Disease relevance of Cholecystitis

• Acceptable definitions of cholecystitis included surgery, pathologic examination, hepatic iminodiacetic acid scan or right upper quadrant ultrasound, or clinical course consistent with acute cholecystitis and no evidence for an alternate diagnosis [1].
• Severe malabsorption required parenteral nutrition support for longer than 1.5 years; this was complicated by unstable blood glucose control, acute calculous cholecystitis, catheter sepsis, and severe venous thrombosis [2].
• Our results suggest that the suppression of gallbladder contractility is the cause of the successive formation of bile sludge, gallstones, and cholecystitis during octreotide therapy in Chinese acromegalic patients [3].
• Total alkaline phosphatase activity assayed in gallbladders from 112 patients with cholecystitis and/or lithiasis showed that activity was significantly lower in patients with pigment stones than patients with cholecystitis and/or cholesterol stones [4].
• We describe five cases of pancreatitis and one case of cholecystitis associated with the use of valproate [5].

High impact information on Cholecystitis

• Cholesterol saturation, not proteins or cholecystitis, is critical for crystal formation in human gallbladder bile [6].
• The role of prostaglandin I2 and biliary lipids during evolving cholecystitis in the rabbit [7].
• We conclude that the effects of histamine on the motility of diseased human gallbladder may depend upon the severity of the cholecystitis [8].
• This pattern was mimicked by chronic cholecystitis in non-CF patients [9].
• Human cholecystitis is associated with increased gallbladder prostaglandin I2 and prostaglandin E2 synthesis [10].

Chemical compound and disease context of Cholecystitis

• Current information suggests that arachidonic acid metabolites are involved in the development of cholecystitis [11].
• BACKGROUND: Previous studies have suggested that thiazide diuretic use increases the risk of cholecystitis [12].
• Apparent ketoconazole failure in candidal cholecystitis [13].
• The purpose of this study was to evaluate gallium scanning in cholecystitis [14].
• Acalculous nontyphoidal salmonellal cholecystitis requiring surgical intervention despite ciprofloxacin therapy: report of three cases [15].

Biological context of Cholecystitis

• Immunohistochemical detection of 8-hydroxydeoxyguanosine, a marker of oxidative DNA damage, in human chronic cholecystitis [16].
• 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) [17].
• RESULTS: Twenty-six pregnancies required parenteral nutrition for the following indications: hyperemesis gravidarum (n = 16), cholecystitis/pancreatitis (n = 3), small bowel obstruction (n = 2), intracranial bleed (n = 2), ulcerative colitis (n = 1), and other (n = 2) [18].

Anatomical context of Cholecystitis

• The inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by an increased prostaglandin formation and is mediated by intramural nerves [19].
• The COX-2 expression rate in the epithelium of non-cancerous adjacent epithelium to cancerous lesion was significantly lower than those not only of cancer, but also chronic cholecystitis, XGC and normal gallbladder [20].
• This study examines the hypothesis that cholecystitis down-regulates Guinea pig gallbladder (GPGB) smooth muscle cholecystokinin (CCK)-stimulated prostaglandin (PG) release [21].
• "Halo" sign on indium-111 leukocyte scan in gangrenous cholecystitis [22].
• Intracellular liposomes and cholesterol deposits in chronic cholecystitis and biliary sludge [23].

Gene context of Cholecystitis

• Gallbladder carcinoma expressed VEGF far more often than adenoma or cholecystitis (p = 0.001); VEGF-positive rates were lower in S1, S2, S3 than S4, S5 by Nevin staging of gallbladder cancer (p = 0.044) [24].
• In severe cholecystitis, CCK contractile effect was reduced by the serotonin receptor antagonist methysergide [25].
• RESULTS: The PCNA and MIB-1 indices in chronic cholecystitis were significantly lower than those obtained in both moderately and poorly differentiated adenocarcinoma of the gallbladder (P < 0.001) [26].
• CONCLUSIONS: These findings indicate that TP53 abnormalities are early and frequent events in the pathogenesis of GBC, starting from chronic cholecystitis [27].
• Acute, non-obstructive, sterile cholecystitis associated with etanercept and infliximab for the treatment of juvenile polyarticular rheumatoid arthritis [28].

Analytical, diagnostic and therapeutic context of Cholecystitis

• One patient with gallstones experienced an episode of biliary colic when octreotide was withdrawn; however, no cholecystitis was found at subsequent cholecystectomy [29].
• CONCLUSIONS: USGPC appears to be the treatment of choice for high-risk patients, especially those with postoperative cholecystitis, severe acute calculous pancreatitis, or total parenteral nutrition [30].
• The problem lies in the fact that the use of CCK as a premedication markedly decreases the sensitivity of the study to detect chronic cholecystitis, since the findings become indistinguishable from patients with normal gallbladders [31].
• In strips with chronic cholecystitis, concentration-dependent contractions were produced by PGF2, PGB2 and PGD2; the responses to PGE1 and PGE2 were sometimes variable but there were concentration-dependent contractions after treatment of the strips with indomethacin [32].
• It is relatively uncommon in Europe, but more frequent in Israel, Chile, Bolivia and in Southwestern Native Americans in the United States. Chronic cholecystitis, choledochal cysts, high body mass index, female gender, age, nicotine and industrial exposure to carcinogens are associated risk factors [33].

References