Comparison of omeprazole and lansoprazole in short-term triple therapy for Helicobacter pylori infection.

BACKGROUND: Effective anti-Helicobacter pylori therapies with few side-effects are needed. AIM: To study the effectiveness of short-term triple therapy with amoxycillin, clarithromycin and either omeprazole or lansoprazole for eradication and healing of peptic ulcers. METHODS: Patients with gastric or duodenal ulcers received amoxycillin (1 g b.d.), clarithromycin (500 mg b.d.) and lansoprazole (30 mg b.d.) (LAC) or omeprazole (20 mg b.d.) (OAC) for 7 days. Endoscopic examinations were performed before treatment and at least 4 weeks after completion of therapy. H. pylori status was confirmed by rapid urease test and histological examination (Giemsa stain) from gastric biopsies taken from both the antrum and the body. RESULTS: A total of 356 patients were randomized in this single-blind study. On a per protocol basis, H. pylori was eradicated in 134 of 170 patients (79%) in the lansoprazole group and in 105 of 146 (72%) in the omeprazole group (P = 0.189); and in intention-to-treat analysis 72% and 62%, respectively (P = 0.043). Healing of the ulcers was obtained in 166 of 186 (98%), and in 139 of 146 patients (95%), respectively (P = 0.357). Side-effects occurred in two patients in the LAC group and in six in the OAC group B (four stopped therapy). CONCLUSIONS: This study has shown that the two regimens are highly effective in healing duodenal ulcers and are well tolerated. Neither treatment achieves the ideal cure rate for H. pylori. Lansoprazole does not appear to have a significant advantage over omeprazole either in ulcer healing or in H. pylori eradication.

Effect of carbenoxolone and cimetidine on gastric mucin.

To determine whether the addition of carbenoxolone to a cimetidine regimen would prevent mucus deficiency in patients with duodenal ulcer, we compared the effect of combined therapy with the effects of treatment with cimetidine alone and carbenoxolone alone. Carbenoxolone proved to be ineffective on gastric mucus induced by cimetidine, the behavior of gastric mucin fractions being similar to that observed in patients treated with cimetidine alone. When used alone, however, carbenoxolone demonstrated mucus-stimulating action.

Rapid improvement of symptomatology with pantoprazole, amoxycillin and metronidazole in Helicobacter pylori-positive duodenal ulcer patients.

BACKGROUND/AIMS: To evaluate the efficacy and tolerability of a new 1-week triple therapy regimen consisting of pantoprazole, amoxycillin and metronidazole. METHODOLOGY: The study involved 51 Helicobacter pylori (H. pylori) positive patients (M:30, F:21, mean age: 52.5 years, range: 24-75) affected with duodenal ulcer in active phase. At baseline and 6 weeks after the completion of treatment, clinical assessment, endoscopy with gastric biopsies, rapid urease test, 13C urea breath test, and serum laboratory analyses were performed. All patients were treated with pantoprazole 40 mg once daily, plus amoxycillin 1 gram tid and metronidazole 250 mg tid for 1 week, and pantoprazole 40 mg once daily for a second week. A clinical diary for daily assessment of symptoms and side effects was completed by patients during the treatment period. RESULTS: Three patients were discontinued from the study. Six weeks after therapy, the ulcer was healed in 47 of 48 patients (97.9%, 95% CI = 93.9-100). The cure rates of H. pylori infection, expressed using both the intention-to-treat and per protocol analyses, were 80.4% (95% CI = 69.5-91.3) and 85.4% (95% CI = 75.4-95.4), respectively. The therapy led to a significant, rapid disappearance or reduction in daytime epigastric pain, from 68.8% on day 1 to 82.2% on day 3 (p < 0.001) and in nocturnal epigastric pain, from 80.6% on day 1 to 93.3% on day 3 (p < 0.001). After 2 weeks of treatment, the percentage of patients completely free of pain was 82.2% for daytime pain and 90.3% for nocturnal pain. A rapid improvement in acid regurgitation, heartburn, nausea and vomiting was also observed with a median value of symptom disappearance of 2 days. The percentages of patients completely symptom-free were 37.5% after 1 day, 54.1% after 3 days, 75% after 2 weeks, and 83.3% after 2 months. H. pylori-cured patients showed a significant decrease in the histological activity of both antral (p = 0.0001) and body (p < 0.008) gastritis. Mild to moderate adverse events were reported by 15 patients. CONCLUSIONS: One week triple therapy with pantoprazole in combination with amoxycillin and metronidazole, followed by a second week of pantoprazole, was well tolerated and highly effective for the 1) rapid improvement or resolution of symptoms; 2) healing of the DU; 3) eradication of H. pylori infection; and, 4) reduction of histological signs of chronic gastritis activity.

[Effect of tiropramide chlorhydrate on intestinal transit time in patients with irritable colon syndrome]. / Azione della tiropramide cloridrato sul tempo di transito intestinale in pazienti affetti da sindrome del colon irritabile.

