Biomedical subjects
E Schrumpf
Publications and source records attributed to E Schrumpf.
[Natural products can be hazardous to health].
Side effects of herbal and health food products have been infrequently reported such as hepatic damage after use of such products. Four such patients were treated in our department in the course of two years. In all four patients, the use of herbal remedies was the probable cause of serious hepatic damage, but both etiology and pathogenesis were difficult to establish. Two major areas of concern are inaccurate formulation and contaminated preparations. As long as no therapeutic effect can be demonstrated from this type of medicine, serious side effects are unacceptable. A critical attitude should be adopted towards these medicines and the use of them.
[Spontaneous bacterial peritonitis].
We describe five patients with spontaneous bacterial peritonitis. The condition is reported more frequently than before and survival has improved. Important clinical features are increasing ascites and unexpected derangement of liver function. Possible predisposing factors, as well as diagnostic and therapeutic measures, are discussed. We emphasize the significance of ascitic polymorph nuclear cell count and bedside inoculation of ascites on blood culture medium, and stress the importance of prompt antibiotic therapy. The choice of empiric antimicrobial treatment is based on the reported frequency of causative agent and toxicity to drugs. Our experience so far indicates that cefotaxime administered as monotherapy is safe and efficient in these patients. Aminoglycosides should be avoided because of increased nephrotoxicity in patients with liver failure.
Antineutrophil cytoplasmic antibodies in primary sclerosing cholangitis, ulcerative colitis, and autoimmune diseases.
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[Peptide-producing neoplasms in the gastrointestinal tract].
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Malignancy in colonoscopically removed polyps.
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Serum concentration of trimipramine (Surmontil) and gastric secretion of acid and pepsin following peroral administration of the drug in healthy humans.
Previous blind studies have shown an increased rate of healing of both duodenal and gastric ulcers following 4 weeks peroral administration of 50 mg trimipramine. The present study shows the effect of 50 mg trimipramine perorally on gastric secretion in relation to that of 25 mg of the drug and placebo. At regular intervals blood specimens were obtained for determination of the serum concentration of trimipramine. In 9 healthy young students it was found that the estimated stabilized values of volume and acid output following 50 mg trimipramine, 33 ml and 3.9 mmol/15 min, respectively, were significantly lower than those following the smallest dose, 37 ml and 4.6 mmol/15 min, respectively. On the other hand, no significant changes of gastric secretion were observed following the peroral administration of 25 mg trimipramine when compared to placebo. Following 50 mg trimipramine the output of pepsin was reduced by about 25%. The values of serum concentration of trimipramine were about 200 nmol/1 at 100 min after administration of 50 mg trimipramine and decreased gradually, whereas the values following the smaller dose were about half of those after the larger one. The results indicate that about 50 mg trimipramine is needed for obtaining a reduction of gastric secretions. Future studies may show whether 25 mg trimipramine, which does not suppress acid secretion when given perorally, is able to promote peptic ulcer healing.
The inhibitory action of somatostatin on the stomach.
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A small dose of somatostatin inhibits the pentagastrin stimulated gastric secretion of acid, pepsin and intrinsic factor in man.
The effect of a small dose of somatostatin (0.05 mg/h) on the gastric secretion of acid, pepsin and Intrinsic Factor (IF) after stepwise increases in the dose of pentagastrin was examined in six healthy volunteers. The gastric secretion of acid, pepsin and IF in response to pentagastrin was significantly reduced by a continuous infusion of somatostatin. The pattern of inhibition indicates that somatostatin is a competitive inhibitor of pentagastrin in the stimulation of gastric secretion of both acid, pepsin and IF. This finding supports the hypothesis of a direct effect of somatostatin on the exocrine secretory cells of the stomach.
Somatostatin inhibits gastric motility in response to distention.
Gastric motility and plasma gastrin concentration have been measured in 6 healthy volunteers before and after stepwise gastric distention. Distention was performed by filling a flaccid thin-walled bag, which was connected with a low pressure transducer for measuring intragastric pressure variations. Stepwise increase in gastric volume from 0-600 ml caused graded increases in gastric motility. No significant change was seen in the plasma gastrin level. When gastric distention was performed concomitantly with constant infusion of somatostatin (0.05 mg/h and 0.50 mg/h) in the same individuals on different days, motility was significantly reduced, without any changes in the plasma gastrin concentration. It is concluded that somatostatin, which probably plays a role in the gastro-intestinal tract, may have a physiological effect in the regulation of gastric motility too. This motility effect of somatostatin seems to be independent of any effect on the gastrin concentration.
Comparison of juice obtained during duodenal aspiration and cannulation of the main pancreatic duct after stimulation with exogenous secretin in man.
