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PubMed2007

Gallbladder mucin production and calcium carbonate gallstones in children.

In contrast to adults, calcium carbonate gallstones are relatively common in children. Their pathogenesis is poorly understood. Cystic duct obstruction promotes calcium carbonate formation in bile and increases gallbladder mucin production. We tested the hypothesis that mucin producing epithelial cells would be increased in gallbladders of children with calcium carbonate gallstones. Archival gallbladder specimens from 20 consecutive children who had undergone elective cholecystectomy for cholelithiasis were examined. In each case, gallstone composition was determined by Fourier transform infrared microspectroscopy. Gallbladder specimens from six children who had undergone cholecystectomy for conditions other than cholelithiasis during the same period were used as controls. Multiple sections were examined in a blinded fashion and scored semiquantitatively for mucin production using two stains (alcian blue and periodic acid-Schiff). Increased mucin staining was observed in 50% or more epithelial cells in five gallbladder specimens from seven children with calcium carbonate stones, compared to 5 of 13 with other stone types (P = 0.17) and none of the control gallbladders (P = 0.02). Gallbladders containing calcium carbonate stones were significantly more likely than those containing other stone types or controls to contain epithelial cells with the greatest mucin content (P = 0.03). Gallbladders containing calcium carbonate stones were also more likely to show the ulcer-associated cell lineage. These results demonstrate an increase in mucin producing epithelial cells in gallbladders from children containing calcium carbonate stones. This supports the hypothesis that cystic duct obstruction leading to increased gallbladder mucin production may play a role in the development of calcium carbonate gallstones in children.

Adolescent↗

PubMed2005

Expression of homeodomain protein CDX2 in gallbladder carcinomas.

PURPOSE: Caudal-related homeobox protein CDX2 plays an important role in the regulation of cell proliferation and differentiation of the intestinal epithelium. CDX2 is associated with intestinal metaplasia and carcinomas of the stomach, but the role of CDX2 in gallbladder carcinogenesis remains unknown. METHODS: We analyzed the expression of CDX2 and intestinal apomucin MUC2 in gallbladder cancer cell lines at the mRNA level by the RT-PCR method. We also investigated the expression of CDX2 and MUC2 in 68 primary gallbladder carcinomas by the immunohistochemical staining method and compared the expression of CDX2 with the clinicopathological factors in the gallbladder carcinoma cases. RESULTS: Expression of CDX2 and MUC2 was found in three of four gallbladder cancer cell lines at the mRNA level. In addition, we found that CDX2 was absent in the normal gallbladder epithelium, but the CDX2 protein was expressed in 25 of the 68 (36.8%) gallbladder carcinomas. Interestingly, in the tubular type gallbladder carcinomas, the frequency of CDX2 expression was much higher in the well-differentiated type than the moderately and poorly differentiated types, the difference being statistically significant (P<0.01). CDX2 expression showed a relationship with expression of MUC2 (P<0.04) in the gallbladder carcinomas. CDX2 was expressed in intestinal metaplasia and dysplasia, which are hypothesized to be premalignant conditions. CONCLUSION: These results imply that CDX2 plays an important role in gallbladder carcinogenesis with intestinal differentiation.

Aged↗

PubMed1988

Peptide YY and gallbladder contraction. Studies in vivo and in vitro.

The purpose of this study was to examine the effect of peptide YY on contraction of the gallbladder in vivo and in vitro and on contraction of the sphincter of Oddi in vitro. In conscious dogs that were prepared with strain-gauge force transducers implanted in the gallbladder wall, peptide YY (400 ng/kg, bolus; 800 pmol/kg.h, infusion) did not affect the resting contractile pattern of the gallbladder, nor did it inhibit cholecystokinin-octapeptide (CCK-8)-stimulated gallbladder contraction. In contrast, the cholecystokinin antagonist proglumide (5, 10, 20, 40, or 80 mg/kg), given in vivo, inhibited CCK-8-stimulated gallbladder contraction in a dose-related manner. The highest dose of proglumide (80 mg/kg) completely abolished contraction of the gallbladder stimulated by CCK-8. In vitro studies showed that peptide YY (0.25, 0.5, or 1 microgram/ml) did not affect the resting tension of rabbit gallbladder strips, and it did not inhibit CCK-8-stimulated contraction of gallbladder strips. Proglumide (0.4, 0.8, 1.6, or 3.2 mg/ml) inhibited CCK-8-stimulated tension of gallbladder strips in a dose-related manner. Peptide YY and CCK-8 had no effect on the motility of the canine sphincter of Oddi in vitro, whereas acetylcholine caused contraction and adrenergic agonists caused relaxation. These results suggest that peptide YY and pancreatone (a peptidelike substance, extracted from ileal and colonic mucosa, that inhibits CCK-8-stimulated gallbladder contraction in vivo) do not appear to be identical.

