[Idiopathic hemorrhage of the gastric mucosa requiring total gastrectomy].
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Biomedical subjects
Publications and source records attributed to G Bommelaer.
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From 16 volunteers with chronic pancreatitis and 36 healthy subjects duodenal biopsies were taken 15--20 cm beyond the papilla of Vater. Several morphometric parameters were calculated. The main results show: a significant decrease of villous area and height but not of the number of intestinal villi; a significant increase of Paneth cells; and a slight decrease in the number of glandular mitoses. This study suggests in man, a possible relationship between exocrine pancreatic secretion and the intestinal mucosa and a trophic action of pancreatic juice on the proliferation and the differentiation of the intestinal mucosa.
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Two males subjects are described with hitherto undescribed glucose-6-phosphate dehydrogenase (G6PD) variants. The first is of French ancestry, the second of Sicilian extraction. Each subject suffered from acute hemolytic anemia following ingestion of broad beans (Vicia fava). In both cases the hemolytic crisis occurred in a late period of life (29 and 58 years). No previous hemolytic crisis was recorded. The electrophoretic and kinetic properties of the mutant enzymes examined after purification from the red cells allowed each to be distinguished from other G6PD variants reported until now. The first variant was named Gd(-) Muret, the other Gd(-) Colomiers.
This work describes a new preparation of dog pancreatic acini which were used to study amylase release in response to various secretagogues. Neither secretin nor vasoactive intestinal peptide stimulated amylase release from acini. Caerulein, carbachol and human synthetic gastrin G17 stimulated amylase release with the same efficacy, but with different potencies. Bombesin nonapeptide did not show any evidence of a direct stimulatory effect on amylase release. These species-related peculiarities stress the necessity of using the same species when comparing pancreatic cell behaviour in vivo and in vitro.
Cytological effects of two H2-receptor antagonists on the gastric and duodenal mucosa were studied during therapy of active duodenal ulcer (D.U.) in man. After endoscopic diagnosis (day 0), subjects were treated with cimetidine or ranitidine and re-examined on day 30. Only subjects with healed D.U. on day 30 were retained in this study. Gastric, pyloric and duodenal endoscopic biopsies were taken and treated for further morphometrical analysis both by light and electron microscopy. The use of the immunoperoxidase technique allowed evaluation of G and D cell populations. Kinetic parameters in proliferative zones were measured after in vitro incubation of biopsies with 3H-thymidine. No differences could be seen between the two H2-receptor antagonists. Increase of tubulovesicles and decrease of canaliculi in parietal cells are closely related to the inhibitory effect of these drugs on acid secretion. However secretory capacities of parietal cells are preserved since the whole membrane (tubulovesicle + canaliculi surface) remained constant. The collapsed aspect of the tubulovesicles on day 30 and the presence of connections between the tubulovesicle membrane, with both vesicle and canaliculi membrane, could support the theory of osmotic membrane expansion during parietal cell acid secretion. H2-receptor antagonists have been shown to be trophic in duodenal mucosa: both villi and microvilli area are increased. Confirming these findings, the proliferative compartment in the intestinal crypts was shown to be enlarged. No variation of G cell number could be seen in the antral mucosa; clear intracytoplasmic granules were increased in D.U. on day 0 but were not further modified on day 30. Somatostatin labelling index decreased. These last findings associated with the lack of G cell variations, suggest the presence of a possible paracrine modulation in the gastric and duodenal mucosa.
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This study was undertaken to determine if the cytoprotective effect of prostaglandin and the H2 histamine receptor antagonist cimetidine involves protection against disruption of the gastric mucosal barrier. Groups of anesthetized, vagotomized rats received one of the following parenterally: saline (control), mepyramine--an H1 histamine receptor antagonist, cimetidine, cimetidine and mepyramine, or 16,16 dimethyl prostaglandin E2. Parameters of barrier disruption were then determined before and after exposure of the gastric mucosa to 40mM acetylsalicylic acid. At the end of the study, gastric lesions were scored according to size and number. Lesion score and fall in potential difference were significantly lower in rats receiving cimetidine, cimetidine and mepyramine, and prostaglandin. Other parameters of barrier disruption--H+ back diffusion, Na+ and K+ influx, and protein outpouring--exhibited the same pattern and correlated with change in potential difference. We conclude that both prostaglandin and cimetidine, but not mepyramine, protect against barrier disruption by topical aspirin, and this may be a factor in the mechanism of their cytoprotective action.
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The effect of somatostatin on the pancreatic exocrine response to different doses of exogenous stimuli and the somatostatin dose-response relationships on pancreatic secretion were studied in conscious dogs. Somatostatin caused a strong inhibition of basal or slightly stimulated pancreatic secretion but failed to inhibit the maximal responses, suggesting that somatostatin interacts with secretin or caerulein by a competitive mechanism. A higher maximal percentage of inhibition and a dose-response relationship was observed with protein outputs and enzyme concentrations. Volumes and bicarbonate outputs were also inhibited but the maximal percentage of inhibition was lower.
Polycystic liver disease, which is generally part of the autosomal dominant polycystic kidney disease, is often asymptomatic. We report a case of obstructive jaundice caused by compression of the biliary tract by a large haemorrhagic liver cyst. The patient was a man with sporadic polycystic liver disease without polycystic kidney disease and with normal renal function for his age. Ultrasound combined with cholangio-MRI provided non-invasive confirmation of intracystic bleeding and intrahepatic biliary dilatation. Obstructive jaundice was confirmed by cyst puncture-aspiration which resolved symptoms and normalized biology. The initial treatment of haemorrhagic liver cyst complicating polycystic liver disease must be medical with cyst aspiration-drainage and sclerotherapy to avoid surgery in these fragile patients.
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