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PubMed1990

Cholecystokinin and cholinergic agents on periodic gallbladder contraction in dogs.

1. The effect of cholecystokinin octapeptide (CCK-OP), methacholine, 2-deoxy-D-glucose (2DG) and gastric distension on gallbladder contraction in relation to interdigestive activity was studied in four conscious dogs with chronic biliary fistulae. 2. The gallbladder contraction in response to CCK-OP was inhibited by atropine and by a ganglionic blocking agent, the characteristics suggesting competitive inhibition. 3. Spontaneous contraction of the gallbladder was still observed after the administration of CCK-OP, methacholine or 2DG. With ganglionic blockade, CCK(-)-OP or methacholine initiated gallbladder contraction, but the spontaneous peak was no longer observed. 4. CCK-OP (100 ng kg-1), methacholine or 2DG advanced the spontaneous contraction of the gallbladder, but did not alter the duration of the cycle. 5. Gastric distension initiated gallbladder contraction. This was abolished by ganglionic blockade. The contraction did not continue in spite of continuous gastric distension, and the spontaneous contraction reappeared 100 min following the pre-distension control.

Animals↗

PubMed2006

Endoscopic gallbladder stent placement for treatment of symptomatic cholelithiasis in patients with end-stage liver disease.

OBJECTIVES: Symptomatic cholelithiasis is a common disease in the general population with an increased prevalence in patients with cirrhosis. While cholecystectomy is the procedure of choice for the treatment of symptomatic cholelithiasis, cirrhotics have an increased risk of complications associated with this therapy. We have found that placement of an endoscopic gallbladder stent is an alternative, less invasive treatment for cirrhotic patients with symptomatic gallbladder disease and describe our experience here. METHODS: A retrospective medical record review of 23 patients with cirrhosis who underwent endoscopic retrograde cholangiography with gallbladder stent placement for symptomatic gallbladder disease from July 1994 to August 2004. RESULTS: Indications for stent placement included recurrent biliary colic (56.5%), acute calculous cholecystitis (39%), acalculous cholecystitis (8.6%), and gallstone pancreatitis (8.6%). All patients experienced resolution of their symptoms following stent placement. Twenty patients (87%) were asymptomatic from 5 days to 3 years post-procedure until transplantation, death, or end of study period. Nine patients (39%) underwent liver transplantation, 5 days to 34 months after the procedure. Eleven patients are well, with ten patients awaiting liver transplantation. Three patients developed late complications and were treated successfully with antibiotics. CONCLUSION: Endoscopic stenting of the gallbladder may be a potential treatment for symptomatic gallbladder disease in patients with cirrhosis awaiting liver transplantation, considered to be high-risk for cholecystectomy.

Adult↗

PubMed2006

Melatonin treatment reverts age-related changes in Guinea pig gallbladder neuromuscular transmission and contractility.

The incidence of gallbladder illness increases with age, but the altered mechanisms leading to gallbladder dysfunction are poorly understood. Here we determine the age-related alterations in gallbladder contractility and the impact of melatonin treatment. Isometric tension changes in response to electrical field stimulation and to agonists were recorded from guinea pig gallbladder muscle strips. [Ca(2+)](i) was determined by epifluorescence microscopy in fura-2 loaded isolated gallbladder smooth muscle cells, and F-actin content was quantified by confocal microscopy. Aging reduced neurogenic contractions, which was associated with the impairment of nitrergic innervation and with increased responsiveness of capsaicin-sensitive relaxant nerves, possibly involving calcitonin gene-related peptide. Melatonin treatment for 4 weeks restored neurogenic responses to normal values, with an associated recovery of nitrergic function and the disappearance of the capsaicin-sensitive component. Aging also reduced the contractile responses to cholecystokinin and Ca(2+) influx. The impaired contractility only correlated with diminished Ca(2+) mobilization in response to activation of Ca(2+) influx. Melatonin improved contractility and increased smooth muscle F-actin content without changing Ca(2+) homeostasis. In conclusion, aging impairs gallbladder function as the result of changes in the inhibitory neuromodulation of smooth muscle contractility and the reduction in the myogenic response to contractile agonists. Impaired contractility seems to be related to decreased Ca(2+) influx and damage of contractile proteins. Melatonin significantly ameliorated these age-related changes.

Acetylcholine↗

PubMed1981

Concentrations of kanamycin and amikacin in human gallbladder bile and wall.

