Helicobacter pylori impairs iron absorption in infected individuals.

BACKGROUND: Infection with Helicobacter pylori is recognised as a major risk factor for chronic gastritis, peptic ulcer disease and gastric cancer. The association between H. pylori infection and iron deficiency anaemia has been established. Multiple mechanisms have been advocated to explain the relationship between H. pylori and iron status and their association might reduce iron deposit. AIM: Aim of this study was to investigate whether H. pylori infection affects iron absorption. METHODS: The study was designed on a prospective basis. Fifty-five subjects underwent upper gastrointestinal endoscopy and biopsy to investigate the presence of H. pylori and, when this was positive, also search of serum anti-CagA was performed. Tests included an oral iron absorption test with the administration of 1 mg/kg of Fe2+. Iron levels were measured before and 2 h after iron administration (delta iron). H. pylori-positive subjects were administered antibiotic therapy for 1 week and, 2 months later, the oral iron absorption test was repeated and urea-breath test was first performed. RESULTS: H. pylori-positive subjects had lower serum level of ferritin and lower delta iron compared to H. pylori-negative subjects. That difference is significant in anaemic women and is independent of the presence of serum anti-CagA antibodies. After H. pylori eradication iron absorption test was similar to those of non-infected subjects. CONCLUSION: H. pylori infection impairs iron uptake. That mechanism, together with others, may contribute to the depletion of iron in infected patients.

Abnormal esophageal acid exposure is common in morbidly obese patients and improves after a successful Lap-band system implantation.

BACKGROUND: The relation between gastro-esophageal reflux disease (GERD) and obesity is controversial. The laparoscopic adjustable gastric band (LAGB) procedure is effective for morbid obesity. Its indication in the presence of GERD, however, is still debated. This study aimed to investigate esophageal symptoms, motility patterns, and acid exposure in morbidly obese patients before and after LAGB placement. METHOD: For this study, 43 consecutive obese patients were investigated by a standardized symptoms questionnaire, stationary manometry and 24-h ambulatory pH-metry, and 16 patients with abnormal esophageal acid exposure were reevaluated 18 months after LAGB placement. RESULTS: Symptom scores and abnormal esophageal acid exposure were found to be significantly higher, Lower Esophageal Sphincter (LOS) pressure was significantly lower in obese patients than in control subjects. After LAGB, esophageal acid exposure was significantly reduced in all but two patients, who presented with proximal of gastric pouch dilation. CONCLUSIONS: There is a high prevalence of GERD in the obese population. Uncomplicated LAGB placement reduces the amount of acid in these patients with abnormal esophageal acid exposure.

Treatment of morbid obesity and gastroesophageal reflux with hiatal hernia by Lap-Band.

BACKGROUND: Esophageal reflux is common in obese patients. Hiatal hernia is considered a potential contraindication to placement of a Lap-Band. METHODS: Esophageal investigation in patients who were candidates for a Lap-Band included clinical evaluation of symptoms (scoring system), endoscopic and radiologic evaluation, 24-h pH test, and stationary manometry. Patients with gastroesophageal reflux (GER) with or without hiatal hernia underwent the Lap-Band procedure. RESULTS: GER was diagnosed in 12/40 morbidly obese patients, 11 of whom received a standard Lap-Band (3 patients were radiologically diagnosed with transient hiatal hernia). One patient with a large hiatal hernia underwent closure of the diaphragmatic esophageal hiatus, and the Lap-Band was positioned similarly to an Angelchik prosthesis. All but 1 patient who was lost at follow-up were symptom-free (range 1-24 months). CONCLUSION: GER with or without hiatal hernia is not a contraindication for obese patients undergoing a Lap-Band procedure. It accomplishes by a single operation satisfactory treatment of these two disturbing diseases.

The influence of severe bulb deformity on duodenal ulcer relapse.

In order to evaluate the prognostic role of duodenal bulb deformation in the recurrence of peptic ulcer, duodenal bulb morphology and the complete healing of duodenal ulcer were endoscopically evaluated in sixty patients, who were subsequently allocated at random to either maintenance therapy with ranitidine or no treatment. Endoscopic checkups were done at regular intervals, up to the first ulcer recurrence. As expected, long-term ranitidine treatment significantly reduced the relapse rate (12 month cumulative relapse rate was 32% versus 86% in the untreated). A set of prognostic factors which might interfere with this result (sex, age, alcohol consumption, history of ulcerous relatives, duration of the disease, previous H2-blocking treatment, previous complications, smoking and morphology of the duodenal bulb) were evaluated by multivariate analysis using the Cox regression model. Only duodenal bulb morphology appeared to have any independent prognostic value. In the untreated group ulcer recurrence seemed to occur earlier (median relapse time = 2 months) in the patients with severe non-stenosing bulb deformity, and later in those with normal or mildly deformed bulb (median relapse time = 8 months); ranitidine treatment delayed relapse in deformed bulb patients (median relapse time = 14 months) and almost eliminated it in those with normal duodenal bulb morphology. No association was found between the presence of duodenal bulb deformity and the above-mentioned covariates. Our study confirms the primary importance of anti-H2 treatment and suggests that anatomical characteristics of the duodenal bulb also influence the occurrence of ulcer relapse.

