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Biomedical subjects

J H Baron

Publications and source records attributed to J H Baron.

At least 19 recordsLinked to original sources
PubMed1992

Improved maintenance of remission in ulcerative colitis by balsalazide 4 g/day compared with 2 g/day.

The efficacy of two doses of balsalazide for the maintenance of remission in patients with ulcerative colitis was compared in a double-blind multicentre trial. Sixty-five patients received a 2 g daily dose, and 68 a 4 g dose. The patient groups were similar at entry for sex, age, and disease distribution. Clinical assessment was carried out at 3-monthly intervals, with sigmoidoscopy, rectal biopsy, and blood tests on entry and at 26 and 52 weeks. Clinical relapse over twelve months was significantly less common on the 4 g dose (36%), than on the 2 g dose (55%), P less than 0.01. There were eight withdrawals on 2 g daily and 13 on 4 g daily, six and nine respectively being mainly due to gastrointestinal intolerance. It is concluded that balsalazide is a well-tolerated drug, and is effective for the maintenance of remission in patients with ulcerative colitis, the optimal dose being greater than 2 g daily.

Adult↗
PubMed1992

Duodenal ulcer: a model of impaired mucosal defence.

There is a new model of chronic duodenal ulcer in which the ulcer is generated by irradiating the lower mediastinum of mice with a single dose of 18 Gy 250 kV x rays. Single ulcers develop in the proximal duodenum of about half the animals. Previous studies have shown a remarkable morphological and behavioural similarity to duodenal ulcer in man. Ulceration occurs because of an imbalance between aggressive and defensive forces within the duodenum and an attempt has been made to elucidate the pathomechanism of this ulcer by determining acid and pepsin secretion. The basal and pentagastrin stimulated secretion of acid, pepsin, and histamine were measured and no changes in acid or pepsin secretion were shown to occur (risk of type II error < 1%). It is therefore concluded that this chronic ulcer is a model of impaired duodenal defence.

Animals↗
PubMed1991

One week eradication regimen for Helicobacter pylori.

Although Helicobacter pylori is both a frequent cause of gastritis and an important factor in duodenal ulcer recurrence, no treatment regimen exists that is completely safe and effective. We have studied a short eradication regimen of tripotassium dicitrato bismuthate 120 mg four times daily and amoxycillin 500 mg four times daily for seven days with metronidazole 400 mg five times daily for three days (days 5-7). 106 patients with peptic ulceration and non-ulcer dyspepsia, who were also infected with H pylori, were entered into the study. H pylori was successfully eradicated in 76/106 (72%) patients (median follow-up 9.3 months). The rate of eradication was higher among patients with metronidazole-sensitive H pylori (40/43, 93%). In 17/30 patients in whom eradication failed, pretreatment metronidazole-resistant strains were subsequently isolated. Side-effects were mild, the commonest (24/106, 24%) being taste disturbance with metronidazole. A one-week eradication regimen is a safe, effective, cheap, and well-tolerated treatment for metronidazole-sensitive H pylori.

Adolescent↗
PubMed1991

Acid blockade by omeprazole or ICI 162846 in a chronic duodenal ulcer model.

Oral treatment with the H2-antagonist ICI 162,846 or omeprazole for five days inhibited both basal and pentagastrin stimulated acid secretion by 50% or more in mice. Either treatment increased the luminal secretion of histamine in the basal (12-fold) and stimulated (9-fold) states. Mice treated with the H2-antagonist had a 27% reduction (p less than 0.05) in mural histamine in the acid-producing area of the stomach. Mice were treated so as to induce duodenal ulcers (abscopal model) and were then treated with the H2-antagonist ICI 162,846, omeprazole or vehicle, orally for one week. Fewer duodenal ulcers were found in animals receiving drug treatments than in the oral vehicle group. Both the H2-receptor antagonist and the proton pump blocker inhibit acid production; acid blockade by either drug is accompanied by a massive increase in secretion of histamine. This rise was associated with depletion of the gastric histamine store only with H2-receptor blocker. Both means of acid inhibition reduce the formation of ulcers in this model.

Adenosine Triphosphatases↗
PubMed1991

Gastric output of pancreatic secretory trypsin inhibitor is increased by misoprostol.