Ampulla of Vater↗

PubMed1992

Effect of oral erythromycin on gallbladder motility in normal subjects and subjects with gallstones.

The action of the motilin receptor agonist erythromycin on human gallbladder contraction, measured by ultrasound, both in normal subjects and those with gallstone disease was studied. In 17 normal subjects, oral erythromycin administration (500 mg; vs. placebo) reduced fasting gallbladder volume at 2 hours (26.2 vs. 19.0 mL; P less than 0.001), and postprandial residual gallbladder volume (9.0 vs. 4.4 mL; P less than 0.001) and the rate constant of gallbladder emptying following the meal was significantly increased. Erythromycin also reduced fasting and residual gallbladder volumes in 13 patients with gallstone disease: in 6 who underwent cholecystolithotomy, fasting volume was 29.5 vs. 22.3 mL (P less than 0.05) and residual volume was 17.7 vs. 6.5 mL (P less than 0.05), and in 7 with gallstones in situ, fasting volume was 23.8 vs. 14.3 mL (P less than 0.05) and residual volume was 17.2 vs. 5.0 mL (P less than 0.05). In 7 of 8 subjects with gallstones and impaired gallbladder emptying, the gallbladder emptied normally following administration of erythromycin, and in 3 of the other 5 gallstone subjects gallbladder emptying was increased. In 6 normal subjects given erythromycin three times weekly for 1 month, the effect was maintained (fasting volume, 18.8 mL, P less than 0.001; residual volume, 3.7 mL, P less than 0.001). Oral erythromycin significantly reduces fasting and postprandial residual gallbladder volumes in both normal subjects and subjects with gallstones and reverses the gallbladder motility defect found in a proportion of subjects with gallstones. This effect is maintained for a month in normal subjects.

Administration, Oral↗

PubMed1989

Nifedipine inhibits cholecystokinin-induced gallbladder contraction.

Nifedipine is a calcium channel blocker which results in relaxation of smooth muscle. Although it has been utilized clinically to treat cardiovascular disease, and more recently spastic disorders of the esophagus and colon, its effects on gallbladder contractility have not been clearly defined. We tested the effects of nifedipine on gallbladder contraction stimulated by cholecystokinin (CCK) in a conscious guinea pig model and in healthy human volunteers. Gallbladder contraction was measured in response to repeated injections of CCK before and after intravenous nifedipine given to groups of five guinea pigs in a dose of 100, 200, or 300 micrograms. Nifedipine virtually abolished spontaneous interdigestive gallbladder contractile activity and decreased resting gallbladder tone. The mean amplitude of gallbladder contraction in response to CCK was decreased by 45, 73, and 67% (P less than 0.01), in response to the nifedipine doses of 100, 200, and 300 micrograms, respectively. The integrated gallbladder contractile response and the rate of rise of gallbladder pressure in response to CCK were also significantly decreased by nifedipine. In nine healthy human volunteers, gallbladder emptying was measured by radionuclide cholescintigraphy in response to CCK infusion; on another day the study was repeated after oral administration of 10 mg nifedipine. Ejection fraction was significantly decreased by nifedipine from 72 +/- 5 to 51 +/- 5% (P less than 0.001). These data demonstrate that nifedipine is a potent inhibitor of gallbladder contractility in guinea pigs and man. This may provide the basis for the use of nifedipine clinically in the treatment of biliary colic and also raises questions about the potential effect of long-term nifedipine use on gallstone formation and cholecystitis.

