Biomedical subjects
M G Korman
Publications and source records attributed to M G Korman.
Low-dose methotrexate therapy and hepatotoxicity.
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In-vivo anti-reflux and raft properties of alginates.
The comparative efficacy of two alginate-containing anti-reflux preparations (Gaviscon, Algicon) was assessed in a single blind crossover study of 20 patients with gastro-oesophageal reflux disease. The clinical efficacy study was preceded by two studies in healthy volunteers to assess the intragastric effects of Algicon and Gaviscon by pH measurement, endoscopic visualization and gamma scintigraphy. Algicon and Gaviscon were shown to form a raft in the fasting and fed human stomach, with Algicon alone having a potent antacid effect below and within the raft. Both Algicon and Gaviscon liquids significantly reduced the frequency and severity of reflux symptoms from baseline when given at their recommended doses (10 ml and 20 ml four times daily, respectively). There were no significant differences between Algicon and Gaviscon, although 12 patients preferred Algicon (vs 5 for Gaviscon) for control of reflux symptoms. It was concluded that both Algicon and Gaviscon were effective for the symptomatic control of gastro-oesophageal reflux disease.
Helicobacter pylori: fact or fiction?
The recent isolation and classification of the spiral gastric bacteria Helicobacter pylori has led to an explosion of worldwide research. The data strongly suggest that H. pylori is the causative agent for type-B active chronic gastritis. The role of H. pylori in duodenal ulcer awaits clarification, and, more importantly, potential treatment regimens need clear documentation and further detailed research. The past decade has revealed many intriguing facts about H. pylori infection. If, during the 1990s, eradication of H. pylori by means of appropriate and safe medication can lead to the control and prevention of gastroduodenal disease, then major clinical and economic benefits can be anticipated.
Campylobacter pylori--a role in non-ulcer dyspepsia?
Non-ulcer dyspepsia (NUD) is a common complaint in which no systematic illness or organic proximal alimentary tract disease can be identified. The pathophysiology of NUD is probably heterogeneous. Eighty-two subjects with NUD were studied in a prospective randomized placebo-controlled study to assess the efficacy of colloidal bismuth subcitrate (CBS) chewable tablets at a dose of four tablets daily for 1 month. The role of Campylobacter pylori and associated histological gastritis was evaluated. Sixty-one percent of NUD patients had C. pylori in the gastric antrum compared with 25% of age-matched controls. C. pylori was associated with acute and chronic inflammation (P less than 0.001) in the antrum. C. pylori was cleared in 59% of CBS-treated subjects compared with only 4% placebo (P less than 0.05). Both acute and chronic inflammation improved in subjects cleared of bacteria. Clearance of C. pylori and histological improvement was associated with a significant decrease in symptoms. In C. pylori negative subjects improvement in symptoms occurred in both the placebo and active treatment groups. This study would suggest that C. pylori and associated histological gastritis may play a role in non-ulcer dyspepsia.
Gastric pH and endoscopic appearance after Algicon administration.
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Algicon in the management of gastro-oesophageal reflux.
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Rational choice of drugs for ulcer therapy.
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Drinking and smoking when taking H2-antagonists.
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Mortality in patients with haematemesis and melaena: a prospective study.
In a prospective study of death in 817 patients with haematemesis and melaena admitted on 894 occasions, the protocol included admission of all patients to a defined unit, early endoscopy and resuscitation, and planned management. Over the three consecutive two-year periods of the study mortality significantly decreased from 9% to 2.4%. Although the operative rate remained the same, the operative mortality fell from 16% to 1.6%. The fall in mortality was greatest in patients with bleeding gastric ulcers. These results suggest that prospective studies with a defined policy can influence the mortality in patients with upper gastrointestinal bleeding.
Bleeding duodenal ulcer: reduction in mortality with a planned approach.
In a 6-year prospective study from 1972 to 1978 266 patients were admitted to a haematemesis and melaena unit with bleeding duodenal ulcer. There were 13 deaths, a mortality of 5 per cent. A comparison between the three consecutive 2-year periods of study showed an initial mortality of 6 per cent for the first 4 years falling to 2 per cent for the 93 admissions during the final 2 years of experience. Of the 120 patients treated surgically, 10 died in hospital, giving an operative mortality of 8 per cent. The trend in operative mortality was from 13 per cent for the initial 2-year period to 8 per cent for the second period and to 3 per cent for the final 2 years. The operative rate was consecutively 45, 50 and 34 per cent. There was 1 death in conservatively treated patients during each 2-year period of study. Three types of operation were performed: vagotomy, pyloroplasty and oversewing of the ulcer; Polya gastrectomy; and vagotomy and antrectomy. There was no difference in morbidity and mortality between these operations. At a mean follow-up of 3.1 years, 90 per cent of the patients had a good result from their operation. It is concluded that a prospective system of management with an active policy of early endoscopy, surgery and regular audit reduces the mortality from bleeding duodenal ulcer.
Long-term cimetidine in duodenal ulcer disease.
