PubMed Health⌕ Search

Biomedical subjects

G J Milton-Thompson

Publications and source records attributed to G J Milton-Thompson.

18 recordsLinked to original sources
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↗
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↗
PubMed1976

Healing of gastric ulcer during treatment with cimetidine.

10 patients with benign gastric ulcer were treated with cimetidine 0-8 to 1-6 g/day for six weeks. Relief of symptoms was rapid. Endoscopy at the end of treatment showed that all the ulcers had healed. Healing was not associated with an improvement of acute atrophic gastritis nor with any change of gastric mucosal potential difference. No untoward clinical or laboratory effects were observed.

Adult↗
PubMed1976

Effect of cimetidine on 24-hour intragastric acidity in normal subjects.

The effect of H2-receptor blockade on intragastric acidity was studied in nine normal males. The pH of their gastric contents was measured at hourly daytime and two hourly nighttime intervals for 48 hours. The subjects ate identical meals, drank identical volumes of fluid, and smoked the same number of cigarettes during the two study days. Their physical activity was unrestricted in a ward environment. Blood cimetidine and plasma gastrin were measured in serial blood samples. The nine subjects were treated in random sequence with cimetidine 0-8-1-0 g on one day and placebo capsules on the other. The drug was given in four divided doses: four subjects received it before, and five after, the three main meals. All took the fourth dose at bedtime. Replicate studies in an additional subject given placebo on both study days showed good reproducibility (r=0-80, P less than 0-01). Cimetidine therapy decreased intragastric acidity in all nine subjects. The decrease was similar in the two groups taking the drug before or after meals, mean 24 h intragastric hydrogen ion activity being lowered by 70 and 72% respectively. Nocturnal anacidity was recorded in only two of 45 samples. Administration of cimetidine before meals produced earlier and higher drug blood levels than post-prandial medication, but when it was taken after food the blood levels were highest at the time when the buffer capacity of the food was waning. Blood concentrations of cimetidine exceeded the secretory IC50 level for most of the time between doses. The results show that cimetidine 0-8-1-0 g/day in four divided doses produces a striking and consistent decrease of intragastric acidity. Although variation in the timing of the dose in relation to meals did not affect the decrease of acidity, the absorption data suggest that patients should take the drug after meals.

Adult↗
PubMed1976

Inhibition of food-stimulated gastric acid secretion by cimetidine.

The effect of cimetidine, a new histamine H2-receptor antagonist, on gastric acid secretion stimulated by a homogenised meal was studied in six normal volunteers using an in vivo intragastric titration technique. The subjects were studied twice, no more than 48 h apart, receiving either cimetidine 200 mg or placebo in random order. Cimetidine administered either 32 men before (three subjects) or with the meal (three subjects) significantly inhibited gastric acid secretion in all the subjects throughout the period of study; 96 min after food, total acid secretion decreased by 67 and 57% respectively. When the drug was taken with the meal absorption was slower (mean peak blood level 2-34 mumol/l, 80-128 min after dosing) than when administered on an empty stomach (mean peak blood level 5-08 mumol/l, 48-64 min after dosing). Blood cimetidine concentration correlated significantly (P less than 0-01) with percentage inhibition of acid output and the calculated concentration resulting in 50% inhibition of gastric acid secretion (IC50) was 1-6 mumol/l. Secretion of gastrin in response to food was unaffected by cimetidine. The results suggest that 200 mg cimetidine effectively inhibits food-stimulated acid secretion and that the bioavailability of the drug may be affected by the timing of dosage in relation to meals. No unwanted effect were observed.

Administration, Oral↗
PubMed1975

24-hour control of intragastric acidity by cimetidine in duodenal-ulcer patients.

The effects of two dose regimens of cimetidine on 24 h intragastric acidity were investigated in six patients with duodenal ulcer. They received placebo capsules on the first day and cimetidine on the second day. Cimetidine 0-8 g/day decreased 24 h mean H+ activity by 55% but 1-6 g/day decreased it by 67%, the difference being due to a greater nocturnal decrease in the high-dose group. Intragastric pH remained below 2-0 for much of the treatment day but similar values were found in four post-vagotomy patients. Cimetidine 0-8-1-6 g/day results in a decrease of intragastric acidity that is compatible with successful medical treatment of duodenal ulceration.

Circadian Rhythm↗
PubMed1975

Relief of duodenal ulcer sysmptons by oral metiamide.

Thirty patients with symptoms of duodenal ulceration were treated for five to eight weeks in a double-blind trial with either metiamide 1 g daily by mouth or a placebo. In the 15 patients receiving metiamide there were significant reductions in nocturnal pain and antacid consumption. Daytime pain was diminished. The results suggest that histamine H2-receptor antagonists are likely to be useful in the medical management of the symptoms of duodenal ulceration.

Administration, Oral↗
PubMed1975

Colonic and small intestinal response to intravenous prostaglandin F2 alpha and E2 in man.

The effects of intravenous infusions of prostaglandins (PGs) F2 alpha(0-4 or 0-8 mug kg-1 min-1) or E2 (0-08 or 0-1 mug kg-1 min equals1) on net colonic movement of water and electrolytes and on ileal flow were measured in eight healthy males by simultaneous ileal and colonic perfusion. Ileal flow was increased by PGF2 alpha (six subjects) from a mean of 1-69 ml min-1 to 4-63 ml min-1 (P smaller than 0-01); it also increased in the two subjects given PGE2. Colonic absorptive function was not significantly diminished by either prostaglandin. These results suggest that diarrhoea due to prostaglandins originates in the small intestine.

Adult↗