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Biomedical subjects

H G Dammann

Publications and source records attributed to H G Dammann.

At least 91 records · Page 5Linked to original sources
PubMed1987

An alprostadil analogue and human gastric secretion. A double-blind placebo-controlled study of the effects of a tablet and lyovial formulation.

The effects of single doses of 800 micrograms and 1200 micrograms of the new alprostadil analogue (prostaglandin E1 16-methyl-16-methoxy derivative) MDL 646, presented as tablet and lyovial formulations, on basal and pentagastrin-stimulated gastric acid secretion, were studied in 10 normal male volunteers using a randomised, double-blind placebo-controlled cross-over design. Compared to placebo, both doses of MDL 646 significantly decreased acid output during the basal and pentagastrin-stimulated periods. No difference between the tablet and lyovial formulations was found. Total basal output (tablet and lyovial data pooled) was reduced by 58% and 68% following 800 micrograms and 1200 micrograms MDL 646, respectively. Stimulated output was reduced to a lesser degree (15% and 27%). Inhibition of the stimulated acid secretion was observed up to 1.5 to 1.75 h after drug administration. Tolerance was good with only one subject reporting nocturnal abdominal pain following each dose of the drug and placebo.

Adult↗
PubMed1986

Comparative clinical trial of enprostil and ranitidine in the treatment of gastric ulcer.

In a randomized, double-bind, parallel, multi-clinic study, the safety and efficacy of enprostil (35 micrograms twice daily) and ranitidine (150 mg twice daily) were compared in the treatment of active gastric ulcer in 93 outpatients (47 enprostil-treated patients and 46 ranitidine). The two treatment groups were well matched for demographic characteristics. The healing rates in the enprostil group were 22, 58, 80, and 86 percent at two, four, six, and eight weeks, respectively. The corresponding rates in the ranitidine group were 22, 66, 84, and 89 percent. None of these differences was statistically significant. The area of the ulcer at baseline and smoking status did not appear to influence healing rates. There were no significant differences between treatment groups in time to relief of ulcer symptoms, frequency of daytime or nighttime ulcer pain, or antacid use. Side effects attributable to enprostil treatment were diarrhea (10 percent versus 6 percent with ranitidine), gastrointestinal pain, and vomiting. These side effects, however, did not influence the patients' assessments of their overall response to enprostil and ranitidine therapy. Six enprostil-treated patients and one ranitidine-treated patient withdrew from the trial prematurely because of adverse experiences. Monitoring of clinical laboratory test results showed no significant changes in the two treatment groups. This study demonstrates that a prostaglandin E2 analogue, enprostil, in a dose of 35 micrograms twice daily, is similarly safe and effective as ranitidine in the treatment of active gastric ulcer.

Adolescent↗
PubMed1986

[Different healing tendencies of reflux esophagitis following omeprazole and ranitidine. Results of a German-Austrian-Swiss multicenter study].

The effectiveness of a single, morning oral dose of 40 mg omeprazole or a twice daily oral dose of 150 mg ranitidine was compared in a randomized endoscopically controlled double-blind trial at 37 clinics in Austria, Germany and Switzerland. A total of 178 out-patients in stages I-IVa (after Savary and Miller) were entered into the trial: 78 in stage I, 60 in stage II, 27 in stage III, and in 13 in stage IVa. As early as at the end of the third treatment week there was a significantly higher rate of complete healing or reduction into a lower stage with omeprazole than ranitidine (85% vs 67%; P less than 0.02). After six treatment weeks, healing tendency after omeprazole compared with ranitidine was 85% vs 45% (P less than 0.04). Omeprazole also brought earlier improvement in symptoms. The difference was statistically significant for heartburn (pyrosis): P less than 0.01. Both drugs were equally well tolerated and there were no clinically significant side-effects. This is the first demonstration that the ATPase inhibitor omeprazole is superior to the H2-receptor antagonist ranitidine in the treatment of reflux oesophagitis.

Administration, Oral↗
PubMed1986

20 versus 30 mg omeprazole once daily: effect on healing rates in 115 duodenal ulcer patients.

In a double-blind, dose comparison multicenter trial 115 patients with duodenal ulcer were treated with either 20 or 30 mg oral omeprazole once daily for 4 weeks. There was no difference in the healing rates for the two groups after 2 and 4 weeks. After 2 weeks with 20 and 30 mg healing frequencies were 79.0 and 72.7%, after 4 weeks 96.5 and 92.7%. No difference was observed between the groups in the number of pain episodes during day and night. No side effects to the drug occurred. A daily dose of 20 mg omeprazole may be effective in ulcer therapy.

Adult↗
PubMed1986

Effects of 800 mg cimetidine once daily on gastric acid secretion.

