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PubMed2001

Ultrasonographic assessment of gallbladder bile exchanges in healthy subjects and in gallstone patients.

Impaired gallbladder motility may contribute to gallstone pathogenesis by providing time for nucleation and aggregation of cholesterol crystals. Simultaneous scintigraphic-ultrasonographic techniques have been proposed to assess alternating phases of gallbladder emptying and filling. To evaluate patterns of gallbladder motility and of postprandial bile flow by means of a single ultrasonographic technique, 12 healthy volunteers and 20 gallstone patients underwent minute-by-minute gallbladder ultrasonography for 3 h postprandially. Mathematical analysis of volume measurements was used to estimate hepatic and cholecystic bile flux through the gallbladder. Compared to controls, gallstone patients showed greater amounts of unexchanged cholecystic-to-hepatic bile (11% vs. 1%, p <.001) and most of them showed impaired gallbladder washout efficacy. Utrasonographic values of bile exchanges were similar to those derived from scintigraphic-sonographic studies in comparable groups of subjects. This study provides new ultrasonographic variables, which better express gallbladder bile retention in gallstone patients and strongly discriminate gallstone patients from controls.

Adult↗

PubMed1995

Epidermal growth factor receptor immunoreactivity in gallbladder and extrahepatic biliary tract tumours.

Elevated levels of epidermal growth factor receptor (EGFR), a transmembrane protein tyrosine kinase receptor, are found in carcinomas from various sites of the body. We investigated the expression of EGFR in carcinoma of the gallbladder (n = 13), common bile duct (n = 7) and ampulla of Vater (n = 9). Non-malignant conditions investigated include chronic cholecystitis (n = 11), gallbladder dysplasia (n = 3) and adenoma (n = 1), and ampullary carcinoma in situ (CIS) (n = 2). Routine immunohistochemistry was employed using a monoclonal antibody against the EGFR protein. Immunostaining was assessed according to both intensity and extent of staining of cells. There was strong immunoreactivity for all gallbladder carcinoma and adenoma, the majority of common bile duct (n = 6; 86%) and ampullary (n = 6; 67%) carcinoma. In contrast, all cases of gallbladder dysplasia, the majority of cases of chronic cholecystitis (n = 7; 64%) and ampullary CIS (n = 2; 67%) had only weak to moderate immunoreactivity. The pattern of immunoreactivity was one of diffuse cytoplasmic and membranous staining. In conclusion, EGFR expression is increased in both gallbladder, common bile duct and ampullary carcinomas but not in non-malignant conditions of the gallbladder and biliary tract. These findings suggest that EGFR overexpression occurs late in the sequential development of gallbladder and biliary tract cancers.

Bile Duct Neoplasms↗

PubMed2003

Correlated expression of inducible nitric oxide synthase and P53, Bax in benign and malignant diseased gallbladder.

Our goal has been to investigate the expression and correlated significance of inducible nitric oxide synthase (iNOS) and P53, Bax in benign and malignant gallbladder diseases. We detected the expression of iNOS, P53 and Bax in the gallbladder wall by SP immunohistochemistry in 16 cases of chronic cholecystitis, 11 cases of chronic cholecystitis with adenomyoma and 24 cases of gallbladder adenocarcinoma. The percentage of positively marked tumor cells was counted under microscope and the intensity of immunoreactivity was graded. SPSS10.0 statistical software was applied for statistical analysis. In this study, we found that: (1) Both benign and malignant diseased gallbladder wall expressed iNOS and Bax. Compared to benign diseased gallbladders, their expression in adenocarcinoma was decreased (p < 0.05), P53 was expressed strongly only in nuclei of adenocarcinoma cells of some cases. (2) In benign and malignant diseased gallbladders, iNOS expression was related positively to Bax (p < 0.01), the expression of P53 and Bax had a negative relationship (p < 0.01). The results suggested that both chronic cholecystitis and chronic cholecystitis with adenomyoma carry the risk of becoming malignant, especially the latter. NO is an important mediated molecule in cancer, there are intimate relationships between gallbladder cancer and apoptosis.

