Renzo Suriani

Gabexate or somatostatin administration before ERCP in patients at high risk for post-ERCP pancreatitis: a multicenter, placebo-controlled, randomized clinical trial.

BACKGROUND ERCP is frequently complicated by pancreatitis. The aims of this study were to assess the efficacy of somatostatin and gabexate for prevention of post-ERCP pancreatitis in high-risk patients and to determine predisposing factors for post-ERCP pancreatitis. A meta-analysis was conducted of all published studies on the use of somatostatin or gabexate for prevention of post-ERCP pancreatitis. METHODS A double blind, multicenter, placebo-controlled trial was conducted in patients at high risk for post-ERCP pancreatitis. Patients were randomized to receive an intravenous infusion of somatostatin (750 mg), gabexate (500 mg), or placebo that was started 30 minutes before endoscopy and continued for 2 hours afterward. Patients were evaluated clinically and serum amylase levels determined at 4 and 24 hours after endoscopy. RESULTS No significant difference in the occurrence of pancreatitis, hyperamylasemia, or abdominal pain was observed among placebo-, gabexate-, and somatostatin-treated patients. A sphincterotomy longer than 2 cm (p = 0.0001), more than 3 pancreatic injections (p = 0.0001), and unsuccessful cannulation (p = 0.008) were predictive of post-ERCP pancreatitis. Hyperamylasemia was predicted by more than 3 pancreatic injections (p = 0.0001) and sphincterotomy (p = 0.02). The meta-analysis of trials of short-term infusion of gabexate or somatostatin did not show efficacy for either drug. CONCLUSIONS Short-term administration of gabexate or somatostatin in patients at high risk for pancreatitis is ineffective for prevention of ERCP-induced pancreatitis. Pancreatic injury is related to maneuvers used to obtain biliary access rather than to any patient characteristic or endoscopist experience.

CagA and VacA Helicobacter Pylori Antibodies in Gastric Cancer

BACKGROUND Infection with different genotypes of virulent Helicobacter pylori strains (cytotoxin-associated gene A [CagA]- and/or vacuolating cytotoxin A [VacA]-positive) can play a role in the development of atrophic gastritis, duodenal ulcer (DU) and gastric cancer (GC). OBJECTIVE To determine whether patients with GC and H pylori-negative histological staining had previously been infected with H pylori CagA- and/or VacA-positive virulent strains. METHODS Twenty-three GC patients with a mean (+/- SD) age of 68.14+/-9.8 years who tested H pylori-negative on histological staining took part in the study. Three control groups were included. The first group comprised 19 patients with past H pylori infection and DUs eradicated 10 years earlier, with a mean age of 58+/-18.2 years. H pylori-negative status for this group was determined every year with Giemsa staining, and follow-up testing occured 120+/-32 months (mean +/- SD) after therapy. The subsequent control groups included 20 asymptomatic children, with a mean age of 7+/-4.47 years, and with H pylori-negative fecal tests; the final group contained 30 patients without clinical symptoms of H pylori infection, with a mean age of 68+/-11.6 years, who tested H pylori-negative by histological staining. RESULTS Prevalence of CagA and VacA seropositivity, respectively was 82.6% and 73.91% in GC patients; 84.2% and 84.2% in H pylori-negative DU patients; 25% and 5% in H pylori-negative children; and 36.6% and 16.6% in the patients without clinical symptoms on histological staining. CagA and VacA antibody positivity was not significantly different between GC patients and patients with DUs that had been eradicated 10 years earlier. Significant positivity was found between the childrens group and the H pylori-negative (with past DUs) group (P<0.001). A statistically significant difference was found in age between groups (P<0.03). CONCLUSIONS Patients with GC, even when H pylori-negative at the time of the present study, may have been infected by H pylori before the onset of the disease, as confirmed by CagA and VacA seropositivity. These data reinforce the hypothesis that H pylori may be a direct carcinogenic agent of GC.

