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Biomedical subjects

J H Baron

Publications and source records attributed to J H Baron.

At least 127 records · Page 7Linked to original sources

Acid, pepsin, and mucus secretion in patients with gastric and duodenal ulcer before and after colloidal bismuth subcitrate (De-Nol).

Basal and pentagastrin stimulated gastric secretion was measured in seven patients with duodenal, and six with gastric ulcers before and after four weeks' treatment with colloidal bismuth subcitrate (as De-Nol), one tablet four times a day. Each duodenal and all but one of the gastric ulcers healed. After De-Nol there were no significant changes in basal, or pentagastrin stimulated volume, acid output, or primary parietal component. There were marked decreases in basal (duodenal ulcer -25%; gastric ulcer -16%) and pentagastrin stimulated total pepsin outputs, (duodenal ulcer -42%, gastric ulcer -36%). There were insignificant decreases in basal output of mucus, but postpentagastrin stimulated mucus output was significantly inhibited (p less than 0.05) in patients with duodenal (-16%) and with gastric ulcer (-27%). The drop in gastric proteolysis after De-Nol is unlikely to be because of the healing of the ulcers and is more likely to be because of the drug. The ulcer healing efficacy of De-Nol may be related to this decline in the proteolytic action of gastric juice, but is unlikely to be because of a quantitative change in mucus, or in acid secretion.

Adult↗

Detecting alcohol consumption as a cause of emergency general medical admissions.

In a general medical unit 27% of 104 admissions and 17% of bed occupancy were attributed to alcohol consumption, although only 10 of these 28 patients had classical alcohol-related conditions. Questioning on the amount of alcohol consumed was the most accurate method of screening for these patients. The brief MAST questionnaire, mean red cell volume, gamma-glutamyl transferase, aspartate transaminase and urate were all inadequate as screening tests. Only 13% of the admissions were defined as 'problem drinkers' on the brief MAST questionnaire, suggesting that harmful effects of alcohol are not confined to 'alcoholics'. Clinical suspicion and questions on the level of alcohol consumption are more efficient than questionnaire, biochemical or haematological screening tests in detecting alcohol-related medical problems.

Adolescent↗

Gastrointestinal histamine after thoracic irradiation in the mouse.

Thoracic irradiation induced duodenal lesions in mice as an indirect effect. We studied the influence of partial thoracic irradiation on endogenous histamine stores in the alimentary canal. Mice subjected to lower mediastinal irradiation had significantly higher (+19%) median gastric histamine, but lower (-44%) distal duodenal histamine than controls. They also had significantly lower proximal (-39%) and distal (-44%) duodenal histamine than mice who received upper mediastinal irradiation. Twenty-three percent of mice after lower mediastinal irradiation had duodenal lesions; these had significantly lower proximal (-30%) and distal (-44%) duodenal histamine than controls. Thus, irradiation to the lower mediastinum induced both duodenal lesions and significant changes in gastric and duodenal histamine stores. Histamine may be involved in the pathogenesis of these lesions.

Animals↗

Basal, sham feed and pentagastrin stimulated gastric acid, pepsin and electrolytes after omeprazole 20 mg and 40 mg daily.

Gastric secretion was measured in nine patients with duodenal ulcer before, and after treatment for four weeks with omeprazole 20 mg or 40 mg daily. Basal acidity and acid output were affected variably by 20 mg, but inhibited totally by 40 mg daily. Sham feed stimulated acid output was reduced by 20 mg daily and completely inhibited by 40 mg daily. Maximal pentagastrin stimulated acid output was halved by 20 mg omeprazole daily and 84% inhibited by 40 mg daily. The reduction in acidity was always greater than the reduction of volume. Pepsin output after pentagastrin was little altered but with the reduced secretory volume pepsin concentrations were increased by both doses. The major cause of reduced aspirate acid output after omeprazole is decreased secretion of the primary acid component of the parietal cell by the proton pump H+K+ ATPase. Duodenogastric alkaline reflux is, however, markedly increased after omeprazole and is an additional factor in the resultant hypoacidity or even anacidity after this drug.

Adult↗

Duodenal pH in health and duodenal ulcer disease: effect of a meal, Coca-Cola, smoking, and cimetidine.

