Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0008325 (cholecystitis)
 3,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prostanoids have been demonstrated to be involved in gallbladder physiology and disease. In previous reports, prostaglandin E (PGE) compounds were found to be increased in inflamed human gallbladders. Prostaglandin synthetase inhibition decreased PGE formation by human gallbladders; however, the relief of symptoms of cholecystitis did not correlate well with the decrease in PGE formation. This suggested that other prostanoids may be involved in cholecystitis. The purpose of this study was to evaluate the production of the proinflammatory arachidonic acid metabolite prostacyclin by gallbladders from patients with calculous cholecystitis. The formation of PGE and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of prostacyclin, in normal human gallbladder mucosal cells and muscle tissue was compared with that produced by diseased mucosal cells and muscle tissue. Normal human gallbladders produced small amounts of 6-keto-PGF1 alpha, and no differences in formation rates were evident when muscle tissue was compared with mucosal cells. Diseased gallbladders produced significantly greater amounts of 6-keto-PGF1 alpha than did normal gallbladders, and diseased gallbladder muscle produced approximately four times greater amounts of 6-keto-PGF1 alpha than did diseased gallbladder mucosa. Prostacyclin formation is increased in diseased human gallbladders and may be an important mediator of the inflammatory changes of cholecystitis.
 ...
PMID:Evaluation of prostacyclin production by human gallbladder. 264 56

In a randomized double-blind trial, the effect of ibuprofen on the pain produced by gallbladder disease and on gallbladder mucosa and muscle wall tissue PGE and PGF production was evaluated to determine if the pain of cholecystitis and prostaglandin formation were altered by administration of a prostaglandin synthetase inhibitor. To ascertain potential differences in extracellular and intracellular prostaglandin production rates, gallbladder mucosal cells and muscle tissues were maintained in tissue culture medium and then subsequently homogenized. PGE and PGF concentrations were measured in culture medium and homogenates utilizing radioimmunoassay. Gallbladder mucosa and muscle tissue produced nanogram per milligram protein amounts of PGE and PGF. As the histological estimation of the degree of inflammation increased, so also did the production of PGE. Increased inflammation was associated with unchanged PGF levels, resulting in an increased ratio of PGE/PGF with increasing inflammation. Oral ibuprofen administration was effective in decreasing PGE production by gallbladder mucosa and muscle and eliminating the significant correlation between PGE levels and the histologic degree of inflammation found in the placebo-treated patients. Ibuprofen significantly decreased the pain of cholecystitis when compared to placebo-treated patients. However, there was poor correlation between pain relief and changes in PGE production by gallbladder mucosa and muscle. PGE may play a mediator role in inflammation associated with cholecystitis. Prostaglandin synthetase inhibition decreases the pain associated with cholecystitis; however, the absence of correlation with decreased PGE formation suggests that other prostanoids may play an important role in producing the symptoms of cholecystitis.
 ...
PMID:Effect of oral ibuprofen on formation of prostaglandins E and F by human gallbladder muscle and mucosa. 389 1