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)

Failure to visualize the gallbladder in its usual location along the right inferior hepatic border suggests many possibilities including acute cholecystitis. The case described here reveals the importance of proper protocol for hepatobiliary imaging with 99mTC-IDA agents, the necessity of quantification of function as an integral part of imaging to enable proper differential diagnosis. A case of bilobed gallbladder presenting as a Valentine heart in an unusual location in the liver is described. The measurement of the CCK-8 induced gallbladder ejection fraction for each lobe facilitated proper diagnosis.
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PMID:Identification and differentiation of congenital gallbladder abnormality by quantitative technetium-99m IDA cholescintigraphy. 174 Jul 14

Hepatobiliary studies were performed over a three-year period on 139 patients suspected of having cystic duct obstruction. Each patient was infused intravenously with sincalide, a C-terminal octapeptide of CCK, 15 minutes prior to the administration of the hepatobiliary imaging agent Tc-99m paraisopropyl iminodiacetic acid (PIPIDA). Analysis of the results demonstrated significant advantages in pretreating patients with sincalide in hepatobiliary studies in a small facility with a relatively large patient load. Most of our studies were completed within 2 hours without jeopardizing the sensitivity (97%) or accuracy (96%) of the test. The specificity (88%) was comparable to percentages reported by others. Most investigators have reported that chronic cholecystitis contributed to the majority of false-positive cases. In addition, inconsistency in the documentation of criteria for the determination of acute cholecystitis (surgical, radiologic, or histologic also could be a cause for such a discrepancy. Knowledge of some important variables may help improve the specificity of the test: an awareness of the following factors during scan interpretation: 1) the effectiveness of the sincalide pretreatment dose, 2) the patient's pretest status (fasting or nonfasting, postanalgesic medication or no analgesics), and 3) time limit for gallbladder visualization. With these variables in mind, the hepatobiliary imaging using pretreatment with sincalide is proven to be a practical procedure protocol with good sensitivity and accuracy as well as specificity.
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PMID:Practical hepatobiliary imaging using pretreatment with sincalide in 139 hepatobiliary studies. 401 80

The following protocols should be observed in evaluating a patient with suspected cholecystitis: In evaluating chronic cholecystitis in patients on a diet containing fat, plain films of the abdomen and oral cholecystogram are the procedures of choice. If the gallbladder fails to fill after ingestion of 3 g iopanoic acid, the procedure is repeated with an additional 3 g the following day. Failure of the gallbladder to visualize after a two-day study, equivocal findings, or persistent symptoms despite a normal study should be followed by ultrasound and, if necessary, cholescintigraphy. The latter two studies should be done in a fasting state, and CCK used to demonstrate gallbladder contraction during both tests. In suspected acute cholecystitis, plain radiography, ultrasound, and Tc-99m-imino diacetic acid derivative scanning should be performed. Again CCK should be used during cholescintigraphy to verify nonvisualization and to stimulate gallbladder emptying.
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PMID:Preoperative diagnosis of gallbladder disease. 716 Jan 62

Cholescintigraphy was performed after pharmacological manipulation in 60 patients with a clinical suspicion of acute cholecystitis and non-visualization of the gallbladder 1 h after 99Tcm-DISIDA cholescintigraphy. Thirty patients received an intravenous (i.v.) injection of morphine sulphate (group I) and the other 30 patients an i.v. injection of CCK (group II). The sensitivity, specificity, positive predictive value and negative predictive value were 94, 100, 100 and 93% in group I and 100, 84, 79 and 100% in group II, respectively. There was a significant difference between groups (P < 0.05). In conclusion, morphine-augmented cholescintigraphy could supply more reliable diagnostic information and is less time-consuming in patients with a clinical suspicion of acute cholecystitis.
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PMID:Morphine-augmented versus CCK-augmented cholescintigraphy in diagnosing acute cholecystitis. 773 22

Pharmacological intervention with either cholecystokinin-8 (CCK-8) or morphine during 99mTc- hepatoiminodiacetic acid (HIDA) cholescintigraphy is required primarily for the assessment of the diseases affecting the gallbladder, the common bile duct, or the sphincter of Oddi. For imaging, the patient should be prepared by an overnight fast, or with 4 hours of minimum fast. Pre-emptying with CCK-8 is probably undesirable and should either be avoided or one should wait for at least 4 hours after CCK-8 to begin the 99mTc-HIDA study to achieve higher specificity of the test for acute cholecystitis. When he gallbladder is not observed by 60 mins in a clinical setting of acute cholecystitis, a dose of 0.04 mg/kg of morphine is administered intravenously and imaging continued for an additional 30 mins. Nonvisualization of the gallbladder by 90 mins with morphine in an appropriate clinical setting is diagnostic for acute cholecystitis. When the gallbladder is not observed by 60 min but is seen with morphine administered after 60 mins, a positive diagnosis of abnormal gallbladder function can be made. When the gallbladder is observed in a clinical setting of biliary pain or chronic calculous or acalculous cholecystitis, CCK-8 at a dose rate of 3.3 ng/kg/min is infused intravenously for 3 mins (10 ng/kg/3 min) for the measurement of the ejection fraction. An ejection fraction value of less than 35% is indicative of calculous or acalculous chronic cholecystitis. The gallbladder emptying is directly related to the total number of cholecystokinin receptors in the smooth muscle. The ejection fraction can be controlled to any desired level simply by controlling the dose rate or the duration of infusion of CCK-8. Morphine and other opiate metabolites circulate for many hours in blood and act on the sphincter of Oddi and decrease the gallbladder ejection fraction. Careful drug history, especially that of opiates, is very critical in all subjects with a low ejection fraction before assigning an abnormality to the gallbladder motor function.
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PMID:Cholecystokinin and morphine pharmacological intervention during 99mTc-HIDA cholescintigraphy: a rational approach. 862 48

The pathogenesis of acute cholecystitis (AC) is controversial. Bile acids may be involved in the pathogenesis of AC because the hydrophobic chenodeoxycholic acid (CDCA) reproduced in vitro the muscle dysfunction observed in AC and was prevented by the hydrophilic ursodeoxycholic acid (UDCA). The present study examined the in vivo effects of UDCA or CDCA on gallbladder muscle dysfunction caused by AC. Guinea pigs were treated with placebo, UDCA, or CDCA for 2 weeks before sham operation or induction of AC by bile duct ligation (BDL) for 3 days. Pretreatment with oral UDCA prevented the defective contraction in response to agonists (acetylcholine [ACh], cholecystokinin 8 [CCK-8], and KCl) that occurs after BDL. Prostaglandin (PG) E(2)-induced contraction remained normal in the placebo and UDCA-treated groups but was impaired in the CDCA-treated group. Treatment with UDCA also prevented the expected increase in the levels of H(2)O(2), lipid peroxidation, and PGE(2) content in the placebo-treated AC group, whereas CDCA caused further increases in these oxidative stress markers. The binding capacity of PGE(2) to its receptors and the activity of catalase were reduced after treatment with CDCA. Treatment with UDCA enriched gallbladder bile acids with its conjugates and reduced the percentage of CDCA conjugates. In contrast, treatment with CDCA significantly decreased the percentage of UDCA in bile. In conclusion, oral treatment with UDCA prevents gallbladder muscle damage caused by BDL, whereas oral treatment with CDCA worsens the defective muscle contractility and the oxidative stress.
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PMID:Hydrophilic but not hydrophobic bile acids prevent gallbladder muscle dysfunction in acute cholecystitis. 1277 24