Inhibition of gastric acid secretion: advantages and risks in short and long-term treatment.

The administration of the currently available H2-blockers (at a dosage that induces only partial inhibition of the intragastric acidity) is effective in nearly all peptic ulcer patients in the short and long- term treatment. The benefits of more profound gastric acid inhibition (as achieved with omeprazole) in the short-term treatment of acid peptic diseases has been demonstrated in clinical studies. However, gastric acid has an important physiological role and the potential consequences of profound inhibition of gastric acid include intragastric bacterial colonization and hypergastrinaemia. Bacterial overgrowth of the stomach renders the gut more susceptible to enteric infection and another possible sequela of intragastric bacteria is the formation of N-nitroso compounds with carcinogenic potency. Hypergastrinaemia has a trofic effect on the gastric mucosa and gastric endocrine cells and, in animal, ECL cell hyperplasia and carcinoid formation has been observed as a result of high serum gastrin levels. So far, these potential risks have precluded the long-term administration of omeprazole.

Cisapride versus placebo in reflux esophagitis. A multicenter double-blind trial.

In a 6 to 12-week double-blind trial, the effect of cisapride (10 mg q.i.d.) was compared with that of placebo in 63 patients with esophagitis confirmed by endoscopy and/or biopsy. In only one patient (3%) in the cisapride group but in 43% of the placebo patients (p = 0.001), symptoms had not improved after 6 weeks. Forty patients continued treatment until week 12. At that time, control endoscopy showed a significantly (p = 0.005) higher rate of healing (no erosions, ulcers, or bleeding mucosa) in the cisapride patients (63%) than in the placebo patients (12%). At week 12, only three of the 21 cisapride patients still had moderate reflux symptoms, whereas eight of the 19 placebo patients had moderate or severe symptoms (p less than 0.05). Cisapride patients also took significantly (p less than 0.001) less antacids during the trial. These results show that cisapride, 10 mg q.i.d., heals esophagitis lesions and greatly reduces associated symptoms. The treatment was well tolerated.

Comparison of pirenzepine and carbenoxolone in the treatment of chronic gastric ulcer. A double-blind endoscopic trial.

The purpose of the present study was to compare the effectiveness of pirenzepine and carbenoxolone in accelerating the healing of chronic gastric ulcer. Sixty-six out-patients with endoscopically proven gastric ulcer, without major systemic diseases, were admitted to the study. Patients were randomly allocated to either pirenzepine, 50 mg three times a day for 6 weeks, or carbenoxolone, 100 mg three times a day for one week followed by 50 mg three times a day for the remaining five weeks. At 6 weeks, the ulcers had healed in 20 out of 34 patients (59%) treated with pirenzepine, and in 15 out of 29 patients (52%) treated with carbenoxolone. Symptomatic improvement was similar with both drugs. Some major side effects (oedema, hypokalaemia and hypertension) occurred in approximately 30% of patients treated with carbenoxolone; of those receiving pirenzepine 25% complained of minor symptoms (e.g. dry mouth, headache, tachycardia). It is concluded that pirenzepine and carbenoxolone are of similar, but rather limited, efficacy in speeding the healing of chronic gastric ulcer, but show important differences with respect to tolerability.

[Plasma levels of cyclic AMP and catecholamines in ischemic cerebrovascular disorders]. / Livelli plasmatici di AMP ciclico e di catecolamine nelle cerebropatie vascolari ischemiche.

We evaluated in this study the relationships between the clinical course of patients affected with ischemic cerebrovascular diseases and plasma catecholamine and cAMP levels. We compared two groups of acute and chronic patients. These results show a different behaviour of plasma catecholamine and cAMP levels. This hematochemical parameter might assume a distance prognostic significance.

Ranitidine vs cimetidine: short-term treatment of gastric ulcer.

We compared the clinical effectiveness and endoscopic results of ranitidine and cimetidine treatment; 71 outpatients, all affected with benign gastric ulcer, were selected for the study (43 type I, 7 type II and 21 type III, according to Johnson's classification). The patients were treated randomly for 4 weeks with ranitidine (300 mg daily) or cimetidine (1 g daily). An endoscopic examination was repeated within 3 days after the end of the treatment. Clinical checks were performed weekly in order to monitor the clinical course of pain and antacid consumption, according to the patient's needs. The patients who did not demonstrate complete healing on endoscopic examination were treated for an additional 4 week period. At the end of this 4 week period, another endoscopic examination was done. Thirty-six patients treated with ranitidine and 33 with cimetidine completed the first period of therapy. The two groups were homogeneous with regard to sex, age, duration of disease, smoking habits, alcohol consumption, and type and size of ulcer. Ranitidine and cimetidine treatments did not demonstrate any significant difference with regard to ulcer healing after the 4th or the 8th week of therapy. Both ranitidine and cimetidine were less effective in healing type I than type II and III G.U., at the 4th week of treatment. No significant differences between the two groups were noted with regard to pain or weekly antacid consumption. No significant side effects were reported.