Different effects of short-term omeprazole, lansoprazole or pantoprazole on the accuracy of the (13)C-urea breath test.

BACKGROUND: Proton pump inhibitors may interfere with the accuracy of the (13)C-urea breath test, but little information is available on the effect of standard doses of various proton pump inhibitors on this test. AIM: To evaluate the effect of short-term standard doses of omeprazole, lansoprazole and pantoprazole on the accuracy of the standardized (13)C-urea breath test. METHODS: A total of 124 patients with Helicobacter pylori infection, diagnosed on the basis of gastric histology, rapid urease test and (13)C-urea breath test, were studied. These patients received omeprazole, 20 mg/day, lansoprazole, 30 mg/day, or pantoprazole, 40 mg/day, for 2 weeks according to a randomized protocol. (13)C-Urea breath test was repeated on days 4, 7 and 14 while on therapy and 7 days after proton pump inhibitor withdrawal. RESULTS: Of the patients receiving omeprazole and lansoprazole, 30% (12/40) and 20% (8/41), respectively, became (13)C-urea breath test negative during therapy, compared with none of the 42 patients treated with pantoprazole (P < 0.05). All the false negative (13)C-urea breath test results returned to positive within 1 week of drug withdrawal, with a mean recovery to 84.7 +/- 15.6% of baseline delta(13)CO(2). CONCLUSIONS: Short-term omeprazole and lansoprazole interfere with the 13C-urea breath test, although a return to positive test results invariably occurs within 1 week of proton pump inhibitor withdrawal. In contrast, the accuracy of the (13)C-urea breath test does not appear to be significantly impaired by short-term pantoprazole, which therefore may not necessarily be withdrawn before this test.

Management of Helicobacter pylori-related gastrointestinal diseases by general practitioners in Italy.

AIMS: To investigate the diagnostic approach to and management of Helicobacter pylori infection at primary care level in Italy 2 years after the Maastricht consensus report. METHODS: A total of 100 randomly selected general practitioners (GPs) answered a 12-item multiple-choice questionnaire, personally delivered and collected by non-medical staff. RESULTS: In 25% of cases, GPs preferred a prompt referral of dyspeptic patients to the specialist. The favourite diagnostic test for H. pylori infection was gastroscopy with biopsies (55%), followed by standard and office-based serology (24% and 18%, respectively), and 13C urea breath test (5%). H. pylori-eradication was prescribed in patients with peptic ulcer, reflux oesophagitis and functional dyspepsia by 64%, 43% and 66% of GPs, respectively. Only 7% of GPs adopted a test-and-treat approach. Proton pump inhibitor-based triple therapies were used by almost all physicians. In peptic ulcer disease, most of GPs re-tested patients in order to confirm H. pylori eradication (50% by gastroscopy with biopsies and 30% by serology only 2 months after therapy). CONCLUSIONS: Uncertainty seems to persist among Italian GPs concerning the indications for H. pylori treatment, the use of diagnostic tests, and patient follow-up. In contrast, no doubts exist regarding the first choice eradication regimens. This survey suggests that further efforts should be made to spread scientific knowledge and guidelines on H. pylori diagnosis and management in primary care in Italy.

Clinical, ultrasonographic and tomographic features on the natural evolution of primary mesenteric fibromatosis: a case report.

Primary mesenteric fibromatosis is a rare, histologically benign, pathology which is characterized by fibrous proliferation in the mesentery and made more serious by biological malignancy as it has a high inclination towards involving the visceral abdominal structures in its growth. While the cases reported in the literature describe the attempts to cure and reduce the tumor growth, this report describes the clinical, ultrasonographic and tomographic features during the natural growth rate of a case of inoperable primary mesenteric fibromatosis during a 20 month follow-up.

Non-steroidal anti-inflammatory drug gastropathy: clinical results with antacids and sucralfate.

The efficacy of antacids in the short- and long-term treatment of peptic ulcers, has suggested a possible use in the prevention and in the treatment of non-steroidal anti-inflammatory drug related gastroduodenal lesions. In short-term prevention studies, significant protection against ASA-related lesions was observed when antacids at high-dose were given before the administration of the offending drug. To the contrary, antacids at low dose did not prevent ASA-induced lesions of gastric and duodenal mucosa. As for long-term prophylaxis, no clinical effect was observed. In the treatment of non-steroidal anti-inflammatory drug-related mucosal lesions in patients who were able to discontinue the offending drugs, antacids proved of some use, when compared with placebo, but were significantly less effective than H2 blockers, as cimetidine. Sucralfate is an effective antiulcer drug thought to provide cytoprotective action. Although initial studies utilizing sucralfate for protection against short-term aspirin administration were encouraging, longer term studies (more than 7 days) were generally disappointing. A comparative study with misoprostol demonstrated that the PGE1 analogue was far superior for the prevention of non-steroidal anti-inflammatory drugs ulcers, and that ulceration rates in the sucralfate group were equivalent to rates in the placebo group. As far as the treatment of non-steroidal anti-inflammatory drug-related mucosal lesions is concerned, sucralfate proved superior to placebo, similar to ranitidine, but significantly less effective than omeprazole.

