Biomedical subjects

H G Dammann

Publications and source records attributed to H G Dammann.

At least 55 records · Page 3Linked to original sources

PubMed1990

[Endoscopic studies on the gastric tolerance of paracetamol and acetylsalicylic acid. A placebo-controlled, double-blind study in healthy volunteers].

Endoscopic Studies on the Gastric Tolerance Following 6 Days Treatment of Paracetamol and Acetylsalicylic Acid/A placebo-controlled double-blind-study in healthy volunteers. In placebo-controlled randomized double-blind cross-over-fashion the gastric and duodenal tolerance of a 6 day treatment with 3000 mg acetylsalicylic acid (ASA; as a commercially available preparation) and 3000 mg paracetamol (Tylenol) were directly compared in 12 healthy volunteers. An endoscopic evaluation of the gastric and duodenal mucosa was performed. 3000 mg ASA daily evoked significant more gastro-duodenal lesions than 3000 mg paracetamol daily and placebo. Difference between Paracetamol and placebo did not reach statistical significance. Based on the comparable analgetic potency of both compounds and the apparently better gastro-duodenal tolerability paracetamol is the drug of choice when a non-inflammatory problem requires an analgesic.

Acetaminophen↗

PubMed1989

[Lowering of the plasma lipid concentration with lovastatin. A clinical study in patients with primary hypercholesterolemia].

A study of 27 patients (18 males and 9 females; median age 57 [35-70] years) with hypercholesterolaemia examined the lipid-reducing effect, clinical reliability and tolerance of lovastatin, an HMG-CoA-reductase inhibitor, given in a single evening dose. After a four-week period on placebo and a lipid-reducing diet the patients received 20 mg lovastatin for four weeks. If, at the end of this period, total cholesterol levels were still above 200 mg/dl, the dose was increased to 40 mg, after a further four weeks to 80 mg. After a three-month treatment period total cholesterol concentration in lovastatin-treated patients was 28% lower than in the placebo group (289.4 +/- 42.2 vs 208.0 +/- 39.9 mg/dl; P less than 0.0001). LDL-cholesterol concentration had fallen by 40% (215.1 +/- 44.4 vs 130.1 +/- 24.7 mg/dl; P less than 0.0001), while plasma triglyceride concentrations had fallen by 15% (166.3 +/- 71.8 vs 141.8 +/- 69.8 mg/dl; P less than 0.01). At the same time, HDL-cholesterol levels had risen by 12% (42.9 +/- 12.4 vs 47.9 +/- 18.2 mg/dl; P less than 0.01). These results confirm the marked lipid-reducing effect of lovastatin.

Adult↗

PubMed1989

[Treatment of non-steroidal anti-inflammatory drug-induced damage to gastric mucosa using ranitidine. Comparison of the effectiveness of 2 dosages].

339 patients with rheumatic diseases suffering from dyspepsia and endoscopically proven gastroduodenal lesion entered an open multicenter study with ranitidine 150 mg bid or ranitidine 300 mg administered at night in a single dose over 4 weeks. For entry the patients had to have been treated for at least 3 months with the non-steroidal anti-inflammatory drugs diclofenac, indomethacin and piroxicam. During the trial all patients were continued on NSAID. The data of 248 patients were evaluable. At entry, patients in both treatment groups had a total gastric damage score of 2.0. The duodenal lesion score was on average 1.43 in the ranitidine 150 mg bid group, and 1.8 in the 300 mg single dose ranitidine at night group. After 4 weeks of treatment the mean lesion score was significantly reduced in the stomach as well as in the duodenum with both ranitidine regimens, no differences being seen between the groups. In addition, rapid symptomatic relief was observed in both groups. After 4 weeks of treatment more than 80% of the patients were symptom-free or markedly improved.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1989

[Nizatidine versus ranitidine in the treatment of acute duodenal ulcer. Comparison of 300 mg nizatidine and 300 mg ranitidine in a single evening dose].