Acute Disease↗

PubMed2003

Epidemiology of gallbladder cancer and trends in cholecystectomy rates in Scotland, 1968-1998.

The aim of this study was to describe the epidemiology of gallbladder cancer in Scotland during the last 30 years. A secondary aim was to describe trends in cholecystectomy rates because it has been suggested that changing rates of cholecystectomy for benign gallbladder disease may be influencing the epidemiology of gallbladder cancer. A retrospective analysis of cancer registration and mortality (gallbladder cancer) and hospital discharge (cholecystectomy) data from Scotland in 1968-1998 was carried out. In Scotland the incidence of, and mortality from, gallbladder cancer have been falling in women since at least 1968, and in men since the late 1980s. Whilst overall survival remains poor, survival in older patients may have improved recently, and survival is better in patients from affluent areas. Cholecystectomy rates increased until 1977 then fell until the introduction of laparoscopic surgery caused them to return to the rates previously observed. The current declining incidence of gallbladder cancer in Scotland is probably, in part, related to the increasing cholecystectomy rates seen prior to 1977. Further studies addressing changes in stage at diagnosis and treatment provided are required to investigate the recent apparent improvement in survival of elderly gallbladder cancer patients.

Adolescent↗

PubMed2001

Laparoscopic cholecystectomy does not demonstrably decrease survival of patients with serendipitously treated gallbladder cancer.

BACKGROUND: The purpose of this study was to evaluate the possibility that laparoscopic cholecystectomy has worsened the prognosis of patients with resected gallbladder cancer; particularly for patients whose cancer was accidentally resected. STUDY DESIGN: We conducted a retrospective review of Connecticut Tumor Registry data and data extracted from individual patient records at 15 of 30 hospitals in Connecticut reporting data to the Registry, at two separate time points, 1985-1988 (immediate prelaparoscopic era) and 1992-95 (laparoscopic cholecystectomy well established). There were 194 and 208 patients in each 3-year period, respectively. Additional information was extracted from hospital records in 82 and 91 patients, respectively. Twenty-five percent of patients in both data sets presented with "local" or Tis, T1, T2 disease. RESULTS: Three-year survival for localized disease was 29% in the prelaparoscopic period and 34% once laparoscopic cholecystectomy was established. But analysis of individual patient records indicated that 36% of patients from the laparoscopic period did not actually undergo a laparoscopic procedure. Fifty-nine patients had their gallbladder cancer discovered in the specimen postoperatively (serendipitously treated). A higher proportion of cancers were discovered postoperatively in the laparoscopic era (44% versus 24%). Three-year survival for these patients was 25%. If the data from the two eras are grouped according to whether or not the cancer-bearing gallbladder was manipulated laparoscopically, 24 of 59 patients (41%) turned out to be at risk for the possibility of increased laparoscopic dissemination of tumor. Survival of these patients (11-month median survival) was not statistically different from survival of patients whose serendipitously discovered gallbladder cancer was never manipulated laparoscopically (16-month median survival); p = 0.54 by log rank test. CONCLUSIONS: The widespread adoption of laparoscopic cholecystectomy did not worsen the survival of patients with gallbladder cancer, and patients with serendipitously treated gallbladder cancers did not have a worse survival after laparoscopic manipulation than after a standard open cholecystectomy. The laparoscopic aspects of operative manipulation of a gallbladder with cancer in it do not appear to be a proximate cause of the poor prognosis in this disease.

Aged↗

PubMedDate not supplied

Role of cyclooxygenase-2 for fluid secretion by the inflamed gallbladder mucosa.

Inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by activation of cyclooxygenase, which leads to an increase in prostaglandin formation. Cyclooxygenase exists as a constitutive (cyclooxygenase-l) and an inducible (cyclooxygenase-2) isoform. The aim of this study was to demonstrate the role of cyclooxygenase-2 in inflammatory fluid secretion of the feline gallbladder. Experiments were performed 10 weeks after a surgical procedure in which chronic cholecystitis was induced in cats by ligation of the cystic duct and implantation of a gallstone in the gallbladder. Gallbladder fluid transport was continuously monitored via a perfusion system. In inflammed gallbladders the continuous fluid secretion was reversed to absorption by intravenous injection of the selective cyclooxygenase-2 blocker, NS 398 (P <0.001). Increased levels of the inducible cyclooxygenase-2 were shown by immunoblotting in inflamed gallbladders. Selective pharmacologic blockage of cyclooxygenase-2 reduced the prostaglandin E2 release to the inflamed gallbladder lumen (P <0.01). These data suggest that cyclooxygenase-2 is involved in the inflammatory response during chronic cholecystitis. Selective cyclooxygenase-2 blockers may offer an alternative to traditional nonsterodial anti-inflammatory drugs with fewer side effects in patients with cholecystitis who are awaiting operation.

Animals↗

PubMed2003

Common presence of Helicobacter DNA in the gallbladder of patients with gallstone diseases and controls.

BACKGROUND: Several species of Helicobacter colonise the biliary tract of animals and cause hepatobiliary diseases. Helicobacter species have also been identified in the gallbladder of a high proportion of Chilean patients with gallbladder cancer. AIM: To determine the presence of Helicobacter species, particularly Helicobacter pylori and Helicobacter bilis, in the gallbladder of patients with non-malignant gallbladder diseases and control patients. PATIENTS AND METHODS: DNA was extracted from gallbladder samples from 122 consecutive patients undergoing cholecystectomy. The presence of Helicobacter genus-specific or Helicobacter pylori and Helicobacter bilis species-specific DNA was determined by polymerase chain reaction and sequence analysis. The presence of Helicobacter pylori-specific immunoglobulin G in the serum (n=84) and bile (n=104) samples was determined by enzyme linked immunosorbent assay. RESULTS: Helicobacter DNA was detected in 61 (50.0%) gallbladder samples: 29 of 60 (48.3%) patients with symptomatic gallstone, six of 10 (60.0%) patients with asymptomatic gallstones, 11 of 15 (73.3%) patients with other biliary diseases, and 15 of 37 (40.5%) control patients, respectively. Among them, 39 samples were positive for Helicobacter pylori but none were positive for Helicobacter bilis. Sequence analysis of Helicobacter genus-positive samples showed that 56 samples were Helicobacter pylori and five were Helicobacter species 'Liver 3' strain. Overall, there was no significant difference in the detection rate of Helicobacter DNA or the levels of serum and bile Helicobacter pylori-specific immunoglobulin G in the various biliary disease groups compared with control patients. Neither was there any significant difference in the blood biochemistry and liver function tests between patients with positive and negative Helicobacter DNA detection. CONCLUSION: Helicobacter species' DNA are commonly present in the gallbladder of patients with gallstone diseases and in controls, implying that Helicobacter infection alone may not play a significant role in the formation of gallstones. However, our results do not exclude the possibility of Helicobacter infection as a cofactor in the development of gallstones.

Antibodies, Bacterial↗

PubMed1998

Gallbladder volume: comparison of diabetics and controls.