Forty patients with chronic duodenal ulcer who had healed endoscopically with a 6-week course of cimetidine were randomized double blind to 1 year of either placebo or cimetidine tablets 400 mg bid (20 patients in each group). Patients were seen at monthly intervals, and endoscopy was performed at clinical relapse or on completion of 1 year. One of 20 patients on active cimetidine relapsed clinically and endoscopically at 3 months; 16 of 20 patients on placebo relapsed clinically and endoscopically within 9 months, the majority within 3 months, and 2 were shown to have asymptomatic chronic ulcers at routine 12-month endoscopy. None of the 19 patients on active cimetidine routinely endoscoped at 12 months showed evidence of ulceration. This study confirms a high relapse rate when short-term cimetidine is ceased and indicates that maintenance treatment with cimetidine prevents relapse.
Effects of long-term cimetidine on serum gastrin in duodenal ulcer.
Basal and food-stimulated gastrin were measured in 16 patients with duodenal ulcer before and during long-term maintenance therapy with 400 mg cimetidine twice daily. Basal gastrin (mean +/- SE) rose significantly from 27.5 +/- 3.1 pmol/liter precimetidine to 32.8 +/- 2.1, 37.2 +/- 2.6, and 38.5 +/- 3.3 pmol/liter at 1, 3, and 6 months, respectively. The total integrated gastrin response to a protein meal was 1.67 +/- 0.18 nmol/liter/120 min pre-, and 2.54 +/- 0.35, 3.29 +/- 0.3, and 4.36 +/- 0.4 nmol/liter/120 min at 1, 3, and 6 months, respectively. These increases were significantly higher at each time period. This study has thus demonstrated a progressive increase in both basal and food-stimulated gastrin during cimetidine therapy, and this increase could theoretically lead to an increase in gastric acid secretion following cessation of cimetidine.
The Mallory-Weiss lesion as a cause of upper gastrointestinal bleeding.
A prospective study of patients with upper gastrointestinal bleeding admitted to a haematemesis and melaena unit has revealed an incidence of Mallory-Weiss tears of 8% (59 of 762 patients undergoing endoscopy). Prior vomiting was present in 60% and an associated upper gastrointestinal lesion in 44 percent. The majority of patients had a recent ingestion of alcohol and/or analgesics, whilst 34% had chronic heavy alcohol intake. Approximately 50% of patients required no blood transfusion, while 37% had over three units of blood. No patient in the group required surgical intervention, and one patient died because of general debility. This study suggests that the Mallory-Weiss tear accounts for a significant proportion of patients admitted with upper gastrointestinal bleeding, but that the mortality and morbidity are low.
The protective effect of cimetidine on stress-induced acute gastric ulceration in the rat.
The effect of intraperitoneal cimetidine, an H2 receptorantagonist, has been assessed on the development of cold-restraint induced acute gastric ulcers in rats. Cimetidine in doses ranging from 20-100 mg per kg body weight significantly reduced the incidence of acute gastric ulceration compared with saline controls in this model. The protective effect of cimetidine suggests a prophylactic role for this agent in stress-induced gastric or duodenal ulceration in man.
The effect of cimetidine on gastrin release in ulcer disease.
The effect of a single dose of 400 mg of the H2-receptor antagonist cimetidine on protein meal stimulated immunoreactive gastrin was assessed in ten patients with gastric ulcer and ten patients with duodenal ulcer. In gastric ulcer patients, serum gastrin (mean +/- SE) rose from 34 +/- 2.2 pmol.l-1 to a peak of 80 +/- 5.0 pmol.l-1 at 45 minutes without and from 36 +/- 2.2 to 107 +/- 8.0 pmol.l-1 at 60 minutes with cimetidine; in duodenal ulcer it rose from 26 +/- 3.0 to 47 +/- 5.1 pmol.l-1 at 45 minutes without and 26 +/- 3.2 to 52 +/- 5.1 pmol.l-1 at 60 minutes with cimetidine. Integrated gastrin responses in gastric ulcer were 4900 +/- 800 pmol.l-1 120 minutes without and 7000 +/- 900 pmol.l-1 120 minutes with cimetidine and 1560 +/- 300 pmol.l-1 120 minutes without and 2620 +/- 400 pmol.l-1 120 minutes with cimetidine in duodenal ulcer patients. These gastrin increases after cimetidine are comparable to those achieved with continuous intragastric neutralisation with alkali.
Serum gastrin after 12 months' continuous cimetidine therapy for duodenal ulcer.
Serum immunoreactive gastrin was measured in 14 patients with duodenal ulcer before and during a 12-month course of cimetidine 400 mg bd. All patients were symptomatically well during the cimetidine therapy and both basal gastrin and that in response to a protein rich meal were assessed before, at six months and at 12 months during therapy. The basal and post-prandial gastrin were significantly higher at six and 12 months on cimetidine than before cimetidine but the six and 12 month levels were similar. This study thus shows that the progressive increase in serum gastrin during six months of continuous cimetidine therapy does not occur beyond this time period.
Long-term cimetidine does not alter serum prolactin.
The effect of repeated cimetidine ingestion on serum prolactin values was studied prospectively in 17 men with proven duodenal ulcers. These patients received 400 mg of cimetidine twice daily for 12 weeks but showed no alteration in their mean serum prolactin levels. Cimetidine-induced hyperprolactinaemia is not the explanation for the development of gynaecomastia in men exposed to this drug.