In a double-blind, endoscopically controlled study on 367 duodenal ulcer patients, we compared the clinical efficacy of 300 mg ranitidine nocte with that of 300 mg nizatidine nocte, which is known to reliably provide selective inhibition of nocturnal acid secretion. Nizatidine was administered to 183, ranitidine to 184 patients. Endoscopy was performed at the start of the study, as well as at 2, 4 and 8 weeks. The presence of ulcer was defined as a benign lesion of the gastric mucosa measuring at least 5 mm in diameter; healing was characterized as complete reepithelialization. In the nizatidine group, as many as 76% of our patients were free from night pain at 2 weeks, and 88% at 4 weeks. Identical values were obtained in the group treated with 300 mg ranitidine nocte. The healing rates at 2, 4 and 8 weeks were comparable in the nizatidine and ranitidine groups (nizatidine: 57%, 87%, 92%, respectively; ranitidine: 63%, 90%, 96%, respectively). Clinically significant adverse effects were seen in neither of the two treatment groups. These results demonstrate that selective inhibition of nocturnal acid secretion achieves healing of duodenal ulcer and freedom from pain as rapidly and effectively as protracted inhibition of acid secretion provided by the administration of 300 mg ranitidine nocte.

Adolescent↗

PubMed1989

[Treatment of acute stomach ulcer with H2 receptor antagonists. A direct therapy comparison with 300 mg nizatidine nightly and 2 times 150 mg nizatidine with twice daily 150 mg ranitidine].

In this endoscopically controlled, double-blind study involving 242 patients with acute benign gastric ulcer, it was shown that the selective inhibition of nocturnal gastric acid secretion with 300 mg nizatidine administered on retiring represents an effective and reliable form of therapy. After four weeks of treatment, 90% of the patients receiving 300 mg nizatidine, no longer experienced nocturnal pain, in comparison with 83% receiving 2 X 150 mg nizatidine daily (n.s.). The total healing rates after four weeks were 60% in the patients receiving 300 mg nizatidine, 60% in those on 2 X 150 mg nizatidine daily, and 58% in those receiving 2 X 150 mg ranitidine daily. After eight weeks, the respective figures rose to 85%, 84% and 84%. Clinically relevant side effects were observed in none of the three groups. With a dose on retiring of 300 mg nizatidine, it is possible to accelerate the healing of a benign gastric ulcer, simply by the nocturnal suppression of gastric acid production, and, during the day, preserving physiological gastric function, thus avoiding the possible risks of protracted hypochlorhydria.

Adolescent↗

PubMed1989

[Inhibition of 24-hour acidity by nizatidine].

In a randomized, double-blind, placebo-controlled, comparative cross-over study, we studied the effect of four H2-receptor antagonists on intragastric 24-hour acidity, nocturnal volume and acid output. Ten healthy male volunteers were administered 300 mg or 150 mg nizatidine, 800 mg cimetidine, 300 mg ranitidine, 40 mg famotidine, or placebo on several days, in each case at 9:000 PM. Nocturnal intragastric H+ concentration (mmol/l) (11:00 PM to 7:00 AM) was significantly reduced by all H2 blockers compared with placebo. We obtained the following inhibition rates: Cimetidine 67%; ranitidine 95%; famotidine 89%; nizatidine 80% (300 mg) and 69% (150 mg). Nocturnal acid (mmol/l) and volume output (ml/h) were also significantly (compared with placebo) inhibited by all four H2-receptor antagonists. Inhibition of nocturnal acid secretion was almost identical on nizatidine 300 mg nocte, ranitidine 300 mg nocte, famotidine 40 mg nocte, and cimetidine 800 mg nocte. Nizatidine 300 mg nocte and 150 mg nocte exclusively reduced acid secretion at night, without an aftereffect into the following day (8:00 AM to 6:00 PM). These results suggest that the clinical efficacy of these H2-receptor antagonists is identical with respect to healing peptic ulcer disease and providing freedom from pain. It is generally accepted today that gastric acid inhibitors used in the treatment of peptic ulcer disease should interfere with daytime gastric acid secretion as little as possible, particularly since the acid protects the stomach from bacteria ingested with the food during the day.

Cimetidine↗

PubMed1989

Comparison of the gastroduodenal tolerance of tenoxicam and diclofenac Na. A double-blind, endoscopically controlled study in healthy volunteers.

The gastroduodenal tolerance of Tenoxicam and Diclofenac Na has been evaluated in a double-blind, parallel group study in 36 healthy male volunteers. The doses used were 20 mg Tenoxicam and 100 mg Diclofenac Na daily in a retard formulation for 14 days. Gastric tolerance was assessed by endoscopy, which was performed at base-line, after the 14 day dosing period and after a 14 day follow-up period without treatment. The mucosal lesions were scored using modified Lanza criteria. Tenoxicam was significantly better tolerated at the end of the 14 day dosing period (mean gastric score: Tenoxicam 1.3; Diclofenac Na 2.2). The two treatment groups had comparable scores at the base-line and post study assessments. Tenoxicam and Diclofenac Na were generally well tolerated. Only two volunteers reported intermittant lack of appetite, heartburn and a feeling of pressure in the stomach.