The concentrations of amikacin and kanamycin were determined in the serum, gallbladder bile, and gallbladder wall of 20 patients undergoing elective cholecystectomy. Of 20 patients, 14 received 500 mg of amikacin intramuscularly and 6 received 500 mg of kanamycin intramuscularly at various times before surgery. In patients receiving kanamycin, detectable levels appeared in bile within 90 min after drug administration, and in five of six patients concentrations ranged from 1.9 to 23 micrograms/ml. Levels of kanamycin in gallbladder wall ranged from 8.0 to 14 micrograms/g. In patients receiving amikacin, detectable levels appeared in bile within 48 min after drug administration and ranged from 1.3 to 7.5 micrograms/ml in 12 of 14 patients. Levels of amikacin in gallbladder wall ranged from 4.7 to 34 micrograms/g. The presence of an obstructed cystic duct did not preclude the entry of either antibiotic into gallbladder bile, and this may reflect passage of antibiotic through the gallbladder wall rather than accumulation via bile secretion.

Adolescent↗

PubMed1982

Piperacillin distribution into bile, gallbladder wall, abdominal skeletal muscle, and adipose tissue in surgical patients.

The concentrations of piperacillin in serum, bile, gallbladder wall, abdominal skeletal muscle, and adipose tissue were measured simultaneously at various times after the intravenous administration of a single 5-g dose to each of 14 patients undergoing biliary tract surgery. Piperacillin concentrated in the bile with peak levels exceeding 4,000 micrograms/ml. In a single patient with cystic duct obstruction, trace gallbladder bile piperacillin levels were measured. Gallbladder wall concentrations of piperacillin tended to be higher than corresponding serum concentrations, with a correlation observed between tissue values and the degree of acute gallbladder inflammation and gallbladder bile piperacillin concentrations. Mean peak muscle and adipose tissue piperacillin concentrations of 31 and 27 micrograms/g, respectively, were reached at between 2 and 3 h after the start of infusion. These concentrations exceeded the minimum inhibitory concentration for a majority of susceptible organisms. A single 5-g dose of piperacillin achieved therapeutic levels in gallbladder wall, intraabdominal skeletal muscle, and adipose tissue and concentrated in the bile of patients with patent biliary tracts.

Abdominal Muscles↗

PubMed2006

Prevalence of Escherichia coli O157:H7 in gallbladders of beef cattle.

Gallbladders and rectal contents were collected from cattle (n=933) at slaughter to determine whether the gallbladder harbors Escherichia coli O157:H7. Both gallbladder mucosal swabs and homogenized mucosal tissues were used for isolation. Only five gallbladders (0.54%) were positive for E. coli O157:H7. Fecal prevalence averaged 7.1%; however, none of the cattle that had E. coli O157:H7 in the gallbladder was positive for E. coli O157:H7 in feces. Therefore, the gallbladder does not appear to be a common site of colonization for E. coli O157:H7 in beef cattle.

Abattoirs↗

PubMed1993

Characterization of leukotriene-induced contraction of the guinea-pig gallbladder in vitro.

Metabolites of arachidonic acid like prostaglandins have an established role in the pathogenesis of gallstone formation and cholecystitis, but any contribution by leukotrienes is less clear. Leukotrienes might contribute to the disease process by contracting the inflamed and (or) obstructed gallbladder, resulting in further inflammatory damage and biliary pain. To better define the role of leukotrienes, we assessed their effects on gallbladder contractility in vitro. Both leukotriene C4 (LTC4) and D4 (LTD4) had a concentration-dependent excitatory effect on guinea-pig gallbladder smooth muscle. The LTD4-receptor antagonist MK-571 (1 microM) competitively depressed the contractile response, to both LTD4 and LTC4. The source of calcium was defined using ryanodine to deplete intracellular calcium stores and nifedinine to block extracellular entry. Ryanodine (10 microM) antagonized gallbladder contraction at low concentrations of LTD4 (10(-10) and 10(-9) M). Nifedipine (1 microM) had a greater inhibitory effect on the contractile response at high concentrations of LTD4 (10(-8)-10(-6) M). LTD4-induced contractions were unaffected in tissues pretreated with the neural blocker tetrodotoxin or the muscarinic antagonist atropine. Thus, leukotrienes act directly on the gallbladder smooth muscle, causing contraction at concentrations found in models of cholecystitis, suggesting that these inflammatory mediators contribute to the symptoms and morbidity associated with gallbladder disease.