The exocrine pancreatic secretion obtained by endoscopic cannulation was compared with that obtained by a conventional duodenal tube after exogenous secretin. The flow rate, bicarbonate output, and amylase output in response to secretin was larger during duodenal aspiration than when collecting during endoscopic cannulation. The majority of samples collected from the duodenum contained bile, whereas those from the pancreatic duct were, with few exceptions, colourless. In all patients the bicarbonate concentration was lower in the duodenal aspirate than in the pancreatic juice. In 5 of the 7 patients, however, the concentration of amylase was higher in the duodenal aspirate than in juice collected by endoscopic cannulation. In these patients the quantitative difference found could not therefore solely be explained by non-quantitative collection of juice from the pancreatic duct and/or contamination of bile, intestinal juice, and gastric juice in the duodenum. Augmentation of the response to secretin by the presence of bile and pancreatic juice in the duodenum and inhibition by the endoscopic cannulation of the pancreatic duct are discussed as alternative explanations.
The effect of TRIMIPRAMINE (Surmontil) on the stimulated gastric secretion and serum gastrin concentration in healthy students.
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Mucosal changes in the gastric stump 20-25 years after partial gastrectomy.
Out of 421 patients who had partial gastrectomy 20-25 years ago for gastric or duodenal ulcer, 108 were examined by endoscopy with multiple biopsy. In no case were the endoscopic appearances of the mucosae interpreted as malignant, though in 2 patients the clinical history suggest malignant disease. Histological examination revealed infiltrating carcinoma in 4 patients, 3 of whom had intramucosal carcinoma only. 3 further patients had severe dysplasia (carcinoma-in-situ). Only 1 patient had a near-normal mucosa close to the anastomosis; in the remainder the gastric remnant showed various degress of dysplasia, metaplasia, or chronic atrophic gastritis. In the patients with carcinoma only 28 (12%) of the 226 biopsy specimens revealed the malignant lesion. Patients who have had partial gastrectomy for benign lesions are at high risk of gastric-stump carcinoma. If, 20 years after operation, they have an endoscopy with multiple biopsy, stump carcinoma may be detected early when the prognosis after operation is probably good.
[Current diagnostic possibilities in pancreatic diseases].
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Secretion of calcitonin and gastrin in rats with transplanted medullary thyroid carcinoma.
Rats transplanted with medullary thyroid carcinoma (MCT) were followed with radio-immuno assay of serum calcitonin (iCT) using antisera to human CT and I125 labelled calcitonin-M. From the 4th month after transplantation, serum from the tumour rats contained iCT in concentrations 8-10 fold higher than serum from the control rats. The tumour cells had retained their ability to react on pentagastrin and calcium injections with increased CT release. It was further shown that the tumour bearing rats had elevated basal gastrin concentratkons in serum. While calcium injection lead to a rise in the serum gastrin concentration in the control group, the adverse effect was seen in the tumour bearing rats. The morphological features and the responsiveness of the rat tumour cells to physiological secretagogues make this tumour a suitable animal model for the study of interactions between CT and gastro-intestinal factors. It is suggested that the gastrin response to calcium might be of interest also in the diagnosis of human MCT.
The effect of somatostatin on pentagastrin-stimulated gastric secretion and on plasma gastrin in man.
Three experiments were carried out in each of 6 healthy students on separate days, in a randomized order. Intravenous saline infusions were given for one hour basally in each experiment. During the second hour either pentagastrin, pentagastrin and somatostatin, or somatostatin alone were given. Gastric juice was collected continuously during all experiments. Somatostatin decreased the volume of gastric secretion and the concentrations of acid and pepsin, and output of acid, pepsin, and intrinsic factor (IF). The plasma gastrin concentration was not changed by somatostatin. A rebound effect was seen on pepsin and IF outputs after cessation of somatostatin, and on blood sugar concentration. The present study suggests that somatostatin acts on gastric secretion either directly or by mechanisms other than by inhibition of gastrin. The rebound of pepsin and IF indicates a release-inhibiting action on these substances similar to the effect of somatostatin on the release of some hormones.
Plasma gastrin and gastric secretory response to duodenal perfusion with liver extract in healthy human subjects.
The stomachs of 8 healthy volunteers were intubated with a Levine tube under radiological control. In addition, a thin polyethylene tube was placed in the proximal duodenum. After a 1-hour period with no perfusion, the duodenum was perfused for two hours with 15% liver extract (LE) (pH 4.5--5.5; 1027 mosm/kg water) at a rate of 100 ml/hour either alone or in combination with intravenous infusion of different doses of exogenous pentagastrin. All subjects were also tested with the tubes in place for 3 hours, but with no perfusion or pentagastrin. Reflux to the stomach was monitored by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin were measured in 15-minute periods. During perfusion of the proximal duodenum, where reflux of the perfusates was less than 4%, only a slight and inconstant change in plasma gastrin was seen. Gastric acid and pepsin outputs were increased to approx. 18% and 25% of the maximal pentagastrin stimulation respectively. Whereas 15% LE was shown to release gastrin by antral perfusion however, such release was not found by duodenal perfusion, except where reflux to the antrum was seen. The results suggest that intestinal stimulation of gastric secretion exists, but has not been found to be gastrin dependent in the present investigation.
The effect of trimipramine (Surmontil) on gastric secretion and the serum gastrin release in healthy young students.
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