Diabetics are known to have an increased prevalence of gallstones. The aim of this study was to investigate whether diabetics have increased gallbladder volumes that would predispose to stasis, nucleation of cholesterol crystals, and gallstone formation. The gallbladder volume of 271 diabetic subjects and 277 controls was determined by ultrasound using the ellipse formula. Gallbladder volume was also determined by the sum of the cylinders method in 143 cases with a strong correlation (r = 0.89) between the two methods. Using analysis of variance, gallbladder volume was influenced by both diabetic type (NIDDM = 33.68 cm3, IDDM = 26.84 cm3, controls = 29.05 cm3; P = 0.018) and the presence of gallstones (gallstones = 32.04 cm3, no gallstones = 27.58 cm3; P = 0.018). The variation in gallbladder volume between NIDDM, IDDM, and control subjects was influenced by the presence of gallstones (P = 0.024, interaction term from ANOVA). Significant differences (P < 0.001) were only found between NIDDM vs IDDM and NIDDM vs control in the nongallstone group (NIDDM = 34.33 cm3, IDDM = 25.08 cm3, control = 25.17 cm3). Males had significantly larger gallbladder volumes than females: 31.98 cm3 vs 27.74 cm3 (P = 0.023). After the inclusion of BMI, HDL cholesterol, triglyceride, and age in a statistical model with gender and diabetic type in those without gallstones, significant differences were still found between NIDDM and IDDM (P = 0.013) and NIDDM and controls (P = 0.005), demonstrating that NIDDM is an independent predictor for increased gallbladder volume.

Adult↗

PubMed1988

Sodium transport in the diseased human gallbladder and the effects of indomethacin.

1. Sodium ion (Na+) transport, a principal function of the gallbladder epithelium, was studied by measuring the flux of 22Na across isolated, inflamed human gallbladder mucosa maintained in a modified 'Ussing' flux chamber. Tissue was obtained from cholecystectomy specimens in symptomatic patients with cholelithiasis. 2. In 30 gallbladders studied, 57% had a net Na+ flux from mucosa to serosa (Na+ absorption), while 23% had a net Na+ flux from serosa to mucosa (Na+ secretion). The remaining 20% showed no overall net Na+ flux. 3. Indomethacin added to the serosal fluid reversed the direction of net Na+ flux in secreting gallbladders and caused an absorption of Na+. In Na+-absorbing gallbladders, indomethacin caused a slight reduction in Na+ absorption. No change in Na+ flux was induced in gallbladders with no initial net Na+ flux. 4. These results demonstrate that instead of absorbing Na+, some inflamed human gallbladders may secrete Na+. As this secretion can be reversed to the more usual absorption by indomethacin, it is likely that this secretion is mediated by prostaglandins.

Biological Transport, Active↗

PubMed2002

Acetazolamide inhibits stimulated feline liver and gallbladder bicarbonate secretion.

Bile acidification is a key factor in preventing calcium carbonate precipitation and gallstone formation. Carbonic anhydrase II (CA II), that is inhibited by acetazolamide, plays a role in regulation of the acid-base balance in many tissues. This study examines the effect of acetazolamide on secretin- and vasoactive intestinal peptide (VIP)-stimulated gallbladder mucosal bicarbonate and acid secretion. Gallbladders in anaesthetized cats were perfused with a bicarbonate buffer bubbled with CO2 in air. In 20 experiments VIP (10 microg kg(-1) h(-1)) and in 10 experiments secretin (4 microg kg(-1) h(-1)) were infused continuously intravenous (i.v.). Hepatic bile and samples from the buffer before and after perfusion of the gallbladder were collected for calculation of ion and fluid transport. During basal conditions a continuous secretion of H+ by the gallbladder mucosa was seen. Intravenous infusion of vasoactive intestinal peptide (VIP) and secretin caused a secretion of bicarbonate from the gallbladder mucosa (P < 0.01). This secretion was reduced by intraluminal (i.l.) acetazolamide (P < 0.01). Bile flow was enhanced by infusion of VIP and secretin (P < 0.01) but this stimulated outflow was not affected by i.v. acetazolamide. The presence of CA II in the gallbladder was demonstrated by immunoblotting. Biliary CA activity has an important function in the regulation of VIP- and secretin-stimulated bicarbonate secretion across the gallbladder mucosa.

Acetazolamide↗

PubMed2000

Gallbladder motility and cholesterol crystallization in bile from patients with pigment and cholesterol gallstones.