Animals↗

PubMed1989

Gallbladder ablation through radiologic intervention: an experimental alternative to cholecystectomy.

Twenty pigs underwent (a) cystic duct occlusion by means of fluoroscopically guided transcatheter endoluminal bipolar radio-frequency (RF) electrocoagulation and (b) gallbladder sclerotherapy with one of two different regimens of ethanol and sodium tetradecyl-sulfate (STS). Serum ethanol levels and hepatic enzyme tests showed no acute toxicity. Postmortem histologic studies showed that the bile ducts beyond the occlusion site remained entirely unaffected in all animals. In three of four animals followed up for 2 weeks, the sclerosants induced necrosis of the gallbladder mucosa, but the adjacent liver, serosa, and blood vessels remained intact. In 13 of 16 animals followed up for 8 weeks, the gallbladder lumen was obliterated by fibrous scar tissue. In the animals treated with 95% ethanol and 3% STS, the gallbladder mucosa was necrotic in all areas after 2 weeks (two of two animals) and eradicated completely after 8 weeks (six of eight animals); the other regimen (70% ethanol plus 1% STS) was somewhat less effective. In this study, the combination of RF-mediated cystic duct occlusion and gallbladder sclerotherapy with ethanol and STS permitted gallbladder ablation in swine without toxic side effects.

Animals↗

PubMed1997

Acalculous gallbladder disease: US evaluation after slow-infusion cholecystokinin stimulation in symptomatic and asymptomatic adults.

PURPOSE: To evaluate the measurement with ultrasonography (US) of the gallbladder ejection fraction after slow-infusion cholecystokinin stimulation in patients with biliary symptoms and in individuals without symptoms. MATERIALS AND METHODS: Gallbladder volumes were calculated in 60 healthy volunteers after a 30-minute infusion of sincalide. The time to maximum response, the gallbladder ejection fraction, and the rate of initial contraction were obtained at US. A total of 100 symptomatic patients were evaluated with this technique. Reference standards included surgical outcome or results of clinical follow-up of at least 1 year. RESULTS: The average ejection fraction +/- 2 standard deviations was 80% +/- 30. A fraction greater than 60% was considered to be a normal response to cholecystokinin stimulation. There was no statistically significant sex difference. Slow infusion did not produce any side effects. A sensitivity of 75% and a specificity of 100% for determination of gallbladder ejection fraction at US were obtained in patients with surgical and histopathologic proof of disease. CONCLUSION: The slow-infusion method is reliable, safe, and reproducible in evaluating gallbladder contraction. The cholecystokinin-stimulated gallbladder ejection fraction test may be useful in determining which patients could benefit from surgery.

Adult↗

PubMed1998

Prospective sonographic evaluation of interleukin-2-induced changes in the gallbladder.

PURPOSE: To describe the changes in the gallbladder induced by interleukin-2 (IL-2) therapy and to correlate the findings with the clinical course. MATERIALS AND METHODS: Twenty-five men with human immunodeficiency virus (HIV) infection were examined prospectively with right upper quadrant ultrasonography (US) before and after receiving IL-2 therapy. Four patients also underwent US after a second course of IL-2. The gallbladder was evaluated for wall thickening, echotexture, and intramural and pericholecystic fluid. Correlation was made between the clinical signs and symptoms, IL-2 dose, CD4 cell count, and the US appearance of the gallbladder. RESULTS: There was significant correlation between symptoms of right upper quadrant pain during IL-2 therapy and US abnormalities of the gallbladder, including an increase in wall thickening (P = .012) and the development of intramural (P = .015) and pericholecystic (P = .006) fluid. More severe abnormalities were seen with higher IL-2 doses. All symptoms resolved with cessation of IL-2 therapy. In patients who underwent repeat US, the gallbladder reverted to a normal appearance. No correlation was found between the CD4 cell count and the development of symptoms or the US appearance of the gallbladder. CONCLUSION: IL-2-induced changes resolve rapidly with cessation of therapy, and no surgical intervention is needed. These changes can be avoided or reduced by decreasing the IL-2 dose during subsequent cycles.

Abdominal Pain↗

PubMed2002

Bile salts potentiate adenylyl cyclase activity and cAMP-regulated secretion in human gallbladder epithelium.

