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 Endoscopic assessment was carried out at 4 and 6 weeks; patients healed after 4 weeks were withdrawn from the trial.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 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.     

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.

     

Peripheral blood dendritic cells and monocytes are differently regulated in the elderly

Dendritic cells (DCs) are the single most central player in all immune responses. To assess whether DC alterations may contribute to the immune dysregulation that affects the elderly, we investigated the effects of ageing on DCs. We analyzed the number, phenotype and function of peripheral blood DCs from 70 healthy subjects aged 20-92 years by using flow cytometric methods that allow cell characterization directly in whole blood samples. We demonstrated that the number of myeloid DCs progressively declines with age. This finding was accompanied by a decrease of CD34+ precursors and increase of circulating monocytes, suggesting that the entire differentiation process of antigen presenting cells is partially dysregulated in the elderly. DCs from aged individuals also appeared to have a more mature phenotype and impaired ability to produce IL-12 upon stimulation. These results may help to clarify the contribution of innate immunity to the development of immunosenescence.     

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.     

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.