BACKGROUND: Little is known about gallbladder motility in patients with black pigment stones when compared to cholesterol gallstone patients, or about their relationship to biliary composition, crystallization and stone characteristics. DESIGN: Fasting and postprandial gallbladder volumes were studied by ultrasonography in 49 gallstone patients with pigment (n = 14) or cholesterol (n = 35) stones and 30 healthy controls. After cholecystectomy stone composition, gallbladder wall inflammation, cholesterol saturation index and appearance of platelike cholesterol crystals in bile were evaluated in gallstone patients. RESULTS: Fasting gallbladder volume was significantly (P < 0.05) increased in cholesterol stone patients (31.7 +/- 1.9 mL) but not in pigment stone patients (21.9 +/- 3.1 mL), compared to controls (21.0 +/- 1.5 mL). Postprandial emptying was delayed in patients (half-emptying time: 31 +/- 2 min, 35 +/- 3 min, 24 +/- 2 min in cholesterol stone patients, pigment stone patients and controls, respectively, P < 0.05) and incomplete (residual volume: 43.2 +/- 2.7%, 40.0 +/- 4.3%, 15.8 +/- 1.6% min in cholesterol stone patients, pigment stone patients and controls, respectively, P < 0.05). The inflammation of the gallbladder wall was mild or absent in all cases. Biliary cholesterol saturation index was 152.3 +/- 8.5% and 92.9 +/- 4.8% in patients with cholesterol and pigment stones, respectively (P < 0.01). Whereas cholesterol crystals never appeared during 21 days in biles from patients with pigment stones, crystal observation time in patients with cholesterol gallstone was 5 days (median) and was significantly shorter in patients with multiple (4 days) than in patients with solitary (12 days) cholesterol stones (P = 0.0019). CONCLUSIONS: Patients with black pigment stones who do not have excess cholesterol and do not grow cholesterol crystals in bile have decreased gallbladder emptying, although to a lesser extent than patients with cholesterol stones. Thus, gallbladder stasis is likely to put a subset of subjects at risk for the formation of pigment gallstones, and pathogenic mechanisms need to be further investigated.

Adult↗

PubMed2000

Effects of phospholipase A2, free fatty acids and 2-lysolecithin on the crystallization of cholesterol in gallbladder bile.

BACKGROUND: Phospholipase A2 (PLA2) and its enzymatic products free fatty acids (FFAs) and 2-lysolecithin are physiological constituents of bile. Their role in the crystallization of cholesterol in gallbladder bile of patients with cholesterol gallstones is still controversial. DESIGN: To clarify this issue we evaluated the activity of PLA2 and the concentration and pattern of FFAs in the gallbladder bile of cholesterol stone patients. We furthermore added PLA2, FFAs and 2-lysolecithin to isotropic gallbladder bile, determined the crystal observation time (COT) and counted the cholesterol crystals in a crystal growth assay for up to 21 days. RESULTS: A PLA2 activity of 1.8 +/- 1.2 U L(-1) and total FFA concentrations of 1.32 +/- 0.71 mmol L(-1) were determined. After incubation of bile for 24 h at 37 degrees C total FFAs increased to 2.72 +/- 1.29 mmol L(-1) (P<0.005). Biliary saturated and unsaturated FFAs were found in equal proportions before and after incubation, pointing to an additional presence of lipases other than PLA2. A COTof 1 day was observed in all gallbladder biles and increased to 1.7 +/- 0.5 days after addition of 5 U L(-1) of PLA2 (P<0.01). An even higher COT of 2.5 +/- 0.8 days was seen after addition of 5 mmol L(-1) of a 'biliary' mixture of FFAs (P<0.005) but the COT remained unchanged after addition of 5 mmol L(-1) of 2-lysolecithin. However, in the crystal growth assay in gallbladder bile addition of 5 U L(-1) of PLA2, of 5 mmol L(-1) of 'biliary' FFAs and of 5 mmol L(-1) of 2-lysolecithin decreased significantly the number of cholesterol crystals formed during follow-up. CONCLUSION: An elevated activity of PLA2 in gallbladder bile may counteract the formation of cholesterol crystals through increased formation of FFAs and 2-lysolecithin. However, regarding the comparatively low activity of PLA2 in gallbladder bile PLA2 seems to be of only minor pathophysiological importance in the formation of cholesterol gallstones.

