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PubMed2002

Epithelial cyst of the gallbladder associated with adenocarcinoma.

Epithelial cyst of the gallbladder associated with papillary adenoma and adenocarcinoma is presented herein. A 70-year-old male patient with general malaise was admitted to our hospital during the follow-up of an elevated mucosal lesion in the fundus of the gallbladder. Endoscopic ultrasonography revealed a cystic lesion adjacent to the elevated lesion, and interruption of the hyperechoic third layer of the gallbladder wall next to the gallbladder bed of the liver. He was diagnosed as having an epithelial cyst of the gallbladder associated with gallbladder carcinoma that directly invaded the gallbladder bed. He underwent resection of the gallbladder with partial resection of the liver and regional lymph node dissection. The resected specimen, which showed multiple cysts with septum formation, measured 1.9 cm in size and was located in the subserosal layer of the gallbladder wall. The wall of the cyst was lined with columnar epithelium and papillary adenoma, and adenocarcinoma was scattered in some portions of the cyst wall. Furthermore, papillary adenoma associated with adenocarcinoma was independently identified in the luminal surface of the gallbladder epithelium covering the cysts. These histological findings were compatible with epithelial cyst of the gallbladder associated with papillary adenoma and adenocarcinoma. The tumor was diagnosed as T1bN0M0, stage I, in the TNM clinical classification. To our knowledge, this is the first report of an epithelial cyst of the gallbladder associated with papillary adenoma and adenocarcinoma, and provides some insight into the relationship between epithelial cyst and adenoma or cystadenocarcinoma of the gallbladder.

Adenocarcinoma↗

PubMed1986

Gallbladder filling and emptying during cholesterol gallstone formation in the prairie dog. A cholescintigraphic study.

We studied gallbladder bile flow before, during, and after cholesterol gallstone formation in the prairie dog using infusion cholescintigraphy with 99mTc-diethyl iminodiacetic acid. In 18 fasting animals partitioning of bile between gallbladder and intestine was determined every 15 min for 140 min, and gallbladder response to cholecystokinin (5 U/kg X h) was calculated from the gallbladder ejection fraction. Ten prairie dogs were then placed on a 0.4% cholesterol diet and 8 on a regular diet, and the studies were repeated 1, 2, and 6 wk later. The proportion of hepatic bile that entered the gallbladder relative to the intestine varied from one 15-min period to the next, and averaged 28.2% +/- 5.1% at 140 min. Partial spontaneous gallbladder emptying (ejection fraction 11.5% +/- 5.6%) was intermittently observed. Neither the number nor the ejection fraction of spontaneous gallbladder contractions changed during gallstone formation. By contrast, the percent of gallbladder emptying in response to cholecystokinin decreased from 72.1% +/- 5% to 25.9% +/- 9.3% (p less than 0.025) in the first week and was 14.3% +/- 5.5% at 6 wk (p less than 0.01 from prediet values, not significant from first week). Gallbladder filling decreased from 28.2% +/- 5.1% to 6.7% +/- 3% (p less than 0.01), but this change was only observed after 6 wk, when gallstones had formed. This study shows that bile flow into the gallbladder during fasting is not constant; the gallbladder contracts intermittently; gallbladder emptying in response to exogenous cholecystokinin is altered very early during gallstone formation; and gallbladder filling remains unaffected until later stages, when gallstones have formed.

Animals↗

PubMed1994

Normal fasting volume and postprandial emptying of the denervated donor gallbladder in liver transplant recipients.

