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

Arachidonic acid metabolites are involved in a wide spectrum of hepatobiliary physiologic functions and disease. Prostanoids alter hepatic bile flow. Prostaglandins with a C9 ketooxygen stimulate a bicarbonate-rich choleresis and those with a C9 hydroxyloxygen produce a chloride-rich choleresis. Prostaglandin F2 alpha stimulates the release of the potent choleretic glucagon and the stimulatory effect of prostaglandin F2 alpha on bile flow is inhibited by cyclooxygenase inhibitors, suggesting that prostaglandins play a role in the release of choleretic hormones as well as in their action. Prostanoids are involved in gallbladder contraction and water absorption. Prostaglandins produce gallbladder contraction in various species and cause gallbladder relaxation in other species. Prostaglandins also may be mediators of cholecystokinetic hormone action; however, cyclooxygenase inhibitors do not inhibit the effect of cholecystokinetic hormones in all species. Prostanoids alter the normal process of water absorption by gallbladder mucosa and induce net water secretion. The inflamed gallbladder secretes rather than absorbs fluid. The demonstration that prostaglandin E2 inhibits gallbladder fluid absorption has led to subsequent studies that demonstrated that the secretion of fluid into the inflamed gallbladder lumen may be mediated by prostanoids. In cholecystitis, the prostanoids may mediate the distention produced by mucosal fluid secretion and the contraction of the diseased gallbladder. The inflammatory changes produced in various experimental models of cholecystitis can be prevented by cyclooxygenase inhibitors. Cyclooxygenase inhibitors decrease gallbladder prostaglandin formation and are effective in producing relief of the symptoms of gallbladder disease. In experimental cholesterol gallstone formation, prostaglandins are involved in the production of mucin, which acts as a nidus for stone formation, and cyclooxygenase inhibitors prevent the formation of experimental cholesterol gallstones. Prostaglandins have been shown to be cytoprotective in various types of experimental hepatic injury and leukotrienes have been shown to be injurious to hepatocytes and biliary tract tissues. Specific prostanoids and lipoxygenase inhibitors may be valuable in treating patients with various acute hepatic inflammatory disease processes. Continued evaluation of the role of arachidonic acid metabolites in hepatobiliary physiology and disease may lead to important new therapeutic modalities.
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PMID:Arachidonic acid metabolites in hepatobiliary physiology and disease. 266 54

13 patients with extrahepatic bile duct carcinoma treated in our institute from 1960 to 1986 are reported. All were proven by pathology. There were 10 moderately differentiated or mucin adenocarcinomas, 2 poorly differentiated and 1 undifferentiated cancers. There were 9 males and 4 females with an average age of 60.6 years. Progressive obstructive jaundice was the most common presenting symptom (11/13). Hepatomegaly was found in 7 patients, distended gallbladder in 4 and gallstone in 2. Before operation, 10 patients were misdiagnosed as hepatitis, cholecystitis or cholelithiasis. During operation, regional lymph node metastasis was observed in the majority of patients. Palliative operation was performed in 10 patients and radical surgery in 3. Three received operation plus postoperative radiotherapy. None survived more than two years. The lesions occurred frequently in the upper bile duct (8 patients). The middle bile duct and diffuse type carcinomas comprised 2 each. One was not recorded clearly. The prognosis is related to the gross type of the tumor and differentiation degree. Finally, carcinogenesis is discussed briefly.
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PMID:[Carcinoma of the extrahepatic bile duct--report of 13 patients]. 285 Jan 47

A MORPHOLOGICAL AND HISTOCHEMICAL STUDY WAS MADE OF EPITHELIOID CELL GRANULOMAS: (a) classical sarcoid type, namely, sarcoidosis, Kveim tests, tuberculosis, farmer's lung, and Crohn's syndrome; (b) sarcoid-like granulomas, often distinguishable from (a) by the presence of extracellular mucin or bile, namely, ulcerative colitis, diverticulitis, cholecystitis, cholangitis, carcinoma of the rectum and lymph nodes, draining tumours. All these granulomas showed similar, numerous cytoplasmic granules in epithelioid and giant cells with the properties of residual bodies, i.e., end products of activated lysosomes. The presence of residual bodies demonstrates the following features the morphological similarity of the granulomas studied, and the phagocytic nature of the affected cells. It suggests a common mechanism of granuloma formation but does not identify any particular exogenous cause. The findings suggest that Boeck's sarcoidosis may be caused by unidentified exogenous agents.
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PMID:"Residual bodies" in sarcoid and sarcoid-like granulomas. 560 72