The effect of tiropramide hydrochloride--a new spasmolytic drug with calmodulin-independent activity--in correcting alterations of intestinal transit, has been investigated in 40 IBS patients (20 with accelerated and 20 with delayed transit time). Intestinal transit has been evaluated by means of radioopaque markers. Tiropramide hydrochloride, at a dose of 100 mg t.i.d. for 4 weeks, was found significantly more effective than placebo both in normalizing intestinal transit time and in inducing symptomatic relief.

Stimulation of prolactin release by intravenous cimetidine: a dose-response study.

The PRL response to iv cimetidine was tested in 8 healthy males and 8 females at 4 different dose levels (0.75, 1.5, 3.0 and 6.0 mg/kg bw). Serum PRL levels were significantly increased in comparison with a placebo study by the second cimetidine dose in both sexes. The PRL response was significantly higher in females than in males at all but the lowest dose tested. A significant correlation between the cimetidine dose and the PRL response was observed. There was no significant modifications in serum GH, LH, FSH, IRI and glucose. Present findings demonstrate that the stimulation of PRL release by iv cimetidine is quite specific and dose-dependent.

Prolactin release by intravenous cimetidine in man: evidence for a suprapituitary locus on action.

In an attempt to identify the sites at which cimetidine stimulates prolactin release, the drug was administered intravenously (6 mg/kg body weight) to healthy subjects under basal conditions, during dopamine infusion (1 microgram/Kg-min for 120 min) and after pretreatment with L-dopa plus carbidopa (250 plus 25 mg every 6 for 1 day). The serum prolactin response to cimetidine was abolished by dopamine infusion and almost completely suppressed by L-dopa plus carbidopa administration. These findings suggest that the drug acts on the central nervous system to stimulate prolactin release. Although the mechanism of this action is unclear, it does not seem to depend on an antidopaminergic effect and may be related to blackade of brain H2 histamine receptors.

Double blind comparison between cimetidine and gefarnate in cases of duodenal ulcer.

Thirty outpatients suffering from duodenal ulcer of recent onset were given cimetidine 1 g/day or gefarnate 250 mg/day for 6 weeks in a double blind trial, randomly balances between the groups. Endoscopic assessment was carried out at 4 and 6 weeks; patients healed after 4 weeks were withdrawn from the trial. In all parameters considered, cimetidine showed a highly significant difference. The healing rate at 4--6 weeks was 67--93% after cimetidine treatment and 27--53% after gefarnate treatment. The effect of cimetidine on the disappearance of symptoms, mainly the nocturnal ulcer pain, and on antacid consumption was greater than that after medication wity gefarnate. After 4--6 weeks of a full dose cimetidine regimen, both basal and pentagastrin stimulated gastric acid secretion were reduced and peptone meal stimulated serum gastrin increased; the basal gastrinaemia remained unchanged.

Effect of dopamine infusion on gastric and pancreatic secretion and on gastrin release in man.

The effect of dopamine infusion on basal and pentagastrin-stimulated gastric secretion, on basal and secretin-CCK-PZ-stimulated pancreatic secretion, and on basal and meal-induced gastrin release has been evaluated in healthy volunteers. Both basal and stimulated gastric acid secretion were significantly inhibited during dopamine infusion with a significant rebound to pre-infusion values after discontinuing dopamine. These effects were prevented by pretreatment with the antidopaminergic drug, metoclopramide. A slight but now significant decrease in amylase and bicarbonate outputs was also observed during dopamine infusion, while gastrin release did not change. These data suggest the existence of dopaminergic mechanisms in the regulation of gastric acid secretion in man.

Prevalence and risk factors of Helicobacter pylori-negative peptic ulcer: a multicenter study.

Peptic ulcer disease (PUD) has been described in the absence of Helicobacter pylori (Hp) infection, suggesting that different factors are involved in its etiopathogenesis. We investigated prevalence and characteristics of Hp-negative (Hp-) PUD in an area of Northern Italy and calculated the rate of Hp-positive (Hp+) patients with PUD in whom Hp might be coincidental and not causal. Four hundred nine consecutive patients with endoscopically diagnosed PUD were enrolled in seven hospitals. Hp infection was assessed by rapid urease test and histologic examination. The attributable risk percentages in different age groups were calculated by appropriate formulas. Of 409 patients, 31 (7.6%) were Hp- (gastric, 8.3%; duodenal, 7.6%). Age, nonsteroidal antiinflammatory drug (NSAID) consumption, and complication rates were significantly higher in Hp-than Hp+ patients with duodenal ulcers (DUs). Of the Hp-patients with DU, 58% did not use NSAIDs. In patients with Hp+ DU, the attributable risk percentage for Hp infection in patients aged <40 years, 40-60 years, or >60 years was 98%, 88%, and 66%, respectively. The prevalence of Hp- PUD was about 8%, mainly unrelated to any known etiologic factor. In about one-third of Hp+ patients with PUD aged over 60 years, Hp infection might be coincidental and not causal.