plays a key role in apoptosis by accelerating cell death after an apoptotic stimulus. The aim of our study was to determine the roles of the Bax proapoptotic gene and the Bcl-2 antiapoptotic gene in the carcinogenesis of gastric cancer. METHODS: One hundred and forty-five gastric biopsy specimens of chronic gastritis, atrophic gastritis, intestinal metaplasia and gastric dysplasia were studied. Using immunohistochemical methods, Bax and Bcl-2 protein expression was observed. RESULTS: Bax was expressed in epithelial cells in all cases of chronic gastritis. Bax was not detected in 26% of specimens of atrophic gastritis. As intestinal metaplasia develops, Bax is further suppressed. In biopsy samples with dysplasia, Bax expression was demonstrated only in 12% of biopsy samples. Although Bcl-2 protein was not detected in chronic gastritis, aberrant expression was found in gastric epithelial intestinal metaplasia and dysplasia. CONCLUSIONS: The suppression of Bax and overexpression of Bcl-2 protein is an early event in gastric tumorigenesis, before gastric dysplastic changes occur.

Esomeprazole versus omeprazole for the eradication of Helicobacter pylori infection: results of a randomized controlled study.

BACKGROUND: Esomeprazole has higher oral bioavailability and increased antimicrobial activity against Helicobacter pylori than omeprazole. GOALS: To compare 7 days esomeprazole with 7 days of omeprazole based triple therapies for the eradication of H. pylori, and to assess whether the administration of higher dose of esomeprazole leads to improved eradication rates. STUDY: One hundred and fifty-six dyspeptic patients with H. pylori received either: (1) 1-week treatment including esomeprazole 40 mg once daily, amoxicillin 1 g, and clarithromycin 500 mg, both twice daily (EAC1 group, n = 52); (2) 1-week treatment of omeprazole 20 mg, amoxicillin 1 g, and clarithromycin 500 mg, all administered twice daily (OAC group, n = 52); or (3) 1-week treatment with esomeprazole 40 mg, amoxicillin 1 g, and clarithromycin 500 mg, all given twice daily (EAC2 group, n = 52). RESULTS: H. pylori was eradicated in 37 of 52 patients in the OAC group (Intension to treat [ITT] 71%), and in 42 patients in the EAC1 group (ITT 81%). High eradication rate was achieved by the EAC2 regimen (ITT; 96%), but more patients reported unwanted effects. CONCLUSION: Seven days of esomeprazole based triple therapy is a satisfactory eradication regimen for H. pylori infection. Higher doses of esomeprazole have excellent eradication rates, but they may lead to increased side effects.

Can somatostatin prevent post-ERCP pancreatitis? Results of a randomized controlled trial.

BACKGROUND: Acute pancreatitis is the most common complication of endoscopic retrograde cholangiopancreatography (ERCP), occurring in 1-10% of patients. Several substances have been used, with negative results, in an attempt to prevent this complication. METHODS: We performed a double-blind randomized trial in 372 consecutive patients undergoing diagnostic or therapeutic ERCP to evaluate the role of somatostatin in preventing post-ERCP pancreatitis. The first group received continuous somatostatin infusion for 12 h starting 30 min before ERCP, the second group received a bolus intravenous injection of somatostatin at the time of cannulation of the papilla, and the third group received a placebo. RESULTS: Two patients in each of the somatostatin groups (1.7%) and 12 patients in the placebo group (9.8%) developed pancreatitis (P<0.05). Serum amylase levels 5 and 24 h after the procedure were lower in both groups that received somatostatin than in the placebo group (P<0.05). CONCLUSION: Somatostatin is useful in preventing post-ERCP pancreatitis. Further studies must be designed to investigate the cost-effectiveness of the drug and to determine the ideal administration route and dosage.

Acute pancreatitis due to pravastatin therapy.

CONTEXT: Few data exist about the incidence of drug-induced pancreatitis in the general population. Drugs are related to the etiology of pancreatitis in about 1.4-2% of cases. Statins are generally well tolerated. Acute pancreatitis has been reported in a few cases treated with atorvastatin, fluvastatin, lovastatin and simvastatin. CASE REPORT: We report the case of a 56-year-old patient who, after 6 months of treatment with pravastatin 20 mg once daily for hypercholesterolemia, presented with acute pancreatitis. Other causes of the disease were ruled out. Five months later, the patient, on his own initiative, reintroduced pravastatin and acute pancreatitis recurred after 3 days. CONCLUSION: To our knowledge this is the first report of pravastatin-induced pancreatitis and further strengthens the fact that statins may cause acute pancreatitis.