BACKGROUND/AIMS: Truncal vagotomy causes gallbladder dilatation and possibly cholelithiasis. During liver transplantation, when the gallbladder is transplanted with the donor liver, the gallbladder and liver are extrinsically denervated. The aim of this study was to determine whether extrinsic denervation affects gallbladder volume and postprandial emptying. METHODS: To evaluate fasting gallbladder volume, 26 transplant recipients underwent ultrasonography. Twenty-eight normal volunteers were controls. To evaluate postprandial contractility, seven transplant recipients underwent radionuclide gallbladder-emptying studies. Gastric emptying and cholecystokinin release were simultaneously determined after a fatty meal to exclude a difference in gallbladder stimulus. Sixteen normal volunteers were controls. RESULTS: There were no differences in fasting gallbladder volume or postprandial contractility, gastric emptying, and cholecystokinin release between transplant patients and controls. Median fasting and postprandial gallbladder volumes for the transplant recipients (95% confidence) were 16 mL (12-34 mL) and 3 mL (0-8 mL), respectively, and for controls were 18 mL (13-21 mL; P = 0.73) and 3 mL (1-6 mL; P = 0.97), respectively. CONCLUSIONS: These data do not show gallbladder dilatation or impaired postprandial gallbladder contraction in the extrinsically denervated gallbladder. This finding suggests that gallbladder dilatation may be caused by the unopposed activity of the sympathetic system after truncal vagotomy.

Adult↗

PubMed2001

Association of p53, p16, and vascular endothelial growth factor protein expressions with the prognosis and metastasis of gallbladder cancer.

BACKGROUND: Tumor suppressor genes were studied in gallbladder disease including cancer for correlation. VEGF (vascular endothelial growth factor) expression was assessed against Nevin staging and metastasis of gallbladder carcinoma. The importance of p53, p16, and VEGF in gallbladder cancer was estimated. STUDY DESIGN: Twenty-four gallbladder carcinomas, 20 gallbladder adenomas, and 18 chronic cholecystitis specimens were immunohistochemically and histopathologically investigated for the relation of p53, p16, and VEGF to Nevin staging and pathologic grading. RESULTS: The expression rate of abnormal p53 in gallbladder carcinomas was significantly higher than that in gallbladder adenoma and chronic cholecystitis (p = 0.003, p = 0.014). The expression rate of abnormal p53 in Nevin staging S1, S2, S3 gallbladder carcinoma was significantly higher than that in S4, S5 (p = 0.01). Abnormal p16 was highest in carcinoma, next in adenoma, and lowest in chronic cholecystitis (p = 0.031, p = 0.017). Gallbladder carcinoma expressed VEGF far more often than adenoma or cholecystitis (p = 0.001); VEGF-positive rates were lower in S1, S2, S3 than S4, S5 by Nevin staging of gallbladder cancer (p = 0.044). CONCLUSION: Mutation of p53 and p16 genes might correlate with progression of of gallbladder carcinoma. Analysis of p53 and p16 can estimate the prognosis of gallbladder cancer. VEGF expression correlates with Nevin staging in gallbladder cancer.

Adenoma↗

PubMed1981

Role of gallbladder mucus hypersecretion in the evolution of cholesterol gallstones.

Because mucin glycoproteins may be important in the pathophysiology of gallstones, we studied the relationship among biliary lipids, gallbladder mucin secretion, and gallstone formation in cholesterol-fed prairie dogs. Organ culture studies of gallbladder explants revealed that the incorporation of [(3)H]glucosamine into tissue and secretory gallbladder glycoproteins was significantly increased at 3, 5, 8, and 14 d of feeding. Peak secretion of labeled mucin occurred at 5 d, when total tissue and secreted glycoprotein production was fivefold greater than control. Gel filtration of the secreted glycoprotein on Sepharose 4B indicated that the majority of radioactivity was present in a macromolecule of > 1 million molecular weight. The increased secretion of gallbladder mucin was organ specific, in that [(3)H]glucosamine incorporation into glycoproteins of stomach and colon was unaffected by cholesterol feeding. Similarly, the incorporation of [(3)H]mannose into gallbladder membrane glycoproteins was not altered by cholesterol feeding. The rate of glycoprotein synthesis and secretion returned to normal upon withdrawal of the cholesterol diet, and ligation of the cystic duct before cholesterol feeding prevented gallbladder mucin hypersecretion. Both results indicate that the stimulus to mucin secretion was a constituent of bile. Gallbladder bile after 5 d contained cholesterol in micelles, liquid crystals, and crystals, whereas hepatic bile remained a single micellar phase throughout cholesterol feeding. For this reason the cholesterol-saturation indices of gallbladder bile were compared in both homogenized and centrifuged samples. The micellar phase of gallbladder bile was appreciably less saturated than homogenized bile at 5 and 8 d, which reflects the continuous nucleation of cholesterol in the gallbladder. Purified human gallbladder mucin gels were shown to induce nucleation of lecithin-cholesterol liquid crystals from supersaturated hepatic bile. These in turn gave rise to cholesterol monohydrate crystals within 18 h. Control supersaturated hepatic bile could not be nucleated by the addition of other proteins, and was stable for days upon standing. These results suggest that the increase in cholesterol content of bile in cholesterolfed prairie dogs stimulates gallbladder mucus hypersecretion, and that gallbladder mucus gel is a nucleating agent for biliary cholesterol.

