Gallbladder Mucosa Of Patients Research Articles

CO-EXISTENCE OF HELICOBACTER PYLORI IN GASTRIC AND GALLBLADDER MUCOSA IN CHOLECYSTITIS PATIENTS: A CROSS-SECTIONAL STUDY

This study was designed to assess the frequency of co-existence of H. Pylori in gastric and gallbladder mucosa of patients with acute cholecystitis or who had symptoms of cholelithiasis. This cross-sectional analysis was conducted at Bahria Town International Hospital Lahore from September 2020 to September 2021. The study consisted of 51 participants, all diagnosed with either acute cholecystitis or symptomatic cholelithiasis. Information regarding the patients' ages, genders, and the H. pylori existence in the mucosa of their gastric and gallbladders was collected and analyzed with SPSS version 22. H. pylori was discovered in the gallbladder mucosa of 22 individuals, which accounts for 43.1% of all cases, and in the gastric mucosa of 16 patients, which accounts for 31.1% of all cases. The co-existence of H. pylori in both the mucosa of the gallbladder and gastric wall was found in six (11.8%) patients. The co-existence of H pylori was significantly greater in patients with acute cholecystitis compared to those with cholelithiasis (p = 0.021). This study showed no significant relationship between age and smoking history with the co-existence of H. pylori in gastric and gallbladder mucosa. The findings of this study indicate that the presence of H. pylori infection is extensive in the gallbladder and stomach mucosa of the patients diagnosed with acute cholecystitis and cholelithiasis. When evaluating patients with gallbladder issues, it should be considered the presence of H. pylori in both the gallbladder and gastric mucosa.

Assessment of the Simultaneous Presence of Helicobacter Pylori in the Gastric Mucosa and Gallbladder Mucosa in Patients Suffering from Cholecystitis: a cross Sectional Study

Aim: The current study was designed to assess the simultaneous presence of H. pylori in gastric and gallbladder mucosa in the patients of acute cholecystitis or symptomatic cholelithiasis. Study design: Cross sectional study Place and duration: This study was conducted at Liaquat University Hospital Hyderabad, Pakistan from March 2020 to March 2021. Methodology: A total of 43 patients suffering from acute cholecystitis and symptomatic cholelithiasis were selected. Their age, gender