Pancreatic secretory trypsin inhibitor (PSTI) is a potent protease inhibitor that also has growth promoting activity. It has recently been identified in the foveolar cells of the stomach, which secrete mucus. We examined the effects of the prostaglandin E1 analogue misoprostol on gastric PSTI output. Seven normal volunteers took part. An initial period of gastric aspiration was followed by four 40 minute periods of gastric perfusion at 5 ml/minute of: 0.14 mol/l saline, 0.17 mmol/l bicarbonate, bicarbonate with misoprostol 400 micrograms, and then bicarbonate again. All perfusates contained polyethylene glycol 4000 as a marker. Misoprostol increased median gastric secretion of PSTI from 11 to 33 micrograms/hour (p less than 0.05), producing concentrations in gastric juice six times higher than those found in jejunal juice and about 1/30 of the values seen in pancreatic juice. Median mucus secretion increased to a lesser extent from 29 to 38 mg/hour during misoprostol. There was no change in intragastric concentrations of protein or of epidermal growth factor during infusion of misoprostol. Infusion of pentagastrin (6 micrograms/kg/hour) had no effect on gastric secretion of mucus, PSTI, or protein. Human gastric mucus was degraded on incubation with trypsin in vitro and this was prevented by the addition of PSTI. These results suggest that gastric PSTI may protect the gastric mucus layer against refluxed pancreatic proteases. Increased output of PSTI during microprostol may contribute to the protective effect of this drug.

Adult↗
PubMed1991

Simplified single sample 13Carbon urea breath test for Helicobacter pylori: comparison with histology, culture, and ELISA serology.

There is no ideal method for detecting Helicobacter pylori. The 'standard' 13Carbon urea breath test (13C-UBT), which involves collecting eight to 15 breath samples and subsequent costly analysis, was modified by pooling 21 samples of expired breath taken at five minute intervals for 40 minutes into a collecting bag, from which a single 20 ml aliquot was taken and analysed by mass spectrometry. This test was evaluated on 50 patients after routine upper gastrointestinal endoscopy, and results were compared with those from the standard 13C-UBT, bacteriology, ELISA serology, and histology--the latter being taken as the gold standard. H pylori were seen in 34 of 50 (68%) patients (in three it was detected in biopsy specimens from the corpus alone). The modified 13C-UBT was positive (pooled excretion delta 13CO2 greater than 5 per mil) in 31 patients and negative in 19 (three false negative results), specificity was 100% (standard 13C-UBT 94%) and sensitivity 92% (standard 13C-UBT 93%). The modified 13C-UBT had a coefficient of variation within subjects of 3.7%. For the ELISA serology and culture the specificities were both 100%, but the sensitivities were 82% and 68% respectively. The 13C-UBT results correlated with the grade of histological gastritis. The modified 13C-UBT is simpler, cheaper, more reproducible, and provides an easy non-invasive method for the detection of H pylori.

Adult↗
PubMed1991

Breakdown of gastric mucus in presence of Helicobacter pylori.

The potential of Helicobacter pylori to degrade gastric mucus was examined. Colonies of H pylori cultured from antral mucosal biopsy specimens of patients with non-autoimmune gastritis were washed with sterile saline, passed through a sterilisation filter, and the filtrate examined for urease, protease, and mucolytic activity. The filtrate failed to hydrolyse bovine serum albumin, or to degrade stable mucus glycoprotein structures of high particle weight that had been separated from human gastric mucus on Sepharose 2B. The high particle weight mucus glycoprotein was, however, extensively degraded when incubated with H pylori filtrate (which possessed urease activity) in the presence of 2 M urea, to release fragments of Mr approximately 2 X 10(6). The high particle weight mucus glycoprotein was also broken down to a comparable extent when incubated with Jack bean urease in the presence of 2 M urea, or 1 M ammonium carbonate, or 40 mM carbonate-bicarbonate buffer (pH 8.7), but not when treated with 4 M urea alone, or Jack bean urease alone. These results indicate that the loss of high particle weight mucus glycoprotein in gastric mucus from patients with gastritis and gastric ulcers is unlikely to be due to the mucolytic action of an extra-cellular protease produced by H pylori, but it may result from the destabilising effects of a carbonate-bicarbonate buffer, generated at the mucosal surface when H pylori urease hydrolyses transuded plasma urea.

Chromatography, Gel↗
PubMed1991

Why do hospital doctors wear white coats?

Seventy-two per cent of all hospital doctors and medical students wear white coats and most wear them greater than 75% of the time. White coats are worn chiefly for easy recognition by colleagues and patients, to put items in the pockets and to keep clothes clean. Psychiatrists and paediatricians try to maximize rapport with patients by deliberately not wearing white coats.

Attitude of Health Personnel↗