Fluid and ion secretion in the gallbladder is mainly triggered by the intracellular second messenger cAMP. We examined the action of bile salts on the cAMP-dependent pathway in the gallbladder epithelium. Primary cultures of human gallbladder epithelial cells were exposed to agonists of the cAMP pathway and/or to bile salts. Taurochenodeoxycholate and tauroursodeoxycholate increased forskolin-induced cAMP accumulation to a similar extent, without affecting cAMP basal levels. This potentiating effect was abrogated after PKC inhibition, whereas both taurochenodeoxycholate and tauroursodeoxycholate induced PKC-alpha and -delta translocation to cell membranes. Consistent with a PKC-mediated stimulation of cAMP production, the expression of six adenylyl cyclase isoforms, including PKC-regulated isoforms 5 and 7, was identified in human gallbladder epithelial cells. cAMP-dependent chloride secretion induced by isoproterenol, a beta-adrenergic agonist, was significantly increased by taurochenodeoxycholate and by tauroursodeoxycholate. In conclusion, endogenous and therapeutic bile salts via PKC regulation of adenylyl cyclase activity potentiate cAMP production in the human gallbladder epithelium. Through this action, bile salts may increase fluid secretion in the gallbladder after feeding.

Adenylyl Cyclases↗

PubMed1988

Bovine gallbladder muscularis: source of a myogenic receptor for cholecystokinin.

Despite being a classic target for the gastrointestinal peptide hormone, cholecystokinin (CCK), the gallbladder CCK receptor is not well characterized. Pharmacological studies of small species suggest that CCK action can be mediated by direct myogenic or by both myogenic and neurogenic receptors. To prepare for the biochemical characterization of a gallbladder CCK receptor and to define the subtype of the receptor being studied, we have performed autoradiographic localization and pharmacological characterization of CCK receptors on bovine gallbladder. Autoradiography demonstrated high-affinity specific CCK-binding sites only on the muscularis. CCK-8 stimulated tonic contraction of longitudinal strips of gallbladder muscularis in a concentration-dependent manner, with an ED50 of 0.2 nM. Antagonism at the cholinergic receptor with 1 microM atropine or axonal transmission with 1 microM tetrodotoxin did not modify CCK-induced contraction, supporting a direct myogenic effect of this hormone. Optimal electrical field stimulation (10 V, 10 Hz, 500 microseconds) to elicit a neuronal response resulted in muscle strip relaxation, which was abolished with adrenergic blockade (1 microM phentolamine, 1 microM propranolol). Although acetylcholine administration stimulated contraction, electrical field stimulation did not, even in the presence of phentolamine, propranolol, and/or CCK. Thus, in bovine gallbladder muscularis, there is evidence for a functional CCK receptor only on smooth muscle cells. Demonstration of a single, high-affinity specific CCK-binding site on an enriched plasma membrane preparation of bovine gallbladder muscularis is consistent with this representing a myogenic CCK receptor.

Animals↗

PubMed1990

Intravenous amino acids stimulate human gallbladder emptying and hormone release.

Gallbladder stasis during prolonged total parenteral nutrition (TPN) has been documented. We have examined the effect of intravenous amino acid infusion on human gallbladder contraction and release of cholecystokinin (CCK). Five healthy adult volunteers were given amino acid infusions at different rates (65, 125, 240, and 600 mg.kg-1.h-1). The volume of the gallbladder was calculated by means of ultrasonographic measurements. Plasma samples were analyzed for CCK immunoreactivity. Gallbladder and hormone responses after intravenous amino acids were compared with responses after a fat meal, after a protein meal, and after ingestion of an oral amino acid mixture. We found that intravenous amino acids stimulated human gallbladder contraction in a dose-related manner. The mechanism of stimulation may be through the release of CCK although significant correlation was not demonstrated. The magnitude of response is similar to that seen after meal stimulation. To compare the delivery of amino acids during a standard meal and during each dose of intravenous amino acids, peripheral plasma levels of dietary amino acids were measured after a standard commercially prepared enteral supplement meal and after each dose of intravenous amino acids. Our lower doses of amino acid infused resulted in levels of circulating amino acid comparable to those after a meal. The induction of gallbladder contraction and release of CCK in human recipients of parenteral nutrition may be of value in some circumstances.

Adult↗

PubMed1996

Membrane cholesterol alters gallbladder muscle contractility in prairie dogs.