Adult↗

PubMed1989

Vasoactive intestinal peptide in the normal and inflamed feline gallbladder.

Intravenous infusion of vasoactive intestinal peptide (VIP) causes gallbladder mucosal fluid secretion by an action on epithelial cell receptors in the cat. Gallbladder fluid secretion is observed also in experimental cholecystitis and this secretion is abolished when the intramural gallbladder nerves are blocked. In the present study, immunoreactive VIP was detected in the gallbladder contents (29 +/- 5 (S.E.M.) pM) in the obstructed lumen of the gallbladder in cats with experimental cholecystitis and gallbladder mucosal fluid secretion, but not in the normal feline gallbladder. During luminal perfusion of the gallbladder in vivo, the calculated secretion of VIP into the gallbladder lumen in animals with experimental cholecystitis was significantly higher (0.31 +/- 0.08 (S.E.M.), pmol/h) than in controls (0.11 +/- 0.02 (S.E.M.), pmol/h) while plasma levels of VIP were similar. Recovery of exogenously administered VIP was similar in normal and inflamed gallbladders. The present results support the hypothesis that intramural VIP-releasing nerve fibers may be activated in cholecystitis.

Animals↗

PubMed1995

Effect of cisapride on gallbladder motility after extracorporeal shock-wave lithotripsy.

BACKGROUND/AIMS: Altered gallbladder motility is regarded as one of the important factors involved in the formation and recurrence of gallstones. Previous studies have suggested that cisapride increases postprandial gallbladder contraction and may therefore be theoretically useful in preventing stone recurrence. The aim of our study was therefore to investigate the effect of cisapride on gallbladder motility in stone-free patients after extracorporeal shock-wave lithotripsy, as compared to healthy volunteers pair-matched for age and sex. METHODS: Each subject received cisapride or placebo in a double-blind, cross-over, random order. Gallbladder volumes were measured by ultrasonography in the fasting state and after intake of a standard liquid meal. Plasma cholecystokinin levels were determined by radioimmunoassay. RESULTS: Fasting gallbladder volumes were smaller in patients as compared to volunteers (20.7 +/- 1.3 ml vs. 46.0 +/- 9.2 ml; p < 0.05) but were not modified by cisapride (21.1 +/- 1.7 ml vs. 58.6 +/- 11.3 ml). The maximal postprandial decrease in gallbladder volume was similar in patients and volunteers (64.5 +/- 12% vs. 62 +/- 10%; NS) and was not significantly altered by cisapride (59 +/- 9.4% vs. 54 +/- 9%; NS). In patients, cisapride increased integrated postprandial gallbladder volume by accelerating gallbladder refilling as compared to placebo by 37 +/- 15% (p < 0.05). Integrated cholecystokinin plasma levels were similar in patients and volunteers and were 13.4 +/- 4.7% higher after cisapride as compared to placebo (p < 0.05). CONCLUSIONS: The results of this study suggest that cisapride does not alter postprandial gallbladder contraction but accelerates gallbladder refilling in patients free from gallstones after extracorporeal shock-wave lithotripsy. This effect of cisapride is probably due to an acceleration of gastric emptying also causing a secondary enhanced cholecystokinin release.

Adult↗

PubMed2000

Impaired human gallbladder lipid absorption in cholesterol gallstone disease and its effect on cholesterol solubility in bile.

BACKGROUND & AIMS: The role of the gallbladder in gallstone pathogenesis is still unclear. We examined the effects of gallbladder mucosal lipid absorption on lipid composition and cholesterol crystallization in bile. METHODS: The in vitro-isolated, intra-arterially perfused gallbladder model was used (1) to compare the absorption rates of lipids from standard bile by gallbladders obtained from 7 patients with cholesterol gallstones and 6 controls; and (2) to measure the microscopic cholesterol crystal detection time in cholesterol-enriched pig bile before and after lipid absorption by the pig gallbladder. RESULTS: Control gallbladders, but not cholesterol gallstone gallbladders, significantly reduced cholesterol (P < 0.02) and phospholipid (P < 0.01) and increased bile salt (P < 0.01) molar percentages in bile over a 5-hour period by efficient and selective cholesterol and phospholipid absorption. A histomorphometric study of the epithelial cells showed significantly higher values for nuclear density (P < 0.01) and nuclear (P < 0.05) and cytoplasmic (P < 0.05) areas in the cholesterol gallstone than the control group. Sequential microscopy of cholesterol-enriched pig bile showed significantly shorter cholesterol filament (P < 0.01) and typical cholesterol plate (P < 0. 02) detection times before than after exposure of bile to the gallbladder lipid absorption. CONCLUSIONS: In cholesterol gallstone disease, the human gallbladder epithelium loses its capacity to selectively and efficiently absorb cholesterol and phospholipids from bile, even if it is hyperplastic and hypertrophic. This epithelial dysfunction eliminates the positive effect that the normal gallbladder exerts on cholesterol solubility in bile and might be a pathogenetic cofactor for cholesterol gallstone formation.