Animals↗

PubMed1992

Percutaneous chemical gallbladder sclerosis after laser-induced cystic duct obliteration: results in an experimental model.

OBJECTIVE: Chemical gallbladder sclerosis has been attempted as a way to defunctionalize the gallbladder in patients who have undergone nonsurgical removal of gallstones and who are unable to undergo surgical/laparoscopic cholecystectomy. The purpose of this investigation was threefold: to study an animal model for chemical sclerosis of the gallbladder with 95% ethanol and 3% sodium tetradecyl sulfate, to attempt chemical sclerosis immediately after percutaneous cystic duct obliteration by laser thermocoagulation, and to assess histopathologic changes in the gallbladder after sclerosis. MATERIALS AND METHODS: Percutaneous cholecystostomy and laser thermocoagulation of the cystic duct was performed in 13 pigs. Eight pigs underwent immediate gallbladder sclerosis with 95% ethanol and 3% sodium tetradecyl sulfate while two pigs received 95% ethanol only. The remaining three pigs served as controls. The cholecystostomy catheter was removed immediately after the procedure. All animals were sacrificed 6 weeks after laser thermocoagulation. Multiple sections through the gallbladder, which included the adjacent liver, the cystic duct, and the common bile duct, were obtained for histologic examination. RESULTS: At autopsy, the gallbladder in all 10 animals who underwent gallbladder sclerosis was reduced in size compared with controls. In all treated animals, the gallbladder mucosa was denuded; however, in nine of 10 cases reepithelialization had occurred. Complete sclerosis without reepithelialization was achieved in one pig who received both ethanol and sodium tetradecyl sulfate. In the two animals who received ethanol only, the depth of wall necrosis around the gallbladder lumen was less than in those pigs who received both ethanol and sodium tetradecyl sulfate. No pigs showed signs of hepatic necrosis or injury to the common bile duct. CONCLUSION: Cystic duct laser thermocoagulation allows immediate gallbladder sclerotherapy without injury to the common bile duct. Sclerosis with ethanol and sodium tetradecyl sulfate results in denudation of the gallbladder mucosa. However, a single therapeutic session with immediate removal of the cholecystostomy catheter was inadequate for gallbladder ablation in this model because of reepithelialization.

Animals↗

PubMed2002

Mucin gene expression in gallbladder epithelium.

BACKGROUND AND PURPOSE: The interaction of mucus, calcium and lipid is important in gallstone formation. The epithelium in stone-containing gallbladders has more mucin than in gallbladders without stones. There is altered mucin gene expression in black pigment stone-bearing gallbladders. In this study, we evaluated mucin gene expression in gallbladders containing cholesterol stones or calcium bilirubinate stones, and gallbladders without stones. METHODS: In situ hybridization with digoxigenin-tailed oligonucleotides was performed on sections of paraffin-embedded epithelial tissue from gallbladders with cholesterol stones (n = 14) or calcium bilirubinate stones (n = 12), and those without stones (n = 10) to identify expression of MUC1, MUC2, MUC3, MUC4, MUC5B, and MUC6. RESULTS: The findings showed mRNA expression of MUC3, MUC5B and MUC6 in most gallbladders in all three groups, but stronger and extensive expression of these mRNAs in gallbladders with stones. MUC2 and MUC4 labeling was absent in gallbladders without stones, but MUC2 labeling was found in 14% and MUC4 in 50% of gallbladders with cholesterol stones. MUC2 expression was found in 25% and MUC4 in 58% of gallbladders with bilirubinate stones. Increased expression of MUC1 was found in gallbladders with cholesterol stones (79%) and calcium bilirubinate stones (83%) compared to those without stones (30%). CONCLUSION: Altered mucin gene expression was found in gallbladders with cholesterol stones and calcium bilirubinate stones, as evidenced by the presence of MUC2 and MUC4 and the increased expression of MUC1, MUC3, MUC5B and MUC6.