Intraluminal duodenal pH was recorded using a combined miniature electrode and logged digitally every 10 or 20 seconds for five hours (basal/meal/drink) in eight control subjects and 11 patients with duodenal ulcer (five on and off treatment with cimetidine). Over the whole test there were no significant differences in duodenal mean pH or log mean hydrogen ion activity (LMHa) between control subjects and patients with duodenal ulcer, but there were significantly longer periods of duodenal acidification (pH less than 4) and paradoxically more periods of duodenal alkalinisation (pH greater than 6) in the duodenal ulcer group compared with controls. After a meal duodenal mean pH and LMHa fell significantly in both controls and patients with duodenal ulcer, with more periods of duodenal acidification and alkalinisation in the duodenal ulcer group. An exogenous acid load (Coca-Cola) significantly increased the periods of duodenal acidification, and reduced alkalinisation, in both groups. Cimetidine significantly increased mean pH and LMHa and abolished the brief spikes of acidification in four of five patients with duodenal ulcer. Peak acid output (but not basal acid output) was significantly correlated with duodenal mean pH and LMHa but not with the periods of duodenal acidification. Smoking did not affect duodenal pH in either group.

Adult↗

Infusion of a novel peptide, PHI, in man. Pharmacokinetics and effect on gastric secretion.

PHI, infused in man, achieved plateau plasma levels of 297 pmoles/1. The plasma half life was 3.1 min, metabolic clearance rate was 16.4 ml/kg/min and estimated volume of distribution was 73.2 ml/kg. No subjective side effects were noted during the infusion and there was no significant alteration in submaximal pentagastrin stimulated gastric acid or pepsin secretion.

Adult↗

Studies of two novel sulfasalazine analogs, ipsalazide and balsalazide.

Sulfasalazine appears to exert its beneficial effect in colitis by releasing 5-aminosalicylic acid in the colon, but its use can be limited by side effects. Ipsalazide and balsalazide are novel sulfasalazine analogs designed to release 5-aminosalicylic acid and a nontoxic carrier molecule in the gastrointestinal tract. They have a low oral toxicity following single or repeat administration to mouse, rat, and ferret, and balsalazide is not mutagenic in the Ames test. Ipsalazide and balsalazide are split in rat and man, and the urinary and fecal excretion pattern of the 5-aminosalicylic acid released is similar to that of sulfasalazine; the carrier molecules are absorbed to a lesser extent than the sulfapyridine derived from sulfasalazine. These two analogs deserve therapeutic trial.

Aminosalicylic Acids↗

Gastric ulcer healing with ranitidine and cimetidine. A multicentre study.

A single-blind study of 339 patients in 19 centres compared the efficacy and tolerance of ranitidine in treating endoscopically confirmed gastric ulcers. Ranitidine (150 mg twice daily) was compared with cimetidine (1 g daily in divided doses) over 4 weeks, followed by a second 4-week treatment for any patient whose ulcer was not healed. In 292 patients who completed the study, endoscopy showed healing in 69% of patients receiving ranitidine and 59% receiving cimetidine after 4 weeks, and 90% and 88%, respectively, by 8 weeks. These results were not significantly different, and, similarly, healing rates for different ulcer sites did not differ. There were no serious adverse drug reactions during the study. Ranitidine is an effective and safe treatment for healing gastric ulcers, with a tendency to produce a faster healing rate than cimetidine during the first 4 weeks of treatment.

Adolescent↗

Gastric acid regulates the release of plasma secretin in man.

Fasting plasma secretin determined in nine healthy subjects, twelve patients with active duodenal ulcer and four with Zollinger-Ellison syndrome were 3.2 +/- 0.4, 5.1 +/- 1.2 and 20.3 +/- 1.3 pmol/l respectively (mean +/- SEM). Cimetidine significantly (P less than 0.05) reduced levels in those with duodenal ulcer, as did gastric aspiration in the Zollinger-Ellison group. A significant correlation (P less than 0.001) was found between basal acid output and mean fasting plasma secretin. After a solid meal and subsequent liquid soft drink, no sustained mean rise in plasma secretin was observed; changes in secretin appeared to coincide in time with rapid falls in duodenal pH, though little relationship could be established between the absolute level of pH and changes in plasma secretin. The mean peak post-prandial rise in plasma secretin observed after solids was significantly (P less than 0.05) greater in duodenal ulcer patients than controls (9.1 +/- 1.1 versus 6.7 +/- 0.5 pmol/l) as was the mean integrated post-prandial release (1002 +/- 110 versus 710 +/- 67 pmol min-1 1(-1)). Cimetidine reduced both rises (P less than 0.05) and was associated with significantly less duodenal pH readings below 4 (P less than 0.001). These results suggest that gastric acid is a major release mechanism for plasma secretin both fasting and after meals but it is likely the acid load rather than absolute pH in the duodenum which determines circulating levels.

Adult↗