Adult↗

PubMed2001

Cisapride improves gallbladder emptying and bile lipid composition in patients with gallstones.

BACKGROUND AND AIM: Biliary cholesterol supersaturation, gallbladder stasis and delayed intestinal transit are the key events in cholesterol gallstone formation. We studied the effect of cisapride, a prokinetic drug, on gallbladder emptying and bile composition in patients with gallstone disease undergoing cholecystectomy. METHODS: Gallbladder emptying, cholesterol saturation index (CSI) and nucleation time were studied in 21 patients with gallstone disease. Eleven patients (cisapride group, age 41.9 +/- 2.9 years) received tablet cisapride 10 mg t.i.d. for 2 weeks, while 10 patients (placebo group, age 42.1 +/- 1.9 years) received placebo for the same duration. Gallbladder emptying was repeated in all patients after a 2-week treatment with cisapride or placebo. Gallbladder bile was obtained at the time of surgery for the measurement of CSI and nucleation time. RESULTS: Residual volume of the gallbladder decreased (mean +/- SE, 18.6 +/- 2.5 mL vs 10.0 +/- 1.1 mL, P = 0.007), and the ejection fraction increased (43.5 +/- 5.3% vs 60.0 +/- 3.2%, P = 0.007) in patients in the cisapride group, while no change was observed in placebo group patients. Nucleation time was higher in the cisapride group than in the placebo group (14.9 +/- 1.3 days vs 8.0 +/- 0.9 days, P = 0.003). Patients in the cisapride group had a significantly lower cholesterol concentration (molar percentage, 5.1 +/- 0.3% vs 6.8 +/- 0.8%, P = 0.049) and CSI (1.0 +/- 0.1 vs 1.36 +/- 0.11, P = 0.034) than patients in the placebo group. CONCLUSION: Cisapride improves gallbladder emptying and bile lithogenicity in patients with gallstone disease.

Adult↗

PubMed2002

Endothelin-3 induces both human and opossum gallbladder contraction mediated mainly by endothelin-B receptor subtype in vitro.

BACKGROUND: Endothelins are produced by gallbladder epithelial cells, suggesting a role in the regulation of gallbladder function. AIMS: To characterize the effect of endothelin-3 (ET-3) on human and Australian possum gallbladder contractility and identify the receptor(s) involved. METHODS: Human and possum gallbladder muscle strips were exposed to cumulative concentrations of ET-3 (10 pmol/L-100 nmol/L). Strips were pretreated with either tetrodotoxin (TTX) (1 micro mol/L), the selective ET receptor antagonists BQ-123 (ET(A)), BQ-788 (ET(B)), alone or together, or the mixed ET antagonist tezosentan (all 1 micro mol/L). Maximal changes in tone were measured and expressed as percentage of carbachol (100 micro mol/L)-induced tone. ANOVA was used for statistical analysis. RESULTS: Endothelin-3 induced a concentration-dependent increase in tone in both human and pos-sum strips (P < 0.05) and at 100 nmol/L represented 44.2 +/- 4.5% and 40.3 +/- 4.6% of carbachol-induced tone, respectively. The effect on human strips was TTX insensitive, whereas the possum concentration-response curve was shifted to the right. Individually, BQ-123 and BQ-788 shifted the human concentration-response curve to the right, but a greater inhibition by BQ-788 was achieved in the possum (P < 0.05). However, BQ-123 plus BQ-788 further reduced the ET-3 effect (P < 0.001) to a level comparable to that observed in the presence of tezosentan in both human and possum strips. CONCLUSION: Endothelin-3 produces potent gallbladder contraction in vitro, acting mainly via ET(B) receptors and also interacting with ET(A)receptors. The receptors are located on the smooth muscle, but in possum gallbladder, neural receptors may also be involved. These findings suggest that ET-3 may regulate motility of possum and human gallbladder.

