Acta hepato-gastroenterologica最新文献

The in vitro fixation of bacterial lipopolysaccharide (LPS) on the plasma membrane of mechanically or enzymatically isolated hepatocytes from rabbits was studied by immunofluorescence technique. Antisera against LPS from E. coli 026:B6 and 0111:B4 were induced in rabbits. Antibody titers up to 1:1024 were determined by the passive hemagglutination test. There was no immunologic cross reactivity between the two antisera. IgG and IgM were prepared from anti-LPS as well as from normal rabbit serum and conjugated with fluorescein-isothiocyanate. The antibody activity against LPS was localized in the IgM fraction. Hepatocytes were isolated by a perfusion technique without enzymes and with collagenase. LPS binding to the hepatocellular plasma membrane increased proportionally with the LPS concentration in a range between 0.01 and 1.0 mg per ml. The fluorescence pattern of the membrane fixed IgM anti-LPS-antibody at the surface of LPS coated hepatocytes was coarse granular. The in vitro reaction of LPS with hepatocytes was not influenced by the presence of complement. The demonstration of binding sites for LPS on the hepatocellular plasma membrane supports the hypothesis that not only Kupffer cells but also parenchymal liver cells are involved in the hepatic clearance activity for endotoxin.

The beta 2 adrenergic agonist Salbutamol was infused intravenously in doses of 0.05, 0.1 and 0.2 microgram/kg-min in conscious dogs with gastric fistulae. Salbutamol inhibited meal-stimulated acid (measured with intragastric titration) by up to 82%. Salbutamol produced dose-related inhibition of acid stimulated by pentagastrin (up to 88%) and by histamine (up to 52%). Pepsin secretion in response to histamine (but not pentagastrin) was also inhibited by salbutamol. The salbutamol infusion caused a marked tachycardia, an increase in pulse pressure, slight hyperkalaemia and hyperglycaemia. The beta-adrenergic antagonist propranolol augmented pentagastrin-stimulated acid and inhibited meal-stimulated secretion. Propranolol abolished salbutamol - induced tachycardia, and blocked the inhibition by salbutamol of pentagastrin-stimulated acid. Salbutamol inhibition of acid in the dog provides further support for the hypothesis that there are beta 2-adrenergic receptors in the stomach.

The potato inhibitors of proteases inhibit the activation of trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A and B induced by trypsin. These inhibitors do not inhibit the activation of trypsinogen induced by enterokinase. Potato inhibitors have no influence on pepsinogen autoactivation and on pepsin activity.

Pneumatosis cystoides intestinalis, an uncommon disease characterized by the presence of gaseous bubbles in bowel wall, is studied by a review of 919 cases of the world literature. The subserous cysts are more frequently found in the small bowel while the submucous localizations are predominant in the colonic wall. The disease, occurring more frequently in males than in females, is associated with several other lesions: pyloric stenosis and scleroderma for small bowel pneumatosis, chronic cardiopathies and dolichocolon for colonic localizations. Jejunoileal bypass for morbid obesity is an increasing iatrogenic cause. Diagnosis is based on radiology and endoscopy with biopsy but is not yet correctly done in many cases. The treatment is essentially medical.

Using the counter-immunoelectrophoresis technique, the presence of HBsAg was determined in sear of 227 cirrhotics, 132 patients with acute hepatitis, and 254 apparently normal villagers and 220 hospital personnel in Southern Iran. Findings show a very high frequency of antigenemia in cirrhotics as compared to the apparently normal population. Of interest was the male predominance of antigenemia both in cirrhotics (50% vs. 27%) and normals (2.1+ vs. 0.4%) but not in patients with acute hepatitis (42.6% vs. 32.8%). This data suggests the importance of HB antigenemia in the pathogenesis of postnecrotic cirrhosis in Iran, and the importance of male predisposition for the development of the carrier state in either healthy or cirrhotic individuals.

From a group of 424 patients with histologically verified fatty liver 92 patients without diabetes mellitus and alcohol abuse were subjected to follow-up examination for 3 1/2 years. 56 patients underwent second liver biopsy at this time; 20 of these patients had shown marked fatty liver at the initial liver biopsy examination. These 20 patients with marked fatty liver and 25 further patients with moderarte fatty liver could be followed up 5 and 7 1/2 years later; the clinical examination, the various liver function tests, liver scan and blind liver biopsy did not show any evidence of progression of fatty liver towards chronic inflammatory liver disorders or precirrhotic states. This clinical study therefore suggests the harmlessness of non-alcoholic fatty liver.

Eleven male and five female gastric ulcer outpatients as well as twenty eight male and seven female duodenal ulcer outpatients received Proglumide (1200 mg/day) or magnesiumtrisilicate (1320 mg/day) in a prospective double blind study. The sizes of the ulcers were assessed by endoscopy before and after 4 weeks therapy. A complete healing of gastric ulcers was observed in 75% (n = 8) of the patients receiving Proglumide and 25% (n = 8) of the antacid treated controls (p less than 0.05; x2 test). The healed area was significantly (p less than 0.05) larger in the Proglumide 91 mm2) than in the anticida group (23 mm2). In addition, the half time of the ulcer-healing was significantly (p less than 0.05) shorter in the Proglumide treated patients (18 days and 26 days respectively). There was no significant effect of the drug on the duodenal ulcers. The spontaneous healing rate was 61% in the antacid (n = 18) and 59% in the Proglumide treated (n = 17) patients. The drug does not effect the basal and pentagastrin stimulated gastric secretion nor the serum gastrin concentration. No side effects on blood pressure, blood cell count, transaminases or blood glucose concentrations could be observed.

Intra-gastric ethanol given daily for 4 weeks caused transient elevations in plasma amylase and total protein with a fall in total calcium. Light microscopic examination of the pancreas at 4 weeks showed areas of acinar cell degranulation and necrosis without an inflammatory cell infiltrate. The pancreatic changes are unlikely to be an artefact, but rather a direct toxic effect of the alcohol as confirmed by the biochemical changes.

Feeding a choline-deficient diet containing 0.5% DL-ethionine induces an acute hemorrhagic pancreatitis in 100% of young female mice. Evidence for deposition of the third component of complement (C3) on acinar cell plasma membranes was sought, during the inductive stages, by a sandwich immunofluorescence technique. Such a localization could not be demonstrated even though the method is capable of detecting less than 8 x 10(-5) microgram of protein/mm2 of cell membrane. Artifactual binding of immunoglobulin reagents was encountered when goat antisera, with high levels of circulating immune complexes, formed the middle layer in the sandwich technique. This was attributed to the appearance of Fc receptors on the plasma membrane of degenerating acinar cells, and could be avoided by ultracentrifuging acinar cells, and could be avoided by ultracentrifuging the goat antisera prior to sue. In view of the fact that C3 cleavage represents an amplification loop in both the calssical and alternate pathways of complement activation, the lack of demonstrable C3 staining in tbe present experiments strongly suggests that complement plays no role in acinar cell necrosis in this model of pancreatitis.