Presence of gastric autoantibodies impairs gastric secretory function in patients with Helicobacter pylori-positive duodenal ulcer.

BACKGROUND: Although the association between Helicobacter pylori infection and gastric autoimmunity is now well established, to date little is known about the significance of anticanalicular autoantibodies in patients with duodenal ulcer (DU). We therefore investigated the prevalence of serum antiparietal cell autoreactivity in DU patients as well as the relationship between these autoantibodies, gastric histopathology and gastric secretory function in this setting. METHODS: Forty-one consecutive patients with H. pylori-positive DU were initially recruited. In all patients, basal (BAO) and pentagastrin stimulated acid output (PAO), fasting and meal-induced serum gastrin levels, as well as serum pepsinogen I concentrations, were measured. Antral and body gastritis was evaluated according to the Sydney system. Serum anticanalicular autoreactivity was determined by the indirect immunoperoxidase technique. RESULTS: Serum anticanalicular autoantibodies were found in 7 out of 34 patients (20%). The presence of these antibodies was associated with a significantly higher grade of body gastritis (activity: 1.9 versus 0.9) as well as with significantly higher fasting and meal stimulated gastrin levels (mean fasting gastrin, 76.4 (15.2) microg/ml versus 59.3 (20.5) microg/ml). In addition, PAO values were significantly lower in patients with gastric autoantibodies than in those without this autoreactivity (mean 0.35 (0.16) mmol kg(-1)h(-1) versus 0.49 (0.16)mmol kg(-1)h(-1)). In contrast, no significant differences were found between patients with and without anticanalicular autoantibodies as regards fasting serum pepsinogen I concentrations. CONCLUSIONS: Serum anticanalicular autoantibodies can be detected in 20% of patients with DU and are associated with a more severe pattern of body gastritis, higher gastrin levels and decreased peak acid secretion values. Their presence could account for the normal or reduced acid output which can be seen in a subset of DU patients.

Upper GI bleeding in healthy full-term infants: a case-control study.

OBJECTIVE: The aim of this case-control study was to evaluate the frequency and the type of mucosal lesions in newborn babies with upper GI bleeding (UGIB), the diagnostic role and safety of upper GI endoscopy, and the recognition of risk factors associated with the hemorrhagic event. METHODS: A population of 5180 infants born from June, 1988 to May, 1997 was examined. A case was defined as any patient who had UGIB within 4 days of delivery. The diagnosis was made by endoscopic examination in an endoscopy room. The following parameters were determined: amniotic fluid features, funicular blood pH, Apgar index at 5 min, neonatal weight, body length, gestational age, and the presence of other pathologies. Biochemical profiles were also evaluated. Clinical and demographic data of the mothers of the newborn babies were analyzed. Sera of cases and the respective parents were tested for gastrin and pepsinogen. As a control group, 53 full-term healthy infants matched for sex and age were randomly selected from the population of infants born in our pediatric department. RESULTS: Sixty-four of 5180 newborn babies (1.23%) suffered from UGIB within 26.5 +/- 20 h of life. In 53 of 64 cases (mean age = 24.2 +/- 25.5 h) it was possible to carry out an endoscopic examination. In one case, endoscopy was limited to the esophagus because of the presence of multiple mucosal ulcers and substenosis of the viscus. Esophageal damage was observed in 24/53 patients. The esophageal lesions were isolated in nine cases, and occurred jointly with gastric or duodenal damage in 14 cases and one, respectively. Gastric and duodenal lesions were seen in 43/52 and 1/52 patients, respectively. There were 17 cases of gastric ulcers and one case of duodenal ulcer. Blood clots were observed in 14 gastric ulcer patients; in one case there was evidence of active bleeding at the margins of a gastric ulcer. There was no significant difference with regard to the demographic and clinical characteristics of the cases and controls. Median values of serum gastrin of the cases and controls were similar. Median serum pepsinogen was significantly higher in the case group. CONCLUSIONS: UGIB in the newborn babies is often associated with clinically relevant mucosal lesions of the upper GI tract. The evolution, after treatment with antisecretory drugs, is generally rapid and favorable, with clinical recovery usually obtained within 24-48 h. The higher serum pepsinogen levels may only represent a significant risk factor of mucosal lesions and complications.