Adult↗

PubMedDate not supplied

Insulin resistance causes human gallbladder dysmotility.

Obesity, diabetes, and hyperlipidemia are known risk factors for the development of gallstones. A growing body of animal and human data has correlated insulin resistance with organ dysfunction. The relationship among obesity, diabetes, hyperlipidemia, and abnormal gallbladder motility remains unclear. Therefore, we designed a study to investigate the association among obesity, insulin resistance, hyperlipidemia, and gallbladder dysmotility. One hundred ninety-two healthy adult nondiabetic volunteers were studied. Gallbladder ultrasounds were performed before and after a standardized fatty meal. A gallbladder ejection fraction (EF) was calculated, and an EF of < 25% was considered abnormal. Serum was analyzed for cholesterol, triglycerides, cholecystokinin, leptin, glucose, and insulin. The homeostasis assessment model (HOMA) was used to determine insulin resistance. The volunteers had a mean age of 38 years (range, 18-77), and 55% were female. Thirty subjects (15%) had gallstones and were excluded from the study. Thirty subjects (19%) had abnormal gallbladder motility (EF < 25%). In lean subjects (n = 96) fasting glucose was significantly increased in the 16 subjects with gallbladder EF < 25% versus the 80 subjects with gallbladder EF > 25% (109 +/- 20 mg/dl versus 78 +/- 2 mg/dl, P < 0.05). Similarly, the HOMA index was significantly greater in subjects with gallbladder EF < 25% versus gallbladder EF >25% (3.3 +/- 1.2 versus 2.0 +/- 0.2, P < 0.05). In obese subjects (n = 66), fasting glucose, insulin, and insulin resistance were not associated with a gallbladder EF < 25%. These data suggest that in lean, nondiabetic volunteers without gallstones, gallbladder dysmotility is associated with an elevated fasting glucose as well as a high index of insulin resistance. We conclude that insulin resistance alone may be responsible for gallbladder dysmotility that may result in acalculous cholecystitis or gallstone formation.

Adolescent↗

PubMed2003

Case of mucinous adenocarcinoma with porcelain gallbladder.

Histologically, the majority of gallbladder cancers are adenocarcinomas. Among the adenocarcinomas, the mucinous adenocarcinoma is relatively uncommon. Porcelain gallbladder is a rare finding and the risk of gallbladder cancer is significantly increased in porcelain gallbladder. We describe a rare case of mucinous adenocarcinoma with porcelain gallbladder. A 46-year-old man was admitted to Chonnam National University Hospital with a 2-week history of right upper quadrant pain. Three and 2 years previously, he had two episodes of cholecystitis with gallstones. An abdominal computed tomography revealed a contracted gallbladder with circumferential mural calcification, and the possibility of gallbladder cancer and porcelain gallbladder were considered. At laparotomy, cholecystectomy, liver wedge resection, and radical lymph node dissection were performed. The resected gallbladder showed thickened wall, luminal narrowing and mucosal irregularity. A histological examination of the resected gallbladder showed a mucinous adenocarcinoma composed of poorly differentiated glandular cells with mucin lakes. Porcelain gallbladder may be an end result of a chronic inflammatory reaction, and this change is associated with the development of gallbladder cancer.

Adenocarcinoma, Mucinous↗

PubMed2001

Medium-term effects of endoscopic papillary balloon dilation on gallbladder motility.

