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Biomedical subjects

R Stockbrügger

Publications and source records attributed to R Stockbrügger.

50 records · Page 3Linked to original sources
PubMed1979

Inhibition of gastric acid secretion by pirenzepine (LS 519) in man.

Pirenzepine is a new tricyclic drug used in the treatment of peptic ulcer disease. The effect of two doses of pirenzepine (25 mg twice daily and 50 mg thrice daily) was examined in ten healthy volunteers during basal acid secretion and under stimulation with two doses of pentagastrin (0.166 microgram/kg . h and 1 microgram/kg.h given as continuous intravenous infusion). Serum drug concentrations were determined by radioimmunoassay, and parallel studies of the salivary function were performed. Pirenzepine, 25 mg twice daily, reduced basal acid output by 50% and 55%, respectively, and inhibited stimulated acid output by 31% and 26%, respectively. The higher dose of pirenzepine, 50 mg thrice daily, augmented the effect insignificantly despite markedly increased serum drug levels. The recommended therapeutic dose of 25 mg twice daily gave no salivary inhibition. Pirenzepine may have an anticholinergic effect on the parietal cell, although systemic side effects were not seen. Pirenzepine does not competitively inhibit pentagastrin-stimulated acid secretion.

Adult↗
PubMed1979

The effect of pirenzepine on basal, pentagastrin- and insulin-stimulated gastric acid secretion in patients with peptic ulcer disease.

The effect of pirenzepine on basal and stimulated acid secretion was tested in five patients with peptic ulcer disease and gastric hypersecretion. Two types of stimulation were compared, namely pentagastrin by intravenous infusion (1 microgram/kg/h) and hypoglycaemia induced by insulin given subcutaneously (0.125 IU/kg). Basal acid output/30 min was reduced by 44% and 69%, respectively. Pentagastrin-stimulated acid output was reduced by 30%/120 min, and insulin-stimulated acid output by 47%. The reduction was similar during the first and second hour of stimulation in both series. These results strengthen our previous impression that pirenzepine may interfere with cholinergic receptors at the parietal cell level. As the inhibition of gastric acid secretion by pirenzepine is similar to that produced by oral doses of cimetidine, pirenzepine may be useful in the treatment of peptic ulcer disease.

Adult↗
PubMed1978

Clinical results of parietal cell vagotomy and selective vagotomy with pyloroplasty in the treatment of duodenal ulcer. Two-year follow-up of a prospective randomized study.

Fifty patients were randomized in a consecutive series of parietal cell vagotomy (PCV) and selective vagotomy with pyloroplasty (SV +P) in the treatment of duodenal ulcer. There were no operative deaths, and the length of the hospital stay and time off from work were the same in both groups. The clinical results were evaluated at 1 and 2 years after operation. Within the first 3 years there were two recurrences after PCV and three after SV +P. The overall clinical result 2 years after surgery did not significantly differ between the two groups; 16/24 after PCV and 17/23 after SV +P classified as excellent results (Visick I). Significantly fewer patients had dumping after PCV (3/23) than after SV +P (13/22). No patient had diarrhoea postoperatively. It is concluded that parietal cell vagotomy gives less dumping than selective vagotomy with pyloroplasty. It is, however, too early to say whether the overall clinical result in a long-term follow-up favours PCV rather than SV +P.

Adult↗
PubMed1978

Mixed endocrine gastric tumors associated with hypergastrinemia of antral origin.

A patient with atrophic gastritis and excessively raised serum gastrin concentrations (4000 to 5000 pg/ml) was found to have multiple polypous tumors of the gastric corpus mucosa. Following gastrectomy, serum gastrin concentrations decreased to undetectable levels. The tumors consisted of a mixed population of endocrine cells. The majority of tumor cells were of the ECL type, but, in addition, enterochromaffin cells of various subtypes as well as agranular cells were found. The tumors were locally invasive and invaded the walls of submucosal blood vessels. The surrounding mucosa showed a severe atrophic gastritis with intestinalization and contained numerous goblet cells, enterochromaffin cells, and cholecystokinin cells. Cholecystokinin cells do not occur in the normal oxyntic mucosa. Hence, the observation of this cell type in intestinalized gastric epithelium suggests that "intestinalization also is associated with changes in endocrine cell populations. Gastrin has been shown to affect the function of the ECL cells. Indications for a trophic action of gastrin on these cells have been obtained. It is discussed whether greatly raised serum gastrin levels in patients with atrophic gastritis may be associated with increased risks for the development of certain types of gastric tumors.

Diabetes Complications↗
PubMed1978

Development of gastric dysfunction in dermatitis herpetiformis.