Absorption↗

PubMed1997

Thickened inner hypoechoic layer of the gallbladder wall in the diagnosis of anomalous pancreaticobiliary ductal union with endosonography.

BACKGROUND: An anomalous pancreaticobiliary ductal union (APBD) is a high-risk factor for biliary tract carcinoma, which often is not diagnosed before overt malignancy. The early detection of APBD is therefore clinically important. We evaluated the gallbladder wall in APBD patients with endoscopic ultrasonography. METHODS: Clinicopathologic features and ultrasonographic findings of the gallbladder in 33 consecutive patients with APBD between 1986 and 1995 were studied in relation to two subtypes of APBD, that is, undilated (n = 17) and dilated (n = 16). The gallbladder wall was evaluated with conventional ultrasonography and/or endoscopic ultrasonography. Histologic examinations of 25 resected gallbladders were made. RESULTS: Fourteen of the seventeen patients with undilated type APBD (82%) had diffuse thickened gallbladder wall of 4 mm or more, whereas 5 of the 16 with dilated type (31%) had this finding (p < 0.01). The thickened gallbladder wall consisted sonographically of two layers: diffuse thickened inner hypoechoic layer and outer hyperechoic layer. Mucosal hyperplasia was histologically found in 8 of 9 cases (89%) with thickened inner hypoechoic layer on endoscopic ultrasonography. Mucosal hyperplasia was observed in 10 of 11 undilated type APBD cases (91%) in which cholecystectomy was performed. In addition, the presence of anomalous union was shown by endoscopic ultrasonography in 9 of 11 patients with undilated type APBD (82%) and all 7 of those with dilated type. The characteristic ultrasonographic pattern of diffuse thickened inner hypoechoic layer was observed exclusively in patients with mucosal hyperplasia of the gallbladder associated with APBD among 2085 endoscopic ultrasonography examinations performed during the study period. CONCLUSIONS: Diffuse thickened inner hypoechoic layer of the gallbladder wall was frequently observed in APBD patients, especially those with the undilated type, on ultrasonography and/or endoscopic ultrasonography. This finding corresponded histologically to mucosal hyperplasia of the gallbladder mucosa. Thickened inner hypoechoic layer is a useful ultrasonographic sign that indicates mucosal hyperplasia of the gallbladder and, particularly, the possible coexistence of undilated type APBD before the appearance of overt malignancy.

Adult↗

PubMed1991

Mucosal changes of the gallbladder in anomalous union with the pancreatico-biliary duct system.

Histological examination of the gallbladder mucosa was made on a total of 39 patients with anomalous union of the pancreatico-biliary duct system. The most characteristic finding was mucosal hyperplasia of the gallbladder. Measurement of the height of the mucosa revealed that 15 cases (38.5%) showed mucosal hyperplasia composed of ordinary gallbladder epithelium without any metaplastic changes, including two cases of primary mucosal hyperplasia of the gallbladder. The other finding was metaplastic changes which were observed in 26 cases in various degrees, of whom 16 cases showed only focal metaplasia. These findings indicate that metaplasia frequently occurred in the gallbladder but the distribution of metaplasia was relatively focal in anomalous union with the pancreatico-biliary duct system. In our present materials there were nine cases of gallbladder adenocarcinoma and based on our classification, they were divided into seven cases of metaplastic type and two cases of non-metaplastic type. This ratio was not different from that of usual gallbladder carcinoma not complicated by this anomaly. These results indicate that the reflux of pancreatic juice into the gallbladder by anomalous union with the pancreatico-biliary duct system may cause two different effects on the gallbladder mucosa, the first being a proliferative effect resulting in mucosal hyperplasia and the other being chronic irritation causing metaplastic changes. The relation between these changes and the pathogenesis of gallbladder carcinoma is briefly discussed.

