Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149520 (acute cholecystitis)
 2,784 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Guinea pigs treated with lincomycin developed colitis, acute cholecystitis and abnormalities in red blood cell morphology. The present study was designed to study the production of clostridial toxins after lincomycin treatment. Lincomycin produced abnormalities in conventional but not in germ-free guinea pigs. Clostridium difficile was cultured from cecal contents of conventional guinea pigs treated with lincomycin. Cecal filtrate from sick guinea pigs was subjected to Sepharose 4B-CL and Sephadex G-200 column chromatography, yielding a partially purified toxin. Both cecal filtrate and partially purified toxin samples contained a heat labile substance which was cytotoxic to human lung fibroblast Wl-38 cells, and which was neutralized by Clostridium sordelli antitoxin. Toxin samples given orally or intraperitoneally killed normal guinea pigs. Finally, toxin samples induced red cell membrane changes in vitro as well as producing features of acute inflammation in healthy explants of guinea pig cecum and gallbladder in organ culture. Lincomycin treated guinea pigs produced Clostridium difficile toxin(s) which in turn caused diffuse cell membrane injury.
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PMID:Toxin-induced cell membrane injury in guinea pigs given lincomycin. 713 62

Further experiments are reported on Lincomycin-induced cholelithiasis in guinea-pigs. The biochemical events in the bile and blood, and the chemical composition of gallstones, have been studied. The gallstones resemble human pigment stones in chemical composition. The clear hepatic bile and the normality of the bile salt--phospholipid--cholesterol equilibrium, the rise in beta-glucuronidase and hexosamine levels with the gallbladder, have reaffirmed that epithelial injury is most probably the primary lithogenic factor. Ligation of the cystic duct and the construction of a common hepatic duct-duodenum bypass did not prevent the development of acute cholecystitis, suggesting the lithogenic factor was mediated through the blood circulation and not through the enterohepatic circulation of bile.
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PMID:Further observations in lincomycin-induced cholelithiasis in guinea-pigs. 743 Nov 43