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Biomedical subjects

J J Misiewicz

Publications and source records attributed to J J Misiewicz.

At least 109 records · Page 6Linked to original sources
PubMed1981

Potentially explosive colonic concentrations of hydrogen after bowel preparation with mannitol.

Hydrogen (H2) concentrations were measured in undiluted samples of intracolonic gas and in expired air in twenty patients undergoing colonoscopy after preparation with either mannitol or castor oil. Potentially explosive intracolonic H2 concentrations were present in six out of ten patients given mannitol, but in none given castor oil. This has important implications for colonoscopic, as well as for surgical, electrosurgery. H2 concentrations in expired air sampled preoperatively did not identify patients with potentially explosive intracolonic hydrogen levels.

Adult↗
PubMed1981

Comparison of the effects of ranitidine, cimetidine and placebo on the 24 hour intragastric acidity and nocturnal acid secretion in patients with duodenal ulcer.

Twenty-four hour intragastric acidity and nocturnal acid secretion were measured in 10 males with duodenal ulcer in four separate 24 hour studies, during which the subjects ate normal meals, had unrestricted physical activity, and consumed their customary quantities of tobacco. The medication consisted of either placebo, cimetidine 200 mg tds and 400 mg at night, or ranitidine 150 mg bd, or 200 mg bd. Ranitidine 150 mg bd decreased mean 24 hour hydrogen ion activity from 41.8 mmol/l to 13.1 mmol/l (-69%, P less than 0.001) and nocturnal acid output from 6.1 mmol/h to 0.6 mmol/h (-90%, P less than 0.01). This degree of inhibition was significantly greater than that due to cimetidine (P less than 0.001 for 24 hours acidity, less than 0.05 for night time acid output). Plasma concentrations of ranitidine were greater than the IC50 for more than eight hours after the 150 mg dose. Ranitidine 200 mg conferred no additional advantage. Ranitidine 150 mg bd should be tested in therapeutic trials.

Adult↗
PubMed1981

Comparison of twice-daily ranitidine with standard cimetidine treatment of duodenal ulcer.

One hundred and three outpatients with endoscopically diagnosed duodenal ulcer were randomly allocated to treatment with either cimetidine 200 mg tds and 400 mg nocte, or ranitidine 150 mg bd for four weeks. The endoscopists were not aware of the treatment and took no part in the clinical management. On completion of treatment ulcers had healed in 43 of 51 (84%) patients given cimetidine and in 40 of 52 (77%) patients given ranitidine. There were no serious unwanted effects in either treatment group. The results show no significant difference between healing rates after four weeks of standard cimetidine therapy or ranitidine 150 mg bd.

Adolescent↗
PubMed1981

Scope and specificity of acarbose in slowing carbohydrate absorption in man.

Fifty-gram carbohydrate tolerance tests were performed on healthy volunteers to test the activity and specificity of an alpha-glucoside hydrolase inhibitor, acarbose (BAY g 5421). Two hundred milligrams acarbose reduced the area under the blood glucose response curve by 89% (P less than 0.001) after sucrose by 80% (P less than 0.002) after starch, by 19% (N.S.) after maltose, with no effect on glucose. Breath hydrogen measurements indicated an almost complete malabsorption of the sucrose. At 50 mg acarbose, some reduction in blood glucose and insulin response to sucrose was still seen, but no significant hydrogen production. It is suggested that at lower doses, acarbose may prolong the time course over which carbohydrate is absorbed as does dietary fiber; as with fiber, it may be a useful adjunct to diabetic therapy.

Acarbose↗
PubMed1981

Investigations on the penetration of ranitidine into the cerebrospinal fluid and a comparison of the effects of ranitidine and cimetidine on male sex hormones.

Cerebrospinal fluid (CSF) ranitidine concentrations were measured in 13 normal subjects undergoing routine myelography following either one, or two doses ranitidine 200 mg. Small amounts of the drug were detectable in the CSF. A separate investigation of duodenal ulcer patients compared the effects of ranitidine 150 mg twice-daily and cimetidine 1 g daily on basal and stimulated levels of male reproductive hormones in the plasma. Although cimetidine treatment resulted in a small rise in basal and stimulated testosterone, neither drug was associated with significant changes in basal or stimulated hormone levels.