In order to study the development of atrophic gastritis, gastric secretory function was examined by a standard pentagastrin test 24 to 78 months after a previous examination (Ex I). The study included 12 patients with dermatitis herpetiformis (DH), 6 patients with functional signs of atrophic gastritis previously, and 8 healthy controls. The surrent examination (Ex II) also included microbiological culture of gastric juice and estimation of gastrin(s), parietal cell and thyroidal antibodies. Most of the controls had increased their maximum acidity and maximum acid output (MAO) between the examinations. This may indicate an altered potency of pentagastrin in recent years. Conversely, 5 of the 6 patients with atrophic gastritis showed a further reduction of maximum acidity and MAO, indicating progressive parietal cell atrophy. In the DH-group, two tendencies were observed: 6/12 patients had an increased MAO at Ex II. They had had lower mean age and higher mean MAO at Ex I, as compared with the remaining 6 patients who had a decreased MAO at Ex II. The latter group more often had parietal cell antibodies.

Adult↗
PubMed1977

Antral gastrin cells and serum gastrin in achlorhydria.

Forty-five patients with achlorhydria due to severe atrophic corpus gastritis or gastric atrophy were studied by determination of serum gastrin, histological examination of multiple biopsy from the antrum, and quantitation of gastrin cells revealed by an indirect immunofluorescence technique. In a reference group of 12 persons with normal gastric secretion and without atrophic antral gastritis the mean number of gastrin cells per field of vision was 52 +/- 6.5 (S.E.M.). In a group of achlorhydric patients having normal antral mucosa (n = 24), the serum gastrin levels was 324 +/- 56 pmol/l and the number of gastrin cells was 79.6 +/- 7.5 cells/field of vision. The corresponding values for a group of achlorhydric patients with chronic superficial antral gastritis (n = 11) were 361 +/- 186 pmol/l and 88.0 +/- 14.4 cells/field of vision. In a group of achlorhydric patients with atrophic antral gastritis (n = 10) serum gastrin was 15.0 +/- 3.3 pmol/l, and the number of gastrin cells was 6.2 +/- 3.3 cells/field of vision. Compared to the subjects in the reference group, the number of gastrin cells was significantly higher in the groups of achlorhydric patients with normal or superficially inflamed antral mucosa and significantly lower in achlorhydric patients with atrophic antral gastritis. It is concluded that serum gastrin in general is a good indicator for the presence or absence of antral atrophic gastritis in achlorhydria.

Achlorhydria↗
PubMed1976

Auto-immune atrophic gastritis in patient with dermatitis herpetiformis.

Seventeen patients with dermatitis herpetiformis were tested for gastric hydrochloric acid secretion. Seven were found to be achlorhydric. Atrophic gastritis in these patients probably had an auto-immune pathogenesis, as judged by elevated serum gastrin level, high prevalence of antibodies against gastric parietal cells and antrum sparing of the gastric atrophy. This type of atrophic gastritis is considered to indicate a precursor state to pernicious anemia.

Adult↗
PubMed1976

Serum gastrin and atrophic gastritis in achlorhydric patients with and without pernicious anemia.

Forty-two patients with pernicious anemia (PA) and 35 patients with achlorhydria but without PA were investigated by means of serum gastrin determination and estimation of circulating parietal cell and thyroidal autoantibodies. In 38 of the 77 patients, gastroscopic and histopathological examinations of the antral and corpus mucosa were performed. The patient groups were similar with regard to distribution of high and normal serum gastrin levels, the frequencey of autoantibodies and antrum-sparing atrophic gastritis. In the present selection of patients, therefore, the achlorhydria group was supposed to represent a precursor state of the group with PA. A minor proportion of patients with severe atrophic gastritis of the antrum as well as of the corpus mucosa was found in the two groups.

Achlorhydria↗
PubMedDate not supplied

Patients with ankylosing spondylitis and healthy relatives do not show increased small intestinal permeability with the lactulose-mannitol test.

Small intestinal permeability was measured in 71 subjects: 26 (24 B27+) patients with ankylosing spondylitis (AS); 20 healthy first degree relatives (13 B27+); 6 patients with active Crohn's disease and 19 healthy controls. We determined the urinary excretion ratio of two ingested sugar probes, lactulose (10 g) and mannitol (0.5 g) by gas-liquid chromatography. The median lactulose/mannitol excretion ratio in AS patients (0.0099) and relatives (0.0090) was not significantly different from the median ratio in healthy controls (0.0095). HLA status or use of NSAIDs did not significantly influence the results. In patients with Crohn's disease, on the other hand, the median lactulose/mannitol ratio (0.021) was significantly increased in comparison to healthy controls (0.0095). Our results confirm that the lactulose-mannitol test can be used to demonstrate increased intestinal permeability in Crohn's disease. For patients with AS and their relatives the lactulose-mannitol test may not be sufficiently sensitive. Alternatively, significantly increased permeability may not occur in most patients with AS.

Adult↗