Adolescent↗

PubMed1989

Human gastric acid secretion following repeated doses of AG-1749.

The effect of increasing doses (15 mg, 30 mg and 60 mg) of the substituted benzimidazole, AG-1749, on gastric acid secretion and fasting serum gastrin concentration has been studied after repeated administration to healthy volunteers. AG-1749 produced a dose-dependent and profound decrease in basal and stimulated gastric acid secretion in all volunteers, with almost total suppression at the highest dose. The extent of inhibition increased between Day 2 and Day 8 with the 15 and 30 mg doses of AG-1749. The inhibitory effect of AG-1749 appears to be fully reversible as control levels of acid output were reached 7 days after drug withdrawal. Seven days' dosing with 60 mg AG-1749 induced a more than threefold increment of fasting serum gastrin concentration, but this increase was still within the normal range. Seven days after cessation of dosing, fasting serum gastrin concentration returned to a pre-dose level.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1989

Sucralfate in the treatment of reflux esophagitis in adults: an update.

Sucralfate was evaluated in several clinical studies on reflux esophagitis, a total of over 400 patients were studied worldwide. In this study 49 patients with reflux esophagitis of stage I-III acc. to Savary and Miller were included. The evaluation was based on 41 patients, 22 received sucralfate suspension 1 g in 5 ml qid, 19 ranitidine 150 mg bid. The patients were treated for 8 weeks, endoscopic controls were performed before treatment and after 8 weeks. The healing rates were 64% in the sucralfate group and 68% in the ranitidine group and exhibited no significant difference (p greater than 0.05). Antacid consumption and symptomatic improvement were comparable in both groups. Sucralfate seems to be a valid alternative to H2-blockers in the treatment of reflux esophagitis.

Adult↗

PubMed1989

Effects of rioprostil on gastric acid and pepsin secretion in man: a review of studies in healthy volunteers.

The antisecretory effect of rioprostil on acid and pepsin secretion stimulated by pentagastrin or a meal, or on the 24-h intragastric acidity is tested in four different studies in 33 healthy male volunteers using a double-blind, crossover design. The oral doses of rioprostil used are 50 micrograms, 100 micrograms, 150 micrograms, 200 micrograms, 300 micrograms and 600 micrograms; these are the results obtained: Rioprostil reduces basal H+ and pepsin output by more than 50%. Rioprostil, 300 micrograms and 600 micrograms, significantly reduces the 3-h pentagastrin-stimulated acid output by 43.5% and 58.9%, respectively, and the 3-h stimulated pepsin output by 41.1% and 66.5%, respectively (p = 0.01). Depending on the method used for intragastric titration the following percentages of inhibition of acid secretion are observed, 40%, 65%, and 75% with 150 micrograms, 300 micrograms, and 600 micrograms rioprostil respectively, with one method and 32%, 34%, and 79% with 25 micrograms, 50 micrograms, and 200 micrograms rioprostil respectively, with a somewhat modified technique. The differences observed in % inhibition between these two studies can be explained by the use of a different intragastric titration technique. Rioprostil, 300 micrograms and 600 micrograms, significantly inhibits night-time acid secretion (AUC x h, 2400 h-0800 h) by 52% and 73.5% when compared with placebo (p = 0.03). The calculated ED50 for acid inhibition is 86.5 micrograms of rioprostil.

Adult↗

PubMed1989

Rioprostil in the acute and long-term treatment of peptic ulcers: a review.

The new prostaglandin E1 analogue, rioprostil, significantly accelerates healing and the elimination of pain in cases of peptic ulcer. The anti-ulcerous potency of this prostaglandin is equivalent to that of cimetidine. In comparison with ranitidine, there is a positive trend in favour of the H2-receptor antagonist, ranitidine, which has a more pronounced antisecretory effect than rioprostil. The differences in the healing rates during treatment with rioprostil and ranitidine are statistically significant in some cases, whereas those relating to pain alleviation are not. In contrast, the therapeutic efficacy of the two substances is almost identical in cases of Ulcus ventriculi. Rioprostil can be used with much the same success as ranitidine for preventing the recurrence of duodenal ulcers. The frequency of diarrhoea during rioprostil treatment, 300 micrograms b.d. and 600 micrograms nocte, is approximately 10%. In only about 1% of the patients does the rioprostil treatment have to be discontinued because of this adverse reaction.