Adult↗
PubMed1981

The effect of ranitidine and cimetidine on the twenty-four hour intragastric acidity profile and nocturnal acid secretion in duodenal ulcer patients.

Ten duodenal ulcer patients were studied during four 36 h periods, receiving either ranitidine 150 mg twice daily, or ranitidine 200 mg twice daily, or cimetidine 200 mg t.d.s. and 400 mg at night, or placebo. Conditions during the four experimental days were standard. Mean 24 h intragastric hydrogen ion activity on placebo (41.8 +/- 1.5 mmol 1(-1)) was decreased to 21.6 +/- 1.2 mmol 1(-1) on cimetidine, and to 13.1 +/- 1.0 and 12.1 +/- 1.1 mmol 1(-1) by the two dose levels of ranitidine. Nocturnal acid output was decreased by 70% by cimetidine and by 90 and 89% by the two dose levels of ranitidine. In this test system ranitidine was more than four times as potent as cimetidine. Greater decreases in daytime acidity and nocturnal acid secretion were produced by twice-daily ranitidine than by the standard four daily doses of cimetidine

Administration, Oral↗
PubMed1979

Evaluation of one-visit endoscopic clinic for patients with dyspepsia.

An evaluation was made of the feasibility of an instant upper-gastrointestinal endoscopy clinic for patients referred to hospital for the investigation of dyspepsia. A total of 200 patients underwent endoscopy using a small-diameter endoscope with only topical pharyngeal anaesthesia but no premedication or sedation. The procedure was successful in 187 of the patients. Its acceptability was high for both patients and doctors. The average duration of the hospital visit was 45 minutes. Instant endoscopy with a small-diameter endoscope provides a convenient and fast primary diagnostic service for patients with dyspepsia.

Adult↗
PubMed1979

Controlled comparison of cimetidine and carbenoxolone sodium in gastric ulcer.

Fifty-four outpatients with endoscopically diagnosed benign gastric ulcer were allocated at random to treatment with either cimetidine 800 mg daily for six weeks or carbenoxolone sodium 300 mg daily for one week then 150 mg daily for five weeks. Ulcers were reassessed by endoscopy at the end of the trial. The endoscopist was unaware of the treatment and did not take part in the clinical care of the patients. Twenty-one of the 27 patients (78%) given cimetidine and 14 of the 27 (52%) given carbenoxolone had healed ulcers. Symptomatic response occurred earlier with cimetidine but was not significantly better. Unwanted effects were more common in the carbenoxolone group: 12 patients developed hypokalaemia, four of whom needed oral potassium supplements. The results suggest that histamine H2-receptor blockade is at least as effective as carbenoxolone sodium for benign gastric ulcer and produces fewer side effects.

Administration, Oral↗
PubMed1979

Medical treatment of duodenal ulcer.

Recent controlled clinical trials have shown that acute episodes of duodenal ulcer can be treated successfully with either anti-secretory (cimetidine), mucosa-protective (carbenoxolone, organic bismuth preparation) or antacid drugs. For prevention of recurrence, only cimetidine has thus far proved effective. A critical review is presented of the advantages and disadvantages of these drugs in conservative ulcer therapy.

Antacids↗
PubMed1979

Controlled trial of cimetidine in upper gastrointestinal haemorrhage.

One hundred and one patients were studied in a double-blind controlled trial to assess the role of oral cimetidine in preventing the continuation or recurrence of acute upper gastrointestinal haemorrhage from various sources, chiefly peptic ulcer. The dose of cimetidine was 800 mg on entering the study followed by 400 mg six hourly. The source of bleeding was identified endoscopically in 96% of patients, peptic ulcer comprising 70%. Bleeding continued or recurred in 11 of 51 (21.5%) of patients on cimetidine and in 12 of 50 (24%) of patients on placebo. Analysis of the effect of cimetidine according to age or severity of bleeding showed no significant advantage for the drug.