We review the pathogenesis of cholesterol gallstones, which occur in five steps: 1) metabolic; 2) chemical; 3) nucleation, 4) growing and maturation of gallstones; 5) clinical. It is emphasized that in the third step it could occur an arenous precipitate formed by cholesterol crystals, calcium bilirrubinate granules, calcium phosphate, or fatty acids anions and calcium, and mucin, called "biliary sludge", which has been associated with cholecystitis and pancreatitis. We describe the gallbladder motor abnormalities that occur during the lithogenesis and the diagnostic approach through scintigraphy and real time ultrasound. We review the pancreatobiliary dyskinesia, a condition associated with the postcholecystectomy syndrome. This later condition can result from anatomic stenosis or dyskinetic dysfunction of the sphincter of Oddi. Likewise, it is pointed out that at the present time, the manometric evaluation of the sphincter of Oddi is the gold standard in the diagnostic approach of this condition.
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PMID:[Laboratory studies and special tests for assessing gallbladder and bile duct function]. 774 24

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

We present the case of a 50-year-old diabetic male who underwent open cholecystectomy for acute gangrenous cholecystitis. At the time of exploration, a 1.5-cm mass was found peripherally in the right lobe of his liver, and an incisional biopsy was performed. Microscopic examination revealed a distinct overgrowth of clear cells in an acinar pattern, with tumor cells emerging directly from bile ducts. The tumor cells were periodic acid-Schiff reactive and diastase resistant, indicating the presence of mucin. No bile canaliculi were demonstrated by immunostaining with carcinoembryonic antigen. CT scans of the chest and abdomen were otherwise normal. Based on these microscopic, immunohistochemical, and clinical data, a diagnosis of clear cell cholangiocarcinoma was established. The patient later underwent reexploration and generous hepatic wedge resection. He did well postoperatively and is free of disease after 12 months.
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PMID:Peripheral clear cell cholangiocarcinoma: a rare histologic variant. 1036 16

Histologically, the majority of gallbladder cancers are adenocarcinomas. Among the adenocarcinomas, the mucinous adenocarcinoma is relatively uncommon. Porcelain gallbladder is a rare finding and the risk of gallbladder cancer is significantly increased in porcelain gallbladder. We describe a rare case of mucinous adenocarcinoma with porcelain gallbladder. A 46-year-old man was admitted to Chonnam National University Hospital with a 2-week history of right upper quadrant pain. Three and 2 years previously, he had two episodes of cholecystitis with gallstones. An abdominal computed tomography revealed a contracted gallbladder with circumferential mural calcification, and the possibility of gallbladder cancer and porcelain gallbladder were considered. At laparotomy, cholecystectomy, liver wedge resection, and radical lymph node dissection were performed. The resected gallbladder showed thickened wall, luminal narrowing and mucosal irregularity. A histological examination of the resected gallbladder showed a mucinous adenocarcinoma composed of poorly differentiated glandular cells with mucin lakes. Porcelain gallbladder may be an end result of a chronic inflammatory reaction, and this change is associated with the development of gallbladder cancer.
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PMID:Case of mucinous adenocarcinoma with porcelain gallbladder. 1285 33