Anti-Ulcer Agents↗

PubMed1989

A single evening dose of rioprostil, 600 micrograms, in the treatment of acute duodenal ulcers.

When administered as 300 micrograms b.d. or as 600 micrograms once in the evening, the new prostaglandin E1 analogue, rioprostil, is capable of reducing nocturnal H+ activity (1200 h to 0800 h) by 52% and 74%, respectively (p less than 0.01). Diurnal acidity (0900 h to 1800 h), on the other hand, is only reduced by 33% and 15% (not significant). A single evening dose of rioprostil, 600 micrograms, is used successfully on 208 patients suffering from acute duodenal ulcer. After 2 weeks and 4 weeks of treatment, the healing rates are comparable to the high values obtained with ranitidine, 300 mg nocte (rioprostil, 600 micrograms nocte: 54.1% and 84.1%; ranitidine, 300 mg nocte: 54.4% and 89.9%). There are also no significant differences between the groups as regards symptomatic improvement. Severe diarrhoea and abdominal complaints do not occur with rioprostil, 600 micrograms nocte.

Adult↗

PubMed1989

[Protective effect of an antacid against acetylsalicylic acid].

The protective action of an magnesium-aluminum-antacid (Mucal-Gel) against acute doses of acetylsalicylic acid (ASA) was studied in healthy subjects (n = 30) by a double-blind cross-over method. The severity of the lesion was determined by endoscopy. In the corresponding placebo experiments, severe lesions of the gastroduodenal mucosa were seen after administration of 1500 mg ASA. These lesions could be prevented only in the presence of high doses of the antacidum mixture. It is concluded from these studies that protective actions against ASA can be achieved only if the intragastric pH-level is adequately raised above 3.5 and higher.

Adult↗

PubMed1989

[Ranitidine ameliorates acemetacin and indomethacin-induced changes of the gastroduodenal mucosa, without modifying the pharmacokinetic behavior of both antirheumatic drugs].

12 healthy volunteers participated in this double-blind, randomized, cross-over study. All subjects were given indomethacin (50 mg tid) or acemetacin (60 mg tid) for 6 days in the presence and absence of ranitidine 300 mg at night. At day 6 120 minutes after the last morning dose an endoscopy was performed and the appearance of the gastric and duodenal mucosa was noted. In the indomethacin experiments mean lesion score averaged 2.2 +/- 0.2 (+/- SEM) when placebo was coadministered. In the corresponding acemetacin-series the lesions score was 1.6 +/- 0.1 (+/- SEM). A reduction in mucosal damage occurred in both NSAID-groups when ranitidine 300 mg at night was given concurrently: The mucosal lesions score was reduced to 1.7 +/- 0.2 and to 1.0 +/- 0.1 (+/- SEM), respectively. This protection afforded by ranitidine was significant when compared with placebo (p less than 0.05). In 8 subjects plasma concentrations of acemetacin and indomethacin were determined on day 1 and day 5. The AUC-values of indomethacin and acemetacin in the presence and absence of ranitidine were almost identical when analysed by the paired T-test. The mean plasma concentrations of both antirheumatic agents did not show any difference when coadministered with placebo or ranitidine. Our data suggest that 300 mg ranitidine at night improves the gastroduodenal tolerability of both indomethacin and acemetacin without affecting main pharmacokinetic parameters of both antirheumatics.

Adult↗

PubMed1989

[Single evening administration of a new antimuscarinic agent telenzepine in therapy of acute duodenal ulcer. Results of a randomized double-blind comparative study versus pirenzepine].

A multicenter, double-blind, randomized controlled study was conducted in 314 duodenal ulcer patients to compare the efficacy and safety of the antimuscarinics telenzepine and pirenzepine in the treatment of duodenal ulcer. Patients received telenzepine 3 mg (156) once-daily at bedtime or 50 mg pirenzepine (158) two times daily for 2 weeks. If ulcerous lesions persisted treatment was extended to 4 weeks. Efficacy was assessed by relief of ulcer pain and endoscopic findings of ulcer healing. Safety was determined on the basis of side effects and results of laboratory tests. The 2- and 4-week healing rates achieved with telenzepine were 21.1 and 67.3%, respectively, and with pirenzepine they were 20.0 an 69.0%, respectively; the differences in healing rates for the two drugs were not statistically significant. Similarly both drugs provided satisfactory relief of pain. The incidence of untoward effects was 24.5% with telenzepine and 29.7% with pirenzepine, dryness of mouth being most prominent (20.4 vs. 19.3%). With telenzepine blurred vision was reported in a significantly lower rate compared to pirenzepine (0.7 vs. 4.2%, p less than 0.05). Clinically relevant abnormal laboratory tests were not observed. The present study shows for the first time that the newly developed antimuscarinic drug telenzepine is in a single nocturnal dosage regimen (3 mg nocte) as effective as pirenzepine (50 mg bid) in the treatment of duodenal ulcer.