Adult↗
PubMed1978

Misleading response of malignant gastric ulcers to cimetidine.

Four patients who apparently had benign gastric ulcer (G.U.) were treated with cimetidine. The ulcers healed and their symptoms disappeared. However, when cimetidine was stopped the symptoms recurred. Intramucosal cancer was found only at histopathological examination of the resected stomachs in two of the four patients, and in all the cases malignancy had not been detected by the initial serial biopsies and brush cytology. Relief of symptoms of malignant gastric ulcers by cimetidine may delay diagnosis and appropriae treatment.

Adult↗
PubMed1978

Peptic ulceration and its correlation with symptoms.

Studies in which the numbers of healed or unhealed ulcers and their correlation with symptoms are availabel are summarized in Table 1. A review of the data and inspection of the Table show that the correlation of GU or DU healing with symptomatic remission is generally poor. The reasons for this are unknown and reflect the very incomplete understanding of the mechanism of ulcer pain and of the pathways through which the pain is mediated. The pathogenesis of pain in GU or DU may be due to the action of acid and pepsin, or of bile, on the tissues exposed in the ulcer crater, to abnormal motility, to normal motility acting on inflamed tissue, to areas of inflammation surrounding the ulcer crater, or to a combination of these factors. The relative importance of each of these variables in DU or GU, or in individual patients (because the mechanism of pain may not be the same in each patient) is not known. Nor is it known how much the pathogenesis of ulcer pain is the result of local release of histamine, kinins, and prostaglandins. These biogenic factors are known to be associated with inflammation and produce, or enhance, somatic pain. Their importance in peptic ulcer in man needs to be studied. Relief of pain after neutralization or buffering of gastric contents with alkali or food suggests strongly that acid must play an important part in the pathogenesis of the ulcer symptoms. The rapidity with which relief of symptoms occurs points towards the direct involvement of hydrogen ions in at least one type of ulcer symptom. Lowering of intragastric acidity by histamine H2- receptor antagonists or high-dose alkali may contribute to the observed discrepancies between ulcer healing and the remission of pain, by creating an environment in the gastroduodenal lumen which favours symptomatic improvement, even in the presence of an unhealed crater. This idea, however, does not explain why there is a discordance between healing and symptoms in patients receiving placebo, or in those treated with other drugs, such as carbenoxolone sodium. In the absence of endoscopic evidence, the presence or absence of symptoms cannot be assumed to indicate with certainty the presence or the absence of a peptic ulcer.

Carbenoxolone↗
PubMed1977

24-hour intragastric acidity and nocturnal acid secretion in patients with duodenal ulcer during oral administration of cimetidine and atropine.

Cimetidine markedly inhibits gastric acid secretion, but from the therapeutic point of view it is important to know whether concurrent treatment with an anticholinergic increases its effect. This possibility has been investigated by measuring the 24 h intragastric acidity and nocturnal output of acid in four duodenal ulcer patients, each receiving on separate occasions cimetidine 1 g/day and placebo, atropine 2-4 mg/day and placebo, cimetidine and atropine, or two placebos. Cimetidine alone decreased mean hourly hydrogen ion activity by 63% of control values, decreased mean hourly hydrogen ion concentration (total acid) by 41%, inhibited nocturnal acid secretion by 83% and resulted in half the nocturnal samples being anacidic. Atropine alone had no effect when compared with control and combined treatment with both drugs was not superior to cimetidine alone. Atropine did not affect the absorption or urinary excretion of cimetidine. Fasting serum gastrin concentrations were not changed by any of the treatments. At the doses studied, the combination of cimetidine with an anticholinergic appears to offer no advantages over treatment with the H2-antagonist alone. Cimetidine is the only potent anti-secretory drug that does not cause acute side-effects and this important advantage would be lost if it were given with a maximal dose of an anticholinergic.

Administration, Oral↗