Adolescent↗

PubMed1994

Gallbladder wall thickening: an in vitro sonographic study with histologic correlation.

RATIONALE AND OBJECTIVES: We compared histologic sections with in vitro sonographic images for 40 resected gallbladder specimens to correlate the histopathologic processes with the sonographic appearance of the gallbladder wall. METHODS: In vitro sonographic images and histologic specimens were obtained by use of a specimen container with a micropositioner. An 8.5-MHz transducer and a scalpel were attached to the micropositioner to obtain the sonographic image and the histologic section. The sonographic images were analyzed for wall thickness and the number and echo texture of the visualized layers and then were correlated with the histologic sections. Each histologic specimen was interpreted as being normal or showing mild, chronic, acute, or gangrenous cholecystitis. RESULTS: One to four sonographic layers were observed in the gallbladder wall specimens. The number of wall layers was fairly evenly distributed among the different types of gallbladder wall inflammation. One to three sonographic layers were observed for most of the different types. In nearly all instances, the findings were attributable to either similar pathologic processes in two or more histologic layers or different pathologic processes in a single histologic layer. The gallbladder wall measured less than or equal to 3 mm in 89% of gallbladders with normal or mild inflammation, greater than 3-6 mm in 71% of cases of chronic cholecystitis, greater than 3 mm in 83% of cases of acute cholecystitis, and greater than 6 mm in 50% of cases of gangrenous cholecystitis. CONCLUSIONS: The sonographic layers in the inflamed gallbladder wall are determined by the pathologic changes present rather than by the normal histologic boundaries. However, because of the overlap of pathologic changes, we cannot predict the type of gallbladder wall pathology on the basis of the sonographic appearance. We found a trend toward gallbladder wall thickening for severely inflamed gallbladder walls.

Acute Disease↗

PubMed1997

The gallbladder also secretes.

The gallbladder is traditionally regarded as an absorptive organ. There is increasing evidence that the gallbladder mucosa can have a secretory function. We studied a patient with primary sclerosing cholangitis whose gallbladder was excluded from his extrahepatic bile ducts by stricture formation. He was admitted into hospital because of cholecystitis and cholangitis and required separate drainage tubes into his gallbladder and common hepatic duct. This unique combination of drains afforded the opportunity to examine hepatic bile and gallbladder secretion. We analyzed samples for fluid volume, protein, electrolyte concentrations and biliary lipids. The simultaneous, yet separate, drainage from the gallbladder and the liver had a striking difference. The former was colorless to opalescent; the latter always golden brown. Hepatic bile flow was continuous but gallbladder drainage was variable in volume, intermittent, and occurred only after a meal. The gallbladder fluid had no bilirubin, bile salts, cholesterol, or phospholipids and had the ionic profile of an extracellular fluid. It was alkaline and contained abundant bicarbonate. We have shown that the gallbladder can secrete. In addition, these observations may also have important implications in the pathogenesis and prevention of gallbladder sludge and stones.

Aged↗

PubMed2003

Influence of cholecystitis state on pharmacological response to cholecystokinin of isolated human gallbladder with gallstones.

We studied the influence of the inflammatory state of the gallbladder with gallstones on its response to cholecystokinin (CCK). Responses to CCK were evaluated in isolated human gallbladder strips incubated with pharmacological antagonists. Gallbladders from patients with gallstones were classified as having mild and severe chronic cholecystitis. Healthy gallbladders were collected from liver donors. In donor gallbladders, the CCK contraction was abolished with the CCK-A receptor antagonist, L-364718, and significantly reduced by indomethacin. In gallbladders with gallstones, only mild cholecystitis showed a decreased contraction to CCK. In gallbladders with gallstones, no involvement of prostaglandins in the CCK response was observed. In severe cholecystitis, CCK contractile effect was reduced by the serotonin receptor antagonist methysergide. In healthy gallbladder, the contraction provoked by CCK is mediated by CCK-A receptors and modulated by prostaglandins. The presence of gallstones in the gallbladder is correlated with a loss of prostaglandins-modulated CCK contraction. However, the excessive release of serotonin in advanced cholecystitis normalizes the contraction to CCK, suggesting that the state of cholecystitis affects the pool of inflammatory mediators responsible for gallbladder CCK-altered motility.

