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)

A case of large protruding cystitis glandularis is reported. A 36-year-old man was admitted to our hospital due to acute cholecystitis, and large protruding masses were incidentally found in the urinary bladder by abdominal ultrasonography. The histological study revealed that they consisted of a large number of Brunn's nests with or without cysts which were often accompanied with columnar epithelial metaplasia, and of glandular structures closely resembling the colonic crypts. The mucin-histochemical study demonstrated glandular lesions in the bladder secreted colonic type mucin, and endocrine cells positive with Grimelius' staining. A review of literature disclosed 19 clinical cases of cystitis glandularis, since 1970, in Japan, but such a large protruding lesion as this case is rare. We first performed detailed histological and mucin-histochemical studies for this clinical case.
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PMID:A case large protruding cystitis glandularis: clinical, histological and mucin-histochemical study. 175 26

This study was undertaken to elucidate the role of autonomic denervation in the pathogenesis of acute acalculous cholecystitis. In Experiment I, the gallbladder was denervated by performing either celiac neurotomy (sympathetic denervation) or truncal vagotomy (parasympathetic denervation), or both, in dogs. In Experiment II, 45-min ischemia and 90-min reperfusion of the gallbladder with or without autonomic denervation were performed by simultaneously occluding the middle hepatic artery and superior mesenteric vein. Celiac neurotomy, and truncal vagotomy, or both, did not cause cholecystitis. Sympathetic denervation, however, decreased the amount of mucin in the gallbladder mucosa and parasympathetic denervation caused reduction of the tissue blood flow, as well as the accumulation of lipid peroxide and xanthine oxidase in the gallbladder mucosa. These changes were most remarkable 1-2 weeks after denervation and were alleviated 4 weeks after denervation. Ischemia-reperfusion 2 weeks after denervation caused more severe cholecystitis than ischemia-reperfusion alone. The most severe inflammation developed in animals that received both celiac neurotomy and truncal vagotomy. These results suggest that autonomic denervation alone does not induce acute cholecystitis, but that it plays an important role in the progression of the inflammatory process in ischemia-reperfusion injury.
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PMID:Experimental study of the pathogenesis of acute acalculous cholecystitis: role of autonomic denervation. 806 1

Experimental studies have shown that prostaglandins increase hepatic bile flow and gallbladder mucin production, cause gallbladder dysmotility, and inhibit intraluminal fluid absorption, thus promoting gallstone formation. By virtue of their positive actions on gallbladder fluid secretion, muscle contraction, and inflammatory properties, prostaglandins may also have a role in the pain of acute cholecystitis. Although only a few clinical studies of the role of prostaglandin inhibitors in gallbladder disease have been done, results show that use of drugs such as aspirin or other nonsteroidal anti-inflammatory agents may prevent gallstone formation and promptly relieve acute pain.
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PMID:Managing gallbladder disease with prostaglandin inhibitors. 832 67

Human mucin genes include membrane-bound mucins (MUC1, MUC3, MUC4) and secretory mucins (MUC2, MUC5AC, MUC5B, MUC6). Our aim was to determine mucin gene expression in human gallbladder cell lines, normal gallbladder from liver donors (N = 7) and surgical specimens with mild chronic cholecystitis (N = 29), chronic cholecystitis (N = 48), and acute and chronic cholecystitis (N = 27). MUC1 mRNA was ubiquitous; however, only rare MUC1 immunoreactivity was detected. MUC3, MUC5AC, MUC5B, and MUC6 mRNA were present in all gallbladder specimens and cell lines examined. Prominent MUC3, MUC5AC, MUC5B, and MUC6 immunoreactivity was present in 86-100% of normal gallbladders. The frequency of MUC5AC reactivity was decreased in specimens with acute cholecystitis (P < 0.05). In contrast, MUC2-reactivity was absent in normal gallbladder and present in 53.8% of acute cholecystitis specimens (P < 0.05). Surface epithelium is characterized by MUC3, MUC5AC, and MUC5B, whereas deeper mucosal folds display MUC5B and MUC6 immunoreactivity. Gallbladder epithelium demonstrates a unique and diverse pattern of mucin core proteins that becomes altered with increasing degrees of inflammation.
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PMID:Altered mucin core peptide expression in acute and chronic cholecystitis. 1087 17