John Christiansen

Placebo-controlled trial with the somatostatin analogue SMS 201-995 in peptic ulcer bleeding

A 5-day, double-blind, placebo-controlled, multicenter trial in 23 centers with a total of 273 patients [241 evaluable patients; 126 on placebo and 115 on a long-acting somatostatin analogue (SMS 201-995, octreotide, Sandostatin)] resulted in no difference in stopping bleeding and preventing rebleeding between placebo (70.6%) and SMS 201-995 (69.6%). Surgery rates, blood transfusion requirements, and time required before bleeding stopped were also not significantly different between the two groups. A retrospective subgroup analysis according to age, sex, localization of the ulcers, severity of the bleeding, and arterial spurting vs. oozing showed homogeneity and did not allow identification of a subgroup that might benefit from treatment with SMS 201-995. The tolerability of SMS 201-995 was very good. No difference was found between placebo and SMS 201-995 with regard to the side-effect profile.

The N-terminal tridecapeptide fragment of gastrin-17 inhibits gastric acid secretion.

After a meal the serum concentrations of the N-terminal tridecapeptide-like fragment of gastrin-17, (1-13)G-17, increased markedly in patients with active duodenal ulcer, but less so in healthy subjects. Consequently the synthetic (1-13)G-17 was infused intravenously in doses that resulted in concentrations similar to those measured in duodenal ulcer patients in order to examine whether the N-terminal fragment influences gastric acid secretion. Doses of 125 and 400 pmol (1-13)G-17/kg per h inhibited the meal-stimulated acid secretion by 36% (P less than 0.05) and 66% (P less than 0.05) respectively. The release of endogenous C-terminal gastrin immunoreactivity was not influenced. The infusion of (1-13)G-17 also inhibited the acid response to exogenous gastrin-34, gastrin-17 and Peptavlon, but not to gastrin-4. The results suggest that the N-terminal gastrin-17 fragment--although devoid of the hitherto considered only active site of gastrin--plays a significant role in the regulation of the gastric acid secretion in patients with active duodenal ulcer.

Complete prolapse of the rectum treated by modified orr operation

During a 25-year period 24 patients were treated for complete rectal prolapse with a modification of the operation described by Orr in 1947. After a median follow-up of five years two recurrences occurred (8 per cent). Of 11 patients who were incontinent for fluid feces or flatus preoperatively, five gained continence after the operation. An actuarial analysis of the data revealed a cure rate after five years of 91 per cent (95 per cent confidence limits: 76–100 per cent).

Fat and Gastric Acid Secretion

To evaluate the importance of the terminal carboxyl group of the oleic acid molecule in the inhibition of gastric acid secretion, 6 normal persons were stimulated twice with duodenal perfusates containing either 20 mM oleic acid or 20 mM oleyl alcohol. Oleic acid significantly inhibited the gastric acid secretion stimulated by pentagastrin (100 ng/kg/h) and increased the levels of secretin in plasma. The effect of oleyl alcohol was insignificant. It is concluded that the carboxyl group of the fat molecule has an important role in the inhibition of gastric acid secretion, and the effect could in part be attributable to the release of secretin into plasma.

Surgical Treatment of Severe Constipation

Severe constipation may be treated surgically provided precise evaluation of colon-transit-time and rectal evacuation can be performed. Colon-transit-time may be studied by straight X-ray of the abdomen after oral intake of small plastic markers, and rectal evacuation may be evaluated by defecography. In patients, where Hirschsprungs disease with a short aganglionic segment is suspected, ano-rectal manometry with evaluation of the recto-anal reflex must be performed. Furthermore, electromyography of the external anal sphincter and puborectal muscle during simulated defecation will be necessary in order to evaluate whether obstructed defecation is due to a spastic condition in the anal sphincter or pelvic floor muscles (anismus). Surgical treatment of obstructed defecation depends on the specific pathology, while treatment of slow transit constipation is subtotal colectomy and ileo-rectal anastomosis. In patients, where constipation is based on a combination of obstructed defecation and prolonged colon-transit-time, surgery for obstructed defecation should be carried out first. In patients, where the constipation is due to prolonged colon-transit-time and an adynamic rectum (rectal inertia) without anatomical abnormalities the only possibility of surgical treatment is total colectomy with an ileo-anal pouch.