Adult↗

PubMed1996

Early mucosal changes of the gallbladder in patients with anomalous arrangement of the pancreaticobiliary duct.

BACKGROUND & AIMS: Anomalous arrangement of the pancreaticobiliary duct (AAPBD) is frequently associated with gallbladder cancer. The aim of this study was to characterize the early epithelial changes of the gallbladder that might be associated with carcinogenesis in patients with AAPBD. METHODS: Routinely fixed tissue specimens obtained from pediatric patients with AAPBD and control patients were examined histologically with H&E, periodic acid-Schiff, and argyrophilic nucleolar organizer region (AgNOR) staining. RESULTS: Epithelial hyperplasia was frequently observed in the gallbladder of patients with AAPBD but not in patients without this anomaly. The incidence of epithelial hyperplasia was significantly higher in the gallbladder of patients in whom the major pancreatic duct joined the common bile duct (P-C type) than in patients in whom the common bile duct joined the pancreatic duct (C-P type). The mean AgNOR number in the gallbladder mucosa was significantly higher in patients with AAPBD than in patients without AAPBD. Patients with C-P type AAPBD had a significantly higher mean AgNOR number of the gallbladder mucosa than patients with C-P type AAPBD. CONCLUSIONS: Patients with AAPBD, especially those with the P-C type anomaly, have increased cellular proliferative activity of the gallbladder mucosa in early childhood.

Bile Ducts↗

PubMed2001

Expression and localization of the multidrug resistance proteins MRP2 and MRP3 in human gallbladder epithelia.

BACKGROUND & AIMS: The multidrug resistance protein (MRP) isoforms MRP2 (ABCC2) and MRP3 (ABCC3) play a decisive role in the hepatic secretion of endogenous and xenobiotic conjugates and are differentially expressed in hepatocytes and cholangiocytes. The epithelium of the gallbladder considerably modifies the composition of primary hepatic bile by absorption and secretion; however, the underlying transport mechanisms were largely unknown. Localization of MRP2 and MRP3 may provide an explanation of how the products of phase II conjugation are effluxed from gallbladder epithelia. METHODS: Expression and localization of MRP2 and MRP3 were analyzed by reverse-transcription polymerase chain reaction (RT-PCR) and immunofluorescence microscopy of human gallbladder tissue. RESULTS: Expression of MRP2 and MRP3 was identified in all gallbladders by RT-PCR followed by sequencing of the amplified fragments. Double immunofluorescence microscopy using 2 specific antibodies for the respective MRP isoform showed the simultaneous expression of MRP2 in the apical membrane and MRP3 in the basolateral membrane of gallbladder epithelia. MRP1 protein expression was not detectable. CONCLUSIONS: Our findings show the expression of MRP2 and MRP3 in distinct plasma membrane domains of gallbladder epithelia and provide evidence for the capacity of the gallbladder to secrete xenobiotic and endogenous anionic conjugates into blood via MRP3 and into bile via MRP2.

Aged↗

PubMed2000

Influence on gallbladder volume of early postoperative gastric supply of nutrients.