Today, the reduction of nocturnal acid secretion is believed to be the most important point in duodenal ulcer therapy. This is supported by the fact that during the day gastric acid secretion is largely buffered by meals. Moreover, independently of food intake the intragastric H+ activity during the day is lower than during the night. During nighttime (2300-0700 h) there was a mean hourly H+ activity of 38 mmol/l--that is, a 65% increase compared with daytime H+ activity with meals--and still a 30% increase without meals. Nocturnal acidity can be suppressed best by single large bedtime doses of H2-receptor antagonists. Cimetidine, 800 mg at night, reduces nocturnal intragastric acidity by 85%; 300 mg ranitidine at night and 40 mg famotidine at night reduce it by 95%. The first clinical trials show that a single nighttime dose of cimetidine or ranitidine is at least as effective in promoting ulcer healing as is twice daily administration.

Administration, Oral↗
PubMed1986

Nocturnal acid suppression with a new H2 receptor antagonist--nizatidine.

To determine the potential efficacy of bedtime doses of the new furan H2 receptor antagonist nizatidine in the suppression of nocturnal acid secretion, this randomized, crossover, single-blind study was performed in 10 healthy male subjects. The actions of a single bedtime (21:00 hour) dose of the H2 receptor antagonists nizatidine (150 mg and 300 mg), ranitidine (300 mg) and cimetidine (800 mg), as well as placebo on nocturnal gastric acid and volume secretion (01:00 to 07:00 hours, and on overall 24 hour H+ ion concentration were studied. Compared with placebo, night-time (23:00 to 07:00 hours) H+ ion concentration was reduced by 70, 79, 95, and 76% (p less than 0.05-p less than 0.01). Nocturnal acid secretion, too, was significantly lower for the H2 blockers than for placebo (p less than 0.05-p less than 0.01). A significant reduction in night-time gastric volume secretion was observed in the hourly intervals from 04:00 to 07:00 hours and in total volume in the whole 6 hours period (p less than 0.05-p less than 0.01). Nizatidine 300 mg nocte, ranitidine and cimetidine significantly decreased H+ concentration for only 1 hour (08:00 to 09:00 hours, p less than 0.05-p less than 0.01) during the subsequent daytime period (08:00 to 13:00 hours). Since no significant pharmacodynamic differences between nizatidine 300 mg nocte, cimetidine 800 mg nocte and ranitidine 300 mg nocte were observed, it may be concluded that at the doses employed, these three H2-blockers will all be similarly effective in the acute therapy of peptic ulcer disease.

Adult↗
PubMed1986

[The action of various doses of the new imidazole H2-receptor antagonist etintidine on intragastric acidity in man].

The chemical structure of etintidine differs from that of cimetidine by the addition of an ethinyl group to the terminal methyl group of the side chain. We investigated the influence of etintidine 300 or 400 mg b.d. and of etintidine 300 or 600 mg nocte, cimetidine 800 mg nocte versus placebo in two different double-blind randomized cross-over studies on 24-h intragastric acidity and nocturnal volume and acid secretion (12:00 midnight to 6:00 a.m.) in 12 and 8 healthy male volunteers, respectively. 5-10 ml of gastric contents were aspirated hourly via a nasogastric tube. The pH of the samples was determined using a glass electrode. The results were expressed in terms of H+-activity (mmol/l). Etintidine 300 or 400 mg b.d. reduced day- and nighttime acidity by 53 and 60% or 41 and 41%, respectively. Nocturnal acid secretion (mmol/l) was inhibited by 38 and 42%, resp. Etintidine 300 or 600 mg nocte and cimetidine 800 mg nocte (9:00 p.m.) lowered nocturnal intragastric acidity by 69, 84 and 79%, resp. Daytime inhibition was not observed. Our results suggest, that 1. etintidine 300 and 400 mg b.d. are equipotent in promoting peptic ulcer healing and 2. that this new imidazole H2-receptor antagonist is also effective in a single bedtime dose.

Adult↗
PubMed1986

[Acute injury to the gastric mucosa by acetylsalicylic acid. A comparative endoscopic study in man with oral prostaglandin analogs, omeprazole and ranitidine].

The deleterious effects of acetylsalicylic acid (ASA) on gastric mucosa have been well documented in experimental and clinical studies. With a direct endoscopic assay system we evaluated in healthy volunteers whether pretreatment with prostaglandin analogues (misoprostol, rioprostil), omeprazole and ranitidine prevented ASA-induced gastric mucosal injuries. Ranitidine (2 X 150 mg/d) in large antisecretory doses almost completely abolished these changes (p less than 0.05). By contrast, misoprostol (4 X 50 micrograms/d and 4 X 200 micrograms/d), rioprostil (3 X 100 micrograms/d), omeprazole (5 mg and 10 mg/d) as well as ranitidine in non-antisecretory doses (2 X 25 mg/d) did not reduce gastric mucosal injury after single-dose ASA administration. The results of this trial indicate that socalled cytoprotective doses of prostaglandins, omeprazole and ranitidine in contrast to animal findings are not effective in preventing acute ASA-induced mucosal damage.

Adult↗