BACKGROUND: Endoscopic papillary balloon dilation (EPBD) for removal of bile duct stones tends to preserve papillary function. However, EPBD may exert beneficial or deleterious effects on gallbladder motility. This was a prospective, medium-term investigation (2 years) of the effects of EPBD on gallbladder motility. METHODS: Twelve patients with intact gallbladders (6 with and 6 without gallbladder stones) who underwent EPBD for choledocholithiasis were enrolled in this study. Gallbladder motility was examined before EPBD and at 7 days, 1 month, 1 year, and 2 years after EPBD. Gallbladder volumes, measured after fasting and after ingestion of dried egg yolk, were determined by US. RESULTS: All patients were asymptomatic during the 2-year follow-up period. Before EPBD, particularly in patients with cholelithiasis, the gallbladder had a larger fasting volume and lower yolk-stimulated maximum contraction compared with normal control subjects. Seven days after EPBD, fasting volume was decreased and maximum contraction was increased, both significantly compared with pre-EPBD values and regardless of the presence or absence of gallbladder stones. At 1 month, 1 year, and 2 years after EPBD, these changes were far less evident and gallbladder function did not differ significantly from baseline. CONCLUSION: EPBD does not adversely affect gallbladder motility in the medium-term (2 years). In terms of gallbladder motility, EPBD does not appear to increase the future risk of acute cholecystitis or gallbladder stone formation.

Aged↗

PubMed1997

Gallbladder motility in response to sham feeding and cholecystokinin in lean and obese subjects.

The risk of developing gallstones is increased in obese subjects. We have investigated whether gallbladder motility in obese subjects is different from that in lean control subjects. In 25 healthy non-diabetic obese subjects and 20 age- and sex-matched lean controls, fasting gallbladder volumes, gallbladder contraction in response to cephalic vagal cholinergic stimulation by modified sham feeding (MSF) and to hormonal stimulation with cholecystokinin (CCK) were studied. Gallbladder volumes were measured during a 30-min MSF period followed 1 h later by a 1-hour continuous i.v. infusion of 0.5 IDU/kg ideal weight of CCK-33. Fasting gallbladder volumes were significantly (p < 0.001) larger in obese (47 +/- 4 cm3) compared to lean subjects (24 +/- 2 cm3). Fasting gallbladder volume was correlated with body mass index (p < 0.01). Gallbladder contraction during MSF was significantly (p < 0.01) reduced in obese (12 +/- 2%) compared to lean subjects (22 +/- 3%). CCK infusion, leading to physiological post-prandial plasma CCK levels, induced a significantly (p < 0.001) greater absolute gallbladder contraction in obese (27 +/- 3 cm3) compared to lean subjects (15 +/- 1 cm3) but the percentage gallbladder contraction was in the same range (64 +/- 3% vs. 67 +/- 4%, respectively). In addition, residual gallbladder volumes after CCK infusion were significantly (p < 0.001) larger in obese (15 +/- 2 cm3) than in lean subjects (7 +/- 1 cm3). Two groups of obese subjects were identified: one with increased (>40 cm3) and one with normal (< or = 40 cm3) fasting gallbladder volumes. Only obese subjects with increased fasting volumes showed abnormal gallbladder motility.

Adult↗

PubMedDate not supplied

Laparoscopic cholecystectomy in patients with porcelain gallbladder based on the preoperative ultrasound findings.

BACKGROUND/AIMS: Porcelain gallbladder is considered a relative contraindication to laparoscopic cholecystectomy, because of a high incidence of gallbladder cancer or gastrointestinal cancer. We examined the management of laparoscopic cholecystectomy in patients with porcelain gallbladder. METHODOLOGY: 1,608 patients underwent cholecystectomy and 13 (0.81%) patients had porcelain gallbladder. All patients underwent preoperative spiral computed tomography after intravenous infusion cholangiography and intraoperative cholangiography. Patients with porcelain gallbladder were classified as Type I to III according to preoperative ultrasound findings. The Type I porcelain gallbladder was indicated for laparoscopic cholecystectomy and Type II porcelain gallbladder was selected for open cholecystectomy. RESULTS: The laparoscopic cholecystectomy was completed in 10 patients with Type I porcelain gallbladder and the microscopie diagnosis demonstrated no cancer in the calcified wall of the gallbladder. In one patient with a non-transected injury to the right hepatic duct, a T-drainage tube was inserted at the site of the injury using the laparoscopic technique. Three patients with Type II porcelain gallbladder underwent open cholecystectomy and one patient had gallbladder cancer, therefore additional hepatectomy and lymphadenectomy was performed. CONCLUSIONS: We conclude that patients with a Type I porcelain gallbladder should be considered for laparoscopic cholecystectomy using a preoperative selection based on the ultrasound findings.