The cause and effect relationship between membrane cholesterol and gallbladder muscle contractility was examined by altering membrane cholesterol to phospholipid mole ratio using cholesterol-rich or cholesterol-free liposomes. Gallbladder single muscle cells, from prairie dogs that were fed either a regular or high-cholesterol (1.2%) diet, were isolated enzymatically with collagenase. Plasma membranes of gallbladder muscle were purified in sucrose gradient. Cholesterol was measured using the cholesterol oxidase method. Phospholipids were measured with the method of G.R. Bartlett (J. Biol. Chem. 234: 466-468, 1959). The results of this experiment are 1) after high-cholesterol feeding, cholesterol contents and cholesterol/ phospholipid mole ratio in plasma membranes of gallbladder muscle increased 90%, and muscle cell contraction in response to cholecystokinin octapeptide decreased 58%; 2) similar changes were observed when normal gallbladder muscle cells were incubated with cholesterol-rich liposomes for 2 h; and 3) the changes induced either in vivo or in vitro were reversed when muscle cells were subsequently incubated with cholesterol-free liposomes for 2-6 h. We conclude that gallbladder muscle may incorporate excess cholesterol into its plasma membrane when exposed to a cholesterol-rich environment, that excess membrane cholesterol impairs muscle contractility, and that these changes appear to be reversible.

Animals↗

PubMed2000

Measurement of gallbladder volume with ultrasonography in pregnant women.

Fasting and postprandial gallbladder volumes were investigated using ultrasonography in three groups (10 subjects in each) of healthy women: third trimester pregnant women, postpartum women up to 10 days after giving birth and nonpregnant controls. The scans were performed at 09:00 after a 12 h fast. After the basal measurement was taken, gallbladder volumes were rescanned in 15 min intervals for 60 mins. At the end of this period, all volunteers received a standard liquid test meal, and scans were performed again for 1 h. The mean basal gallbladder volume was 22.2+/-4.2 mL in the nonpregnant (control) group. In the third trimester group, the basal volume was 37.8+/-10.5 mL -70.5% higher than in the nonpregnant group (P<0.001). In the postpartum group, the mean basal volume was 37.9% lower (27.4+/-6.5 mL) than that of the third trimester group (P<0.02). This basal volume was 23.6% greater than that of the control group (P<0.05). After administration of a test meal, the postprandial gallbladder volumes decreased during the first few minutes compared with baseline values. The volumes decreased by 10.2% to 39.8% (23.5+/-7.3 to 34.0+/-10.2; P<0.01) in the third trimester group, by 14.9% to 43.2% (16.6+/-4.3 to 23.3+/-5.5; P<0.01, 0.001) in the postpartum group and by 19.2% to 51.6% (11.9+/-3.5 to 17.9+/-3.6; P<0.02, 0.05, 0.01, 0.001) in the control group. Postprandial mean gallbladder volumes of the third trimester (P<0. 02) and postpartum groups (P<0.02 to 0.01) were significantly different from those of the control group. In conclusion, incomplete emptying of the gallbladder after eating during the third trimester of pregnancy may contribute to cholesterol-gallstone formation, and pregnancy may thus increase the risk of gallstones.

Adult↗

PubMed2004

Overexpression of epithelial cell adhesion molecule antigen in gallbladder carcinoma is an independent marker for poor survival.

PURPOSE: Gallbladder carcinoma is an aggressive type of cancer that is difficult to cure by conventional procedures. There thus is a need to identify novel molecular markers for the assessment of prognosis and as potential therapeutic targets. This retrospective study was designed to investigate the prognostic significance of epithelial cell adhesion molecule (Ep-CAM) overexpression in human gallbladder carcinoma. EXPERIMENTAL DESIGN: Ep-CAM expression was examined immunohistochemically on paraffin-embedded tissue specimens from 99 patients who underwent surgical treatment for gallbladder carcinoma in the period between August 1988 and May 1999. RESULTS: Ep-CAM overexpression was found in 63 (63.6%) of the tumor samples. Kaplan-Meier curves showed that Ep-CAM overexpression was significantly related to decreased overall survival (P < 0.01). Overall survival gradually worsened with increasing Ep-CAM scores. Notably, in the subgroup of pT1 tumors (n = 17), patients without Ep-CAM overexpression had a 5-year overall survival rate of 100% compared with 38% (P = 0.01) for patients with Ep-CAM-overexpressing tumors. By univariate analysis, no correlation was found with conventional clinicopathological parameters. Multivariate analysis, including Ep-CAM expression, pT stage, tumor grade, and resection margin involvement, showed that Ep-CAM overexpression was an independent prognostic marker in gallbladder carcinoma (P = 0.03; relative risk, 1.8). CONCLUSIONS: These results demonstrate for the first time that Ep-CAM overexpression is an independent prognostic marker in gallbladder carcinoma and that its prognostic impact should be validated prospectively. Furthermore, the Ep-CAM antigen represents an attractive target for specific therapies with monoclonal antibodies or specific vaccines in patients with Ep-CAM-overexpressing gallbladder carcinoma.