Re-treatment with interferon-beta of patients with chronic hepatitis C virus infection

Objective To evaluate the efficacy of interferon-beta (IFN-β) in the re-treatment of patients with chronic hepatitis C who did not respond to IFN-α monotherapy. Patients and methods Thirty patients (24 men and six women; mean age, 41 ± 13 (SD) years; range, 23–62 years), with chronic hepatitis C that was non-responsive to a standard course of IFN-α therapy, were re-treated with recombinant human IFN-β-1a. All patients received IFN-β, 12 MIU subcutaneously, three times weekly for 3 months, after which time patients’ responses were evaluated. Responders (normal alanine aminotransferase, and negative for serum hepatitis C virus RNA) continued to receive IFN-β, 12 MIU, for a further 3 months. Non-responders had their dose increased to 18 MIU for the remaining 3 months of treatment. After 6 months of treatment, therapy was stopped and patients were followed-up for a further 6 months. Results Overall, six (20%) of the 30 patients exhibited a response at the end of treatment. One patient (3.3%) maintained a sustained virological response at the end of post-treatment follow-up. Conclusions Treatment with recombinant IFN-β, at doses of up to 18 MIU for 6 months, is safe and well tolerated. However, the results of the trial do not support the use of IFN-β monotherapy in patients with chronic hepatitis C that is resistant to IFN-α.

Intrahepatic localization of the surface (HBsAg) and core (HBcAg) antigenic determinants associated with hepatitis B virus in biopsy samples from patients with liver disease.

Summary109 biopsy samples from 35 HBAg serologically positive and 74 negative patients were examined by IFL for the presence of the surface and core antigenic determinants associated with the Dane particle. In no serologically negative case was specific IFL detected. Different patterns were observed in serologically positive patients: negative in acute hepatitis, strongly positive cytoplasmic HBs fluorescence in chronic HBAg carriers with normal liver, and discrete HBsAg parenchymal and mesenchymal staining and variable HBcAg staining in chronic liver disease, with HBsAg appearing more frequently in inactive and HBcAg in active disease. These results are compared with recent reports in this field and the clinical significance of the intrahepatic localization of HBAg is discussed.

6948 Multicentre trial on the endoscopic ablation of barrett's esophagus with argon plasma coagulation (apc): comparison between apccombined medical or surgical treatment of gastroesophageal reflux (ger).

The endoscopic ablation of BE in a GER controlled environment has recently been reported with a non-contact Argon-plasma coagulation (APC) technique. Aim: to evaluate the follow up results of endoscopic ablation of BE using APC and to compare medical versus surgical laparoscopic control of GER to be combined with APC of BE. Methods: from November 1996 to November 1999, 42 patients with intestinal BE of 2 -11 cm lenght (mean 4.2 cm) have been treated by endoscopic APC and in a multicentric Italian trial (G.O.S.P.E.). Suppression of GER has been obtained previously by medical (Omeprazole 40 mg per day; 17 patients) or by surgical laparoscopic fundoplicatio (25 patients). Data of the coordinating centre are part of a pilot study for the O.E.S.O.-B.S.G. international multicentric randomized study on treatment of BE. Control of GER was verified by 24 hours pH-metry in all patients. Histological follow up after the completed ablation is ranging from 1 to 27 months (mean 8.4 months). Biopsies were taken after 1, 3, 6, 12 months following the completion of APC treatment and thereafter on annual basis. Results: The number of APC session/patient ranged from 2 to 9. Histologically, squamous re-epithelization was observed in 33 out of the 42 patients, 22/25 in the surgical group and 11/17 in the medical group of patients. Small islands of intestinal metaplasia were observed under the neosquamous epithelium in 9 patients. Recurrence of large metaplastic areas of BE was seen in only 1 patient (of the medical group), 3 months after BE ablation. Thus the global failure rate of the procedure was 21%: 12% in the surgical group and 35% in patients treated with omeprazole. There were no significant complications. Conclusion: endoscopic APC of BE in a GER controlled environment can restore a persistent squamous lining to the lower esophagus. Surgical therapy of GER may produce a better histological pattern of re-epithelization after ablation. Small islands of intestinal metaplasia under the new squamous epithelium may persist in few patients, indicating that ablation of Barrett esophagus must be confined to controlled clinical trials.