Aged↗

PubMed1994

Postprandial release of cholecystokinin and pancreatic polypeptide in health and in gallstone disease: relationships with gallbladder contraction.

OBJECTIVES: The present study investigated endogenous postprandial release of cholecystokinin (CCK) and pancreatic polypeptide (PP) in relation to gallbladder dynamics in healthy subjects and patients with gallstones. METHODS: Gallbladder volume (by ultrasonography) and plasma concentrations of CCK and PP (by radioimmunoassay) were evaluated in 18 patients with gallstones and 14 healthy controls before and after administration of a semi-liquid test meal (250 ml, 1450 kJ). Gallbladder contractility was previously assessed on a separate day by intravenous infusion of ceruletide (2.5 ng/kg/min). RESULTS: Basal gallbladder volume was not different in patients (32 +/- 5.9 cm3) and controls (26 +/- 2.7 cm3). Postprandial gallbladder contractility was impaired in gallstone patients, who showed a reduced integrated response (-3718 +/- 349 vs. -5251 +/- 376 cm3/2 h, p < 0.01) and a delayed time to maximal gallbladder contraction (67 +/- 7.4 min vs. 37 +/- 2.4 min, p < 0.002). Maximal gallbladder contraction after ceruletide infusion was also reduced (44.1 +/- 5.0% vs. 72.5 +/- 3.2%, p < 0.001), but not delayed (15.8 +/- 2.4 vs. 15.7 +/- 1.4 min) in gallstone patients. Basal CCK and PP plasma levels were similar in both groups. Postprandial CCK release was impaired in gallstone patients, predominantly due to a decreased response over the first 30 min (3.8 +/- 1.8 vs. 20.0 +/- 4.9 pmol/L/30 min, p < 0.005). Postprandial PP release was not different between groups. A direct linear correlation between postprandial release of CCK and PP was found in healthy controls but not in patients with gallstones. Postprandial gallbladder volume at any moment was inversely correlated with CCK plasma levels in healthy subjects, but not in gallstone patients. No correlation between postprandial PP response and gallbladder dynamics was observed. CONCLUSIONS: Based on a multivariate logistic approach, a reduced and delayed postprandial gallbladder contractility and an impaired CCK release in the early postprandial phase are significantly associated with gallstone disease. Our data provide further evidence for the predominant role of endogenous postprandial CCK release in gallbladder contraction. A role for PP in modulating postprandial gallbladder dynamics is not supported.

Cholecystokinin↗

PubMed1997

Biochemical and morphological correlations in human gallbladder with reference to membrane permeability.