We report 49 cases of gallbladder carcinomas that extended into or originated from Rokitansky-Aschoff sinuses (RAS), all of which were resected by laparoscopic cholecystectomy. Twenty-one tumors were in situ carcinomas that extended along RAS; six in situ carcinomas arose in adenomyomatous hyperplasia and 22 were invasive adenocarcinomas with extension into RAS. Thirty-seven patients were women and 12 men. Forty patients had cholelithiasis. The age of the patients ranged from 55 to 84 years (mean 67 years). All in situ carcinomas were incidental microscopic findings in gallbladders removed for cholelithiasis and/or cholecystitis. No patient with in situ carcinoma died as a result of the tumor, including two with in situ carcinoma that originated in adenomyomatous hyperplasia and showed microinvasion. In contrast, of 15 patients with invasive well to moderately differentiated adenocarcinoma extending into RAS and invading the muscle layer or subserosal connective tissue, 8 died 2 to 4 years after surgery. Seven patients survived 1 to 8 years after cholecystectomy. Useful clues to separate RAS with in situ carcinoma from tubular neoplastic invasive glands were the following: connection of the epithelial invaginations to the surface epithelium, recognition of normal biliary epithelium admixed with neoplastic epithelium, presence of inspissated bile in long dilated spaces, and lack of invasion to the smooth muscle bundles. In situ carcinoma spreading along RAS consisted of long tubular often dilated structures extending through the intermuscular connective tissue, whereas neoplastic glands were usually small or of medium size that invaded smooth muscle bundles or intermuscular connective tissue. Perineural invasion was seen only in invasive glands located in the subserosal connective tissue. Two cases of in situ carcinoma that arose in adenomyomatous hyperplasia and three invasive adenocarcinomas that were composed predominantly of tall columnar mucin containing cells similar to gastric foveolar cells with varying degrees of atypia and cells with biliary phenotype bear some resemblance to intraductal papillary mucinous carcinoma of the pancreas or to mucinous cystic pancreatic neoplasm. Metaplastic pyloric glands often seen in the muscle layer and subserosal connective tissue maintain their lobular pattern and should not be confused with invasive glands. Our findings indicate that distinction of in situ carcinoma spreading into RAS from tubular neoplastic glands of invasive adenocarcinomas is crucial to determine prognosis in this group of patients with gallbladder carcinoma.
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PMID:In situ and invasive adenocarcinomas of the gallbladder extending into or arising from Rokitansky-Aschoff sinuses: a clinicopathologic study of 49 cases. 1510 50

Gallstones are common in Western countries and due to pain and complications pose a substantial burden on health care systems. In general, cholesterol gallstones are distinguished from bilirubin gallstones. Bilirubin gallstones form if the ion product of unconjugated bilirubin and calcium in gallbladder bile exceeds the solubilisation capacities of mixed micelles and vesicles. Cholesterol gallstones develop if the amount of cholesterol in gallbladder bile exceeds the maximum concentration that is soluble at the given concentration of bile salts and phospholipids. In addition, cholesterol gallstone formation requires hypomotility of the gallbladder and a mucin gel as nucleation matrix for monohydrate crystals. The individual risk of gallstone formation is determined by interactions of lithogenic alleles of gallstone susceptibility genes and multiple environmental factors. For asymptomatic gallstones, expectant management is recommended, whereas an episode of gallstone-associated pain substantially increases the risk of complications such as cholecystitis, cholangitis and pancreatitis and therefore necessitates cholecystectomy.
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PMID:Hereditary liver disease: gallstones. 2095 75

Metachromatic leukodystrophy (MLD) is an autosomal recessive lysosomal storage disorder caused by a deficiency of arylsulfatase A enzyme. This deficiency leads to accumulation of sulfatides in the central nervous system and other organs, such as the gallbladder. Here the authors discuss a 9-year-old Middle Eastern patient with late-infantile-type MLD who presented with symptoms of cholecystitis. Radiographic studies revealed an enlarged gallbladder with a thickened wall and a pericholecystic fluid collection with peripheral calcifications. Gross examination of the gallbladder showed multiple small to medium-sized papillary projections involving the entire mucosal surface. Sections through the gallbladder wall revealed multilocular dilated mucin-producing cystic spaces. Microscopically, the mucosa showed numerous papillary projections with complex folds lined by mucin-producing cuboidal to tall columnar cells. The cystic spaces were composed of numerous markedly distended Rokitansky-Aschoff sinuses filled with mucin. Ultrastructurally, the epithelial cells and macrophages showed frequent secondary lysosomes containing closely packed lamellar amorphous to prismatic material with alternating leaflets and tubules, imparting a "herringbone" or "tuffstone" pattern. This case illustrates the features of gallbladder involvement in MLD and the potential role of ultrastructural examination in diagnosis of MLD.
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PMID:Metachromatic leukodystrophy and its effects on the gallbladder: a case report. 2208 3


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