Acetylcholine↗

PubMed1999

Effects of ursodeoxycholic acid therapy on in vitro gallbladder contractility in patients with cholesterol gallstones.

During treatment with ursodeoxycholic acid (UDCA), the fasting gallbladder volume increases by a yet unknown mechanism. The present study tests whether in vitro human gallbladder contractility in response to acetylcholine and cholecystokinin is affected by UDCA therapy. Gallbladder tissue was obtained from 15 patients treated with UDCA (10 mg/kg/day) during three weeks prior to surgery, and from 15 comparable patients not treated. Data were correlated with in vivo contractility, bile composition, and gallbladder wall inflammation. The inflammation score was lower in the treated patient group. UDCA treatment enhanced gallbladder contractility in vitro: Dose-response curves for acetylcholine and cholecystokinin were both shifted to the left, and the maximal contractile stress generated in response to cholecystokinin was higher in the treated group, whereas the maximal acetylcholine-induced stress was not increased. Maximal cholecystokinin-induced stress correlated positively with fasting gallbladder volume and negatively with the biliary cholesterol saturation index, but not with bile salt hydrophobicity or gallbladder wall inflammation score. In conclusion, UDCA treatment improves in vitro gallbladder contractility, possibly related to a reduced biliary cholesterol saturation. Increased fasting gallbladder volumes during UDCA treatment thus do not appear to result from decreased gallbladder muscle contractile strength.

Acetylcholine↗

PubMed2002

High resolution chromosome 3p, 8p, 9q and 22q allelotyping analysis in the pathogenesis of gallbladder carcinoma.

Our recent genome-wide allelotyping analysis of gallbladder carcinoma identified 3p, 8p, 9q and 22q as chromosomal regions with frequent loss of heterozygosity. The present study was undertaken to more precisely identify the presence and location of regions of frequent allele loss involving those chromosomes in gallbladder carcinoma. Microdissected tissue from 24 gallbladder carcinoma were analysed for PCR-based loss of heterozygosity using 81 microsatellite markers spanning chromosome 3p (n=26), 8p (n=14), 9q (n=29) and 22q (n=12) regions. We also studied the role of those allele losses in gallbladder carcinoma pathogenesis by examining 45 microdissected normal and dysplastic gallbladder epithelia accompanying gallbladder carcinoma, using 17 microsatellite markers. Overall frequencies of loss of heterozygosity at 3p (100%), 8p (100%), 9q (88%), and 22q (92%) sites were very high in gallbladder carcinoma, and we identified 13 distinct regions undergoing frequent loss of heterozygosity in tumours. Allele losses were frequently detected in normal and dysplastic gallbladder epithelia. There was a progressive increase of the overall loss of heterozygosity frequency with increasing severity of histopathological changes. Allele losses were not random and followed a sequence. This study refines several distinct chromosome 3p, 8p, 9q and 22q regions undergoing frequent allele loss in gallbladder carcinoma that will aid in the positional identification of tumour suppressor genes involved in gallbladder carcinoma pathogenesis.

Carcinoma↗

PubMed2000

Acute intraduodenal bile salt depletion leads to strong gallbladder contraction, altered antroduodenal motility and high plasma motilin levels in humans.