Adult↗

PubMed1989

[Endoscopic studies of gastroduodenal tolerance of 100 mg versus 500 mg acetylsalicylic acid daily: a randomized double-blind study with healthy probands].

Acetylsalicylic acid (ASS) is increasingly used in the prevention of cardiovascular diseases. In recent years lower daily ASS-doses (100-300 mg) have been given for this indication. However, only marginal knowledge is available about the upper GI-tolerability of ASS in this dosage regiment. In a randomized double-blind study we have evaluated the gastroduodenal tolerability of 100 mg ASS and 500 mg ASS daily in 20 healthy volunteers using upper GI-endoscopy. Both ASS-dosages have been taken over a period of 4 weeks. Endoscopic controls were performed at entry and repeated after 7, 14 and 28 days of treatment. 100 mg ASS daily induced during the whole period significant less gastroduodenal damages than 500 mg ASS daily (p less than 0.05). The lesion score of both groups on day 7 and day 28 were almost identical. Our data suggest that even low doses of ASS (100 mg daily) produced gastroduodenal injuries and that no adaptative phenomena did occur during the treatment period.

Adult↗

PubMed1989

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

The effects of single oral doses of 800 and 1200 micrograms of the new alprostadil analogue mexiprostil (prostaglandin E1 16-methyl-16-methoxy derivative, MDL 646), presented as tablet and capsule formulation, on basal and pentagastrin-stimulated acid secretion, were studied in 10 healthy volunteers, using a randomized, double-blind, placebo-controlled, 5-way crossover design. Compared to placebo, administration of mexiprostil resulted in a significant inhibition of basal gastric acid secretion, at both doses and formulations. Pentagastrin-stimulated gastric secretion was reduced to a lesser degree and the differences compared to placebo did not achieve statistical significance when adjustments were made for basal effects present before starting stimulation. Total volume of gastric secretion, under basal conditions, was decreased by both doses and formulations, though the changes were significant only at 1200 micrograms for both formulation. The decrease in volume of gastric secretion during pentagastrin infusion did not reach statistical significance. Basal intragastric pH was increased by both doses and formulation, but the changes were significant only for the capsule formulation, at either dose. Neither dose of mexiprostil prevented the decrease in intragastric pH produced by pentagastrin infusion. Tolerability of mexiprostil was excellent with no unwanted effects reported either during or after the study. No changes in heart rate and systemic blood pressure were observed. Laboratory safety parameters were not altered by mexiprostil. There was no significant difference between the effects of both formulations of mexiprostil on any pharmacodynamic parameter.

Adult↗

PubMed1988

Optimal reduction of gastric acid secretion in the treatment of peptic ulceration.

Pronounced and sustained inhibition of acid secretion is currently the therapeutic principle most frequently applied in the treatment of peptic ulcer disease. Since theoretically short term risks of complete inhibition of acid secretion cannot be totally ruled out, anti-secretory anti-ulcer drugs should interfere as little as possible in the physiology of gastric acid secretion. This concept is presently best achieved through the single bedtime dose of H2-blockers, which has been shown to be as effective as a twice daily dosage regimen in peptic ulcer disease. This reduces only nocturnal acid secretion, while daytime acidity remains unaffected. But there is a close correlation between the extent of the reduction of nocturnal acid secretion, healing rates and pain relief. Additionally, large clinical trials with peptic ulcer patients have shown that after 14 days' treatment with H2-blockers 30 to 50% of patients still complain about ulcer pain and about 20 to 40% of patients take supplementary antacids. As a result of this there is undoubtedly a need for an additional medication that produces a more pronounced reduction of acidity than current treatment with H2-receptor antagonists as a single evening dose. Obviously this dosage regimen does not always fulfil the therapeutic requirements (i.e. pain relief) of the individual patient. Therefore a more flexible form of application should be introduced. In general clinical use it is not feasible to identify patients with a higher treatment requirement by acid secretion analysis. However, what is feasible is the recommendation to increase the dose and frequency of administration of H2-blockers in relation to the symptoms of pain.

Depression, Chemical↗