BACKGROUND & AIM: The gallbladder volume is a predictor of biliary stasis and the formation of biliary sludge. Biliary stasis and sludge have been recently recognized as the precursors of acute acalculous cholecystitis, as well as 'idiopathic' postoperative pancreatitis, rare but very serious complications after surgery. The aim of the study was to establish how early postoperative gastric supply of nutrients affects the gallbladder volume in patients after noncardiac and cardiac surgery. METHODS: In the two prospective, randomized studies 40 patients (study I-noncardiac surgery) treated at surgical ICU after major elective extrahepatobiliary and extragastrointestinal surgeries (7 thoracic, 19 vascular, 14 urological) and 40 patients (study II-cardiac surgery) treated at cardiosurgical ICU after CABG surgery were analyzed. In both studies the patients were divided into two groups: control group C (study I: 20 patients, age 45+/-18 yrs, male 65%; study II: 20 patients age 58+/-7 yrs, male 60%) and group E (group of early postoperative gastric supply of nutrients) (study I: 20 patients, age 52+/-17 yrs, male 50%; study II: 20 patients; age 59+/-8 yrs, male 65%). For the first 24 hours the patients in group C received only crystalloid solutions and the gallbladder volume was verified 24 hours after the surgery. In group E, postoperative gastric supply of nutrients began 18 hours after surgery (Osmolite, Ross; first 3 hours 30 ml/h and second 3 hours 50 ml/h; total 240 ml after 6 hours). In all patients sonographic measurement of gallbladder volume was performed immediately before surgery and 6 hours after the start of feeding (24 hours after surgery). The measurement was done with ultrasonographic scanner Hitachi 405 EUB (convex probe 3.5-5MHz) by the same specialist, and the volume was calculated using the ellipsoid method. RESULTS: The gallbladder volume measured by ultrasonography 24 hours after surgery in study I (noncardiac surgery) in group E amounted to 43+/-25 ml while in control group C it was significantly higher, i.e. 67+/-30 ml (P<0.05). In study II (cardiac surgery) in group E gallbladder volume amounted to 59+/-15 ml while in control group C it was also significantly higher, i.e. 71+/-11 ml (P<0.05). CONCLUSION: An early postoperative gastric supply of nutrients after both noncardiac and cardiac adult surgery diminishes the volume and probably stimulates the motility of the gallbladder, thus preventing biliary stasis and the formation of biliary sludge.

Adult↗

PubMed2003

[Unsuspected gallbladder carcinoma--the CAE-S/CAMIC registry].

INTRODUCTION: Results of earlier surveys raised the prospect that laparoscopic surgical procedures may specifically increase the risk of port wound metastasis and generally of tumour cell seeding if at the time of operation an unsuspected gallbladder cancer existed. Other observations lead to presume that laparoscopic technique could deteriorate the prognosis of gallbladder cancer. These assumptions are going to be verified by the CAES/ CAMIC-registry. MATERIAL AND METHOD: The Workgroup Surgical Endoscopy (CAE) of the German Society of Surgery has started 1997 a registry of all cases of cholecystectomy--laparoscopic as well open--with a postoperative incidental finding of a gallbladder carcinoma. The aim of our registry is to compare the prospectively collected follow up data on the outcome of these patients and to answer the question whether laparoscopic cholecystectomy affects the course and the prognosis of patients with unsuspected gallbladder cancer. RESULTS: Until now 142 cases of incidental gallbladder cancer following laparoscopic and 79 cases following open cholecystectomy as well as 24 cases after intraoperative conversion to the open procedure have been recorded. The median follow up runs up to 27 (1-69) months. Following laparoscopic primary procedure we registered 10 port site metastases (7 %), following open primary procedure 4 (5.1 %) wound recurrences. The total recurrence rate at the moment is about 27 % after laparoscopic treatment and 31 % for conventionally operated patients. 70 of the 245 patients underwent a second radical procedure after diagnosis of gallbladder carcinoma. A postoperative combined radio- and chemotherapy was undertaken in 4 cases, a chemotherapy alone in 14 cases. 64 patients already died due to the underlining disease. DISCUSSION: At the present, after a median follow up of 27 months, the incidence of abdominal wall recurrences is very similar following laparoscopic and conventional procedure (7 % vs. 5.1 %). The total incidence of recurrences is at the moment slightly higher following open cholecystectomy (31 % vs. 27 %). The access technique, open or laparoscopic, doesn't seem to influence the prognosis of unsuspected gallbladder carcinoma. Until now we could not find disadvantages for the laparoscopically operated group.

Adenocarcinoma↗