Adult↗

PubMed2004

Effect of intraduodenal administration of ursodeoxycholic acid on interdigestive interaction between gallbladder motility, pancreatic secretion and endocrine activity.

BACKGROUND: Gastroduodenal motorfunction, gallbladder motility, and pancreatic secretion are closely related during the interdigestive state. The extent to which application of ursodeoxycholic acid (UDC) influences this process is only partly understood. AIM: As UDC is widely used for the therapy of gallbladder stones and of cholestatic liver disease, we wanted to define the immediate effect of UDC on interdigestive gallbladder and antroduodenal motility, biliary-pancreatic secretion and hormone release in man. METHODS: Interdigestive gastrointestinal function in 10 healthy males (26-35 years) was studied twice after 12-hour fasting on 2 different days. Antroduodenal motility was continuously recorded manometrically over a complete interdigestive migrating motor complex (MMC) cycle. Gallbladder volume was evaluated sonographically in 5- to 7-min intervals during the MMC cycle. Pancreatic and biliary secretion was determined by a standard duodenal perfusion technique measuring chymotrypsin, amylase, lipase and bile salts in duodenal aspirates every 15 min. Plasma levels of pancreatic polypeptide (PP) and motilin were determined by radioimmunoassay in 15-min intervals. On 2 separate days, 7-10 days apart, each subject received intraduodenally either 10 mg/kg UDC (pH 8) or placebo 30 min after the first recorded duodenal MMC cycle phase III. RESULTS: With placebo, the fasting gallbladder volume decreased slightly from phase I (32 +/- 8 ml) to the end of phase II (24 +/- 13 ml), but increased significantly from 31 +/- 14 ml (phase I) to 46 +/- 11 ml (phase III) after intraduodenal UDC application (p < 0.01). Pancreatic secretion was significantly reduced after UDC application at the end of phase II (secretion of chymotrypsin 10 +/- 3 U/min vs. 5 +/- 2 U/min, p < 0.01). Serum levels of PP were also reduced by UDC during the entire MMC cycle. This reached statistical significance at the end of phase II (84 +/- 8 pg/ml vs. 57 +/- 14 pg/ml; p < 0.05) and during phase III (86 +/- 19 pg/ml vs. 64 +/- 22 pg/ml; p < 0.05), while motilin slightly increased during the MMC cycle after UDC application. UDC instillation did not affect antroduodenal motility. CONCLUSION: UDC exerts significant inhibitory effects on interdigestive gallbladder contractility, pancreatic secretion, and PP release. Whether these inhibitory effects are mediated by cholinergic pathways or other mechanisms requires further investigation.

Adult↗

PubMed2005

Gallbladder sludge and acute pancreatitis induced by acute hepatitis A.

In this case report, a young woman with gallbladder sludge and acute pancreatitis due to acute hepatitis A (HAV) is presented. She was admitted to our hospital with abnormal hepatic enzymes. Five days prior to her admission, an initial abdominal ultrasound was performed at another hospital and revealed no abnormality, while her serum aspartate aminotransferase (AST) level was at the upper limit of normal (ULN) x 8. A second ultrasound was performed at our hospital and revealed a gallbladder wall thickness (9.3 mm), gallbladder sludge in the gallbladder lumen, pancreatic edema, ascites, and hepatomegaly while AST was at the ULN x 50. Magnetic resonance imaging and magnetic resonance cholangiopancreatography revealed imaging features of an acute stage of pancreatitis and gallbladder wall thickness with coexisting sludge in the gallbladder lumen. HAV infection was diagnosed by the detection of immunoglobulin M against HAV in the serum. The patient underwent two repeated abdominal ultrasound examinations on the 5th (AST was at the ULN x 3) and the 20th days (AST was at the normal) after her discharge, and both revealed normal findings. In our case, we observed reversible changes in the hepatobiliary and pancreatic system which was related to the severity of hepatic necro-inflammation. HAV-associated pancreatitis may be due to the formation of biliary sludge during the acute phase of the viral illness, but this association needs further investigation.

Acute Disease↗