Cholecystokinin is the main hormone involved in postprandial gallbladder contraction. There is also considerable gallbladder contraction in the fasting state, associated with phase III of the gastrointestinal migrating motor complex and release of the hormone motilin. It has been proposed that intraduodenal bile salts exert a negative-feedback control on postprandial cholecystokinin release and resulting gallbladder contraction. We wanted to elucidate whether a similar control mechanism on gallbladder contraction exists in the fasting state. We therefore performed gallbladder ultrasonography and 24-h antroduodenal motility registrations and determined plasma cholecystokinin and motilin levels in six healthy subjects before and after acute (4 g) and chronic (8 days; 8 g day(-1)) oral cholestyramine. Acute cholestyramine strongly decreased gallbladder volumes and increased motilin without changed cholecystokinin levels. There was a negative relationship between gallbladder volumes and plasma motilin levels. Although there was a persistent fasting pattern of antroduodenal motility, its cycle length was increased (P < 0.03) with markedly longer phase II (P < 0. 005). Fasting gallbladder volumes 24 h later were still strongly decreased but gradually increased to pretreatment levels. Before and after 8 days cholestyramine, interdigestive and postprandial gallbladder emptying, intestinal migrating motor complex and hormone levels did not differ. We conclude that acute (but not chronic) intraduodenal bile salt depletion with cholestyramine affects gallbladder and antroduodenal motility, possibly partly related to motilin release.

Adult↗

PubMed1996

Gallbladder emptying and gallstone formation: a prospective study on gallstone recurrence.

BACKGROUND & AIMS: Gallbladder emptying is reduced in many patients with cholesterol gallstones. To clarify the role of impaired gallbladder motility in recurrent gallstone disease, the effect of gallbladder emptying on the formation of recurrent stones was studied prospectively. METHODS: In 54 consecutive patients with single radiolucent gallbladder stones, postprandial gallbladder emptying was assessed sonographically before lithotripsy and 1.8 +/- 0.1 years (mean +/- SE) after gallstone disappearance. Patients were followed up for gallstone recurrence for 0.6-4.1 years (median, 2.6 years). RESULTS: After gallstone disappearance, gallbladder fasting volume (33.7 +/- 3.4 vs. 27.8 +/- 3.0 mL; P = 0.007) and residual volume (12.6 +/- 1.9 vs. 9.7 +/- 1.3 mL; P = 0.010) decreased, whereas the ejection fraction remained unchanged. However, gallbladder volume did not differ whether initial or recurrent stones were present. Gallbladder emptying was more impaired in patients with than patients without later recurrence (47% +/- 5% vs. 63% +/- 2%; P = 0.001). Cox analysis showed that gallbladder emptying was an independent determinant of the risk of gallstone recurrence (P = 0.002). Within 3 years, recurrent stones formed in 53% (actuarial analysis) of patients with an ejection fraction of < 60% but in only 13% of patients with an ejection fraction of > or = 60%. CONCLUSIONS: Gallbladder emptying is an important factor in the formation of recurrent gallstones.

Biliary Tract↗

PubMed2005

Endoscopic ultrasound-guided fine-needle aspiration in the evaluation of gallbladder masses.

BACKGROUND AND STUDY AIMS: There are very few data on endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) of gallbladder masses. The aim of this study was to assess the utility and safety of EUS-FNA in the evaluation of patients with gallbladder masses. PATIENTS AND METHODS: Six patients who underwent EUS-FNA of gallbladder masses over a 2-year period between 2002 and 2004 were studied retrospectively. Reports of endoscopic ultrasound (EUS) procedures, EUS images, cytology results, and clinical records were reviewed. Abdominal computed tomography (CT) prior to EUS had revealed a definitive gallbladder mass in only one of the six patients and no gallbladder masses were identified in any of the patients who had undergone prior transabdominal ultrasound. RESULTS: At EUS, all the patients were found to have an echo-poor mass arising from the gallbladder wall or within the lumen of the gallbladder. EUS-FNA of the gallbladder masses revealed adenocarcinoma in five patients and benign disease in one patient. After a mean follow-up period of 127 days (range 90 - 187 days), three patients had died, two were undergoing palliative chemoradiotherapy, and one had been confirmed as having chronic cholecystitis at surgery. No complications occurred. CONCLUSIONS: In patients with obstructive jaundice and equivocal ultrasound or CT findings, evaluation of the gallbladder for the presence of a primary malignancy by EUS is useful. In patients with gallbladder masses, EUS-FNA can be performed safely and can help to make a definitive diagnosis.

Adenocarcinoma↗