There is good evidence that gallbladder epithelium is permeable to a diverse range of molecules which move into the epithelial cell from the lumen or the basement membrane. Morphological investigations have shown both secretory mucous droplets, components of the endocytosis pathway together with evidence of a system allowing passage of molecules across the basement membrane. This indicates that the gallbladder epithelium may be influenced by molecules presented via the apical and basal membranes, complicating our understanding of gallbladder function, particularly in disease. Gallbladder disease increases the proteoglycan content of the basement membrane, but the implication of this in terms of permeability remains to be defined. Indeed, it remains unknown whether this precedes disease or is a manifestation of the disease process. The removal of water from hepatic bile by gallbladder involves two counter ion transport systems. Autoradiography shows that ion transport occurs into the lateral intracellular spaces but it remains unclear whether this leads to a hypertonic solution in these spaces causing an osmotically driven water absorption or if the process involves an osmotically linked isotonic secretion. These ion pumps are reversible, for water is absorbed during the interdigestive phase but fluid is secreted into the lumen during digestion or in the presence of disease. Appropriate neural stimulation can increase or decrease fluid absorption from the lumen while vasoactive intestinal peptide or secretin promote fluid secretion, probably mediated by prostaglandins leading to raised cyclic AMP acting at the cellular level. Immediate control may depend on intracellular Ca2+ which activates a calmodulin-protein kinase, phosphorylating the counter ion transporters to downregulate their activity. Failure of this regulatory process may explain the initial increase in bile concentrating potential seen in the development of gallstones although the mechanism of such failure remains unknown. More concentrated bile increases movement of biliary compounds into gallbladder epithelial cells which alter gallbladder function in a complex manner. Secondary bile acids are raised in gallstone disease and increase permeability of the gallbladder epithelium to molecules including cholesterol. This cholesterol absorbed from the lumen may have paramount importance to gallbladder function. Raised biliary cholesterol reduces gallbladder motility, possibly by increasing the amount of cholesterol in gallbladder muscle membranes and reducing contraction in response to cholecystokinin. However, increased secondary bile acids are also associated with an alteration in phospholipid acyl groups which may alter ion transport activity and/or cholesterol solubility within the micelle/vesicle. As the acyl groups show increased arachidonate levels the production of prostaglandins could be raised, although currently it is not known if this phospholipid arachidonate enters the epithelial cells. In addition, gallbladder inflammation is associated with raised phospholipase A2 activity, leading to formation of fatty acids and lysophospholipid which causes membrane damage. The fatty acids are likely to displace cholesterol from the micelle but may also act directly on the epithelium, possibly increasing prostaglandin production and thus stimulating mucin secretion. Increased mucin secretion is seen early in gallstone disease but the evidence presently available cannot determine if this is a causative factor.

Absorption↗

PubMed1989

Plasma cholecystokinin and gallbladder responses to intraduodenal fat in gallstone patients.

Impaired gallbladder emptying is one of the various factors suggested to be involved in the pathogenesis of gallstones. The present study was undertaken to determine whether gallbladder emptying, endogenous cholecystokinin (CCK) secretion, or their interrelation is altered in patients with gallstones. After intraduodenal administration of 60 ml corn oil, plasma CCK concentration was measured by a sensitive and specific radioimmunoassay and gallbladder emptying by cholescintigraphy. Patients with gallstones (N = 20) produced significantly less endogenous CCK (105 +/- 17 pmol/liter 60 min; P less than 0.001) than control subjects (191 +/- 11 pmol/liter 60 min, N = 20); gallbladder emptying in the patients was significantly decreased at 5, 10, 40, 45, and 50 min but the reduction in gallbladder emptying did not reach statistical significance at 60 min (patients 44 +/- 8%, control subjects 60 +/- 4%). In addition, the gallbladder responsiveness to intravenous infusion of the synthetic CCK analog cerulein was investigated. Based on the results of gallbladder emptying in response to endogenous and exogenous CCK, four subgroups of gallstone patients were identified: (1) a group (N = 7) with normal gallbladder sensitivity to CCK, (2) a group (N = 6) with significantly increased gallbladder sensitivity to CCK, (3) a group (N = 6) with impaired gallbladder emptying after corn oil due to a significantly reduced endogenous CCK secretion but with normal gallbladder sensitivity to CCK, and (4) one patient whose gallbladder was unresponsive to CCK and was found to have chronic cholecystitis at surgery.

Ceruletide↗

PubMedDate not supplied

Sonographic findings of anomalous position of the gallbladder.

Anomalous position of the gallbladder is relatively rare and has been reported only in isolated case reports. We tried to determine its ultrasound (US) findings on the basis of 18 such patients. In the left-side gallbladder group (nine patients), the gallbladder was imaged as an oval cystic mass in front of the pancreas. In all patients, the narrow neck of the gallbladder was clearly detected by US in the usual location before the main portal vein. Four of nine patients had small gallbladder stones. The retrohepatic gallbladder group (four patients) showed marked atrophy of the right lobe of the liver. Two patients had multiple gallstones in the bile ducts of the right lobe. All patients in the suprahepatic retrohepatic gallbladder group (four patients) were cirrhotic, and the anterior segment of the right lobe was markedly atrophied. In the intercostal scan, the gallbladder mimicked a perihepatic fluid. In the floating gallbladder group (one patient), the gallbladder was imaged as a cystic mass in the anterior abdominal wall. Surgical intervention showed a severely inflamed gallbladder, with small stones adhered into the anterior abdominal wall and partially ruptured. Knowledge of the wide range of US findings of malposition of the gallbladder helps in avoiding misdiagnosis.

Adult↗

PubMed2001

Sludge and stone formation in the gallbladder in bedridden elderly patients with cerebrovascular disease: influence of feeding method.

PURPOSE: The incidence of gallbladder sludge or gallstone formation in bedridden patients with cerebrovascular disease (CVD) remains obscure. The aim of this study was to determine the incidence, relationship to feeding method, and mechanisms of gallbladder sludge and gallstone formation in elderly patients with CVD. METHODS: Using ultrasonography, we determined the development of gallbladder sludge and gallstone over a 12-month period, the area of the gallbladder, the gallbladder contractile response to cerulein, and fasting levels of plasma cholecystokinin (CCK) in 40 bedridden elderly patients with CVD. The patients were divided into three groups based on the feeding method: oral ingestion (OI), nasogastric feeding (NF), and total parenteral nutrition (TPN). RESULTS: Gallbladder sludge and gallstone were not observed in any of the 14 OI patients, but occurred in 6 and 1 of the 11 NF patients, and in 14 and 3 of the 15 TPN patients, respectively. Fasting gallbladder areas were significantly larger in the TPN group than in the other two groups. The TPN group showed a marked decrease in cerulein-induced gallbladder contractility. Fasting plasma CCK levels were lower in the TPN group than in the OI group. CONCLUSIONS: Our results indicate that elderly patients with CVD confined to bed over long periods are not necessarily at risk of gallbladder sludge or gallstone formation, and the development of these features may be associated with the feeding method. The predisposition of CVD patients on TPN to gallbladder disease is probably caused by failure of gallbladder contraction, resulting from insufficient secretion of CCK and impaired sensitivity of the gallbladder to CCK.

Aged↗

PubMed1984

Cardiovascular and T2-T4 dorsal horn cell responses to gallbladder distention in the cat.

Effects of gallbladder distention on blood pressure, heart rate, and T2-T4 dorsal horn cell activity were determined in 18 cats anesthetized with alpha-chloralose. Distention of the gallbladder (10-100 mm Hg) increased blood pressure in 17 of 18 cats, but heart rate was altered in only 2. The gallbladder pressure-blood pressure relation was derived for 11 cats. Pressor responses were greater with greater distending pressures over the gallbladder pressure range of 20-80 mm Hg. The maximum increase in blood pressure was 21 +/- 6 mm Hg at a gallbladder pressure of 80 mm Hg. Effects of gallbladder distention were tested on 64 T2-T4 dorsal horn neurons which met the following criteria: they had a somatic receptive field and were excited or inhibited by electrical stimulation of the left greater splanchnic nerve. In addition, all 64 neurons responded to stimulation of cardiopulmonary sympathetic afferent fibers. Gallbladder distention excited 17 cells and inhibited 9 cells. Responses usually consisted of phasic and tonic components. Significant increases or decreases in cell activity were elicited at a gallbladder pressure of 40 mm Hg. Pressor responses as well as changes in cell activity were abolished or greatly attenuated when both greater splanchnic nerves were sectioned. Vagotomy had no effect. Gallbladder pressure thresholds for a change in blood pressure (27 +/- 3 mm Hg) and cell activity (29 +/- 4 mm Hg) were not significantly different. Cells responding to gallbladder distention were located in laminae IV-VII of the T2-T4 segments. We conclude that gallbladder distention alters cell activity in the upper thoracic spinal cord and increases blood pressure. These findings may explain the phenomenon of chest pain which results from disease of the gallbladder.

Angina Pectoris↗