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Biomedical subjects

F Halter

Publications and source records attributed to F Halter.

At least 37 records · Page 2Linked to original sources
PubMed1990

Loss of acid suppression during dosing with H2-receptor antagonists.

The suppression of intragastric acidity with H2-receptor antagonists may diminish with repeated administration. To assess the degree and dose-dependence of this tolerance after short-term dosing, two doses of the H2-receptor antagonists, ranitidine (300 mg nocte or q.d.s.) and sufotidine (300 mg or 600 mg b.d.), were given to healthy volunteers for 1 and 2 weeks, respectively. After 1 and 7 days of dosing with ranitidine 300 mg q.d.s. the median 24-h and night-time pH, measured by continuous 24-h pH-metry, dropped from 3.7 to 2.2 and 5.8 to 3.2, respectively (P less than 0.0001 for both). The decline in median pH with ranitidine 300 mg nocte was only significant during the night (from 4.1 to 2.9) (P less than 0.04). There was little change in plasma gastrin concentrations between days 1 and 7 with either dosage. With sufotidine 300 mg b.d. and 600 mg b.d. for 1 and 14 days, the median 24-h pH fell from 3.7 to 2.1 and from 4.6 to 2.6, respectively (P less than 0.0001). The equivalent medians for the night decreased from 6.3 to 2.3 and from 6.6 to 3.1 (P less than 0.0001). Gastrin concentrations did not change after 14 days of dosing with sufotidine 300 mg b.d., but increased significantly during dosing with sufotidine 600 mg b.d. (P less than 0.001). Significant tolerance developed in 7-14 days and it seemed to show some dose relationship. The mechanisms behind tolerance and the role of gastrin are discussed, but remain unclear.

Adolescent↗
PubMed1989

Sucralfate and ranitidine in the treatment of acute duodenal ulcer. Healing and relapse. Ulcer Study Group.

Healing and relapse of acute duodenal ulcer were investigated in an endoscopically controlled multicenter study using a double-blind design. Patients with acute uncomplicated duodenal ulcer were randomly assigned to treatment with sucralfate (1 g four times per day) or ranitidine (150 mg twice per day) for four to eight weeks. After healing, all anti-ulcer treatment was discontinued except for low-dose antacids needed for occasional upper abdominal pain, and the patients were observed for up to one year. Endoscopy was repeated after one year or at any time earlier if symptoms suggested ulcer relapse. Of the 83 patients who entered the study, 75 (sucralfate 40, ranitidine 35) underwent endoscopy after four weeks and could be fully evaluated. Healing rates after four and eight weeks were similar in the two groups (four- and eight-week healing rates after sucralfate and ranitidine: 78 and 74 percent, and 95 and 94 percent, respectively). Fifty-three patients with healed ulcers (sucralfate 29, ranitidine 24) were observed for up to one year. Duodenal ulcers occurred somewhat later after sucralfate than after ranitidine treatment, but life table analysis showed no significant difference. Thus, this study confirms a similar efficacy of sucralfate and ranitidine in healing of duodenal ulcer. A tendency to delayed relapse early after discontinuation of sucralfate failed to reach statistical significance.

Acute Disease↗
PubMed1989

[Diagnosis and therapy of stomach ulcer].

The patient suffering from gastric ulcer disease needs more attention than one suffering from duodenal ulcer disease, especially regarding the necessity of endoscopic bioptic control of healing, which is vital to ensure that malignancy is not missed. Greater patience is also necessary during therapy, since a gastric ulcer is generally larger than a duodenal ulcer and more time is thus necessary for complete healing. Otherwise the natural course of the disease and the therapeutic requirements for acute and maintenance treatment are similar. This also relates to the indication for surgery.

Acute Disease↗
PubMed1989

Enprostil reduces the increase of gastric corpus mucosal mass induced by the hydrogen-potassium-stimulated adenosine triphosphatase inhibitor BY 831-78 in the rat.

We studied whether enprostil, a synthetic prostaglandin E2 derivative, might inhibit gastrin release and the trophic effects on gastric oxyntic mucosa induced by prolonged treatment with an inhibitor of hydrogen-potassium-stimulated adenosine triphosphatase, the substituted benzimidazole BY 831-78. Rats were treated intragastrically with enprostil (1 or 15 micrograms/kg b.i.d.), BY 831-78 (15 mumol/kg once daily), the combination of enprostil and BY 831-78, ranitidine (300 mumol/kg b.i.d.), and placebo. Plasma gastrin and somatostatin levels and gastric acid secretion were measured during a 1-day treatment in animals fitted with chronic gastric fistulas and repeatedly during 9 wk of treatment in intact rats. Despite inhibiting acid secretion, enprostil did not increase plasma gastrin. When combined with BY 831-78, enprostil transiently reduced the BY 831-78-induced increase of integrated plasma gastrin (1375 +/- 206 vs. 2137 +/- 256 pmol/L.12 h, p less than 0.05) in fasted rats with fistulas, but failed to prevent the marked hypergastrinemia following 9 wk of treatment with BY 831-78 (717 +/- 80 vs. 731 +/- 56 pmol/L) in intact rats. However, enprostil reduced the BY 831-78-induced increase of oxyntic mucosal volume (458 +/- 31 vs. 567 +/- 33 mm3, p less than 0.01), whereas BY 831-78 prevented the enprostil-induced increase of antral mucosal volume (42 +/- 3 vs. 56 +/- 3 mm3, p less than 0.01). These results demonstrate that some of the trophic effects induced by a hydrogen-potassium-stimulated adenosine triphosphatase inhibitor are not exclusively governed by gastrin.

Adenosine Triphosphatases↗
PubMed1989

Smoking and pH response to H2-receptor antagonists.

Smoking has been shown to impair the therapeutic effect of H2-receptor antagonists. To evaluate the acid-reducing capacity of H2-receptor antagonists in relation to smoking habits, we tested the effect of ranitidine (Ran) and famotidine (Fam) under physiologic conditions, using ambulatory pH-metry. Intragastric pH was measured over 20 h. Each of 18 healthy volunteers, 9 smokers and 9 nonsmokers, received 40 mg Fam, 300 mg Ran, or placebo in a double-blind, randomized study as a single evening dose. With both drugs 20-h acidity was markedly suppressed. After Fam treatment mean inhibition was 61% in smokers and 76% in nonsmokers and after Ran 51% and 67%, respectively. When areas under the pH curves for each individual were calculated and treatment compared with placebo (= 100%), the response was smaller in smokers than in nonsmokers with either drug (Fam, 153 +/- 21% versus 214 +/- 19%, p less than 0.01; Ran, 176 +/- 21% versus 232 +/- 29%, p less than 0.05) during the first 4 h after drug intake. A similar effect was observed in the morning period from 0600 to 1000 h (Fam, 118 +/- 19% versus 206 +/- 19%, p less than 0.001; Ran, 133 +/- 21% versus 207 +/- 31%, p less than 0.02). During the nighttime there were no significant differences. These findings indicate that smoking impairs the response to both drugs tested.

Adolescent↗
PubMed1988

[Endoscopic stone extraction from the biliary tract--current status].

Endoscopic removal of bile duct stones has become a routine procedure. The present situation is analyzed in the light of patients treated in 1985 and 1986 by the same team. We report on 114 patients (46 men, 68 women, median age 74 years). Clearance of bile ducts was possible at first attempt in 80 patients (70%) and at second attempt in a further 8 patients (7%). Procedure-related mortality was 0.9%: one patient died after developing necrotizing pancreatitis. The complication rate was 10.6%. Among the 39 patients with gallbladders left in situ, 4 (10.8%) had to undergo cholecystectomy after an interval of 1 to 7 months. It is concluded that endoscopic removal of bile duct stones is a method with a high rate of success. However, even in experienced hands complications are by no means negligible.

Adult↗
PubMed1988

Influence of prostaglandins, omeprazole, and indomethacin on healing of experimental gastric ulcers in the rat.

We investigated whether the trophic actions of prostaglandins, omeprazole, and indomethacin on gastric mucosa lead to accelerated healing of gastric ulcers in the rat. Cryoulcers were produced in the corpus area and treated with 16,16-dimethyl prostaglandin E2 (5 or 100 micrograms/kg b.i.d., intragastrically), omeprazole (40 mumol/kg once daily, subcutaneously), indomethacin (2 mg/kg b.i.d., subcutaneously), or placebo. At the end of the treatment, plasma gastrin, cell labeling index (autoradiography with [3H]thymidine), and the size and depth of mucosal defects were measured. Compared with placebo, omeprazole accelerated ulcer healing as indicated by a smaller ulcer area [1.1 +/- 0.2 vs. 4.8 +/- 1.2 mm2 (mean +/- SEM)] and smaller ulcer depth (383 +/- 31 vs. 488 +/- 41 microns) after 10 days of treatment. Prostaglandins did not affect ulcer healing despite thickening of gastric corpus mucosa. Indomethacin delayed ulcer healing and reduced the labeling index. Omeprazole induced a marked hypergastrinemia (208 +/- 12 vs. 66 +/- 12 pmol/L on day 5, and 469 +/- 23 vs. 58 +/- 16 pmol/L on day 10). The results indicate that abolishment of acid secretion by omeprazole accelerates healing. Trophic actions and "cytoprotective" effects by prostaglandins are not relevant for ulcer healing in this model.

16,16-Dimethylprostaglandin E2↗
PubMed1988

Mechanism of gastrointestinal toxicity of NSAIDs.

Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the gastrointestinal tract, mainly the stomach, by a local effect and by systemic interactions with prostaglandin synthesis. A local damaging effect was first suggested by Davenport, who demonstrated that aspirin, at an acid pH, enters the gastric mucosa by non-ionic diffusion, leading to a disruption of the gastric barrier and subsequent back-diffusion of hydrogen ions into the mucosa. Consequently, this leads to local haemorrhage and cell necrosis. Systemic damage is thought chiefly to occur by inhibition of prostaglandin synthesis, with consequent interaction of the defensive functions of the gastric mucosa. Inhibition of cyclo-oxygenase is the specific target of NSAIDs. However, the lipoxygenase pathway is also affected indirectly since cyclo-oxygenase inhibition results in a spill-over effect of leukotrienes, as both prostaglandins and leukotrienes are produced from arachidonic acid. Indeed, leukotriene B4, an extremely potent vasoconstrictor, may be responsible for some of the NSAID damage. In addition, cyclo-oxygenase inhibition blocks the integrity and synthesis of mucus, the secretion of bicarbonate and profoundly changes the life cycle of gastric mucosal cells. Following acute NSAID medication, the overall cell migration from the proliferative zone to the surface is accelerated and cell shedding is increased. However, during prolonged NSAID treatment, adaptation to the noxious effects of NSAIDs can occur with increased cell reproduction and subsequent compensation of the initially increased cell loss.

Animals↗
PubMed1987

Is it really more difficult to treat prepyloric ulcers?

Prepyloric and duodenal ulcers have some common characteristics: gastric acid secretion is increased and there is an association with blood group O. Many, therefore, have considered prepyloric ulcers to be a variety of duodenal ulcer disease. From an anatomical point of view, however, prepyloric ulcers are clearly gastric ulcers. After proximal selective vagotomy, the recurrence rate is very high, amounting to more than 30% in 5 years; this is significantly higher than the rate for duodenal ulcers. Better results are obtained in prepyloric ulcers, if vagotomy is combined with a drainage procedure. In recent years, some evidence, primarily from Scandinavia, has accumulated indicating that prepyloric ulcers are more resistant to treatment with histamine H2-receptor antagonists than duodenal ulcers or ulcers located in other parts of the stomach. In addition, the recurrence rate is particularly high in prepyloric ulcers. One must, however, consider that not only have all of these studies included relatively small numbers of patients, but also the prepyloric ulcer healing rates in other studies were similar to those observed for both duodenal ulcers and ulcers located elsewhere in the stomach. Prospective studies with large numbers of patients are, therefore, necessary before a clear-cut conclusion can be reached. There are several reasons why prepyloric ulcers could be more resistant to treatment. Impaired gastric emptying, duodeno-gastric reflux or chronic gastritis, especially in conjunction with Campylobacter pylori infection, must be considered. At present, one can only speculate on the validity of any of these hypotheses.

Anti-Ulcer Agents↗
PubMed1987

Effect of 16,16-dimethyl prostaglandin E2 on small intestinal mucosa in suckling rats.

Suckling rats were treated every 8 h by intragastric instillation of 16,16-dimethyl prostaglandin E2 (PG) in a dose of 25 micrograms kg-1 (PG25), or 100 micrograms kg-1 (PG100), or saline from postnatal day 7-11. PG increased small intestinal villus length and crypt depth, most markedly in the duodenum, leading to a mucosal height of 543 +/- 24 microns after saline, 670 +/- 26 microns after PG25 and 823 +/- 40 microns after PG100. In the proximal small bowel, PG100 raised the mean activities of sucrase by 439%, maltase by 98%, trehalase by 584%, lactase by 58% and alkaline phosphatase by 76%. In the distal small intestine, only sucrase and trehalase activities were stimulated whereas other enzymes were depressed. PG25 caused similar but less pronounced changes of enzyme activities. Eight hours after both the last PG25 and the last PG100 dose, plasma gastrin and corticosterone levels were decreased while thyroxine remained unchanged. The effect of a single dose of 100 micrograms kg-1 PG or saline was also tested on 5- and 11-day-old rats; they were killed 16 h after PG administration. An increase in villus length occurred along the entire small intestine of rats treated on day 5, and also in the ileum of rats treated on day 11. In the proximal intestine, maltase and trehalase were stimulated after early and late treatment and, in addition, sucrase and lactase after late treatment. Serum corticosterone levels were found to be significantly higher 2-6 h after PG100 than in the controls and then decreased gradually.(ABSTRACT TRUNCATED AT 250 WORDS)

16,16-Dimethylprostaglandin E2↗
PubMed1987

Prophylactic treatment of acute gastroduodenal stress ulceration. Low-dose antacid treatment without and with additional ranitidine.

Low-dose antacid treatment without and with additional ranitidine in the prevention of acute gastroduodenal stress ulceration in high-risk patients was compared in a randomized, double-blind clinical trial with endoscopic examination of the upper gastrointestinal tract before entry and after the 7-day study period. Of 67 patients who entered the study, 56 could be evaluated. Only one patient, allocated to antacid and placebo, had massive acute upper gastrointestinal bleeding, arising from a gastric ulcer. Although gastric intraluminal pH was better controlled with additional ranitidine treatment, the occurrence of mucosal lesions did not depend on the assigned treatment. We conclude that there is no significant difference between the two regimens in terms of endoscopically visible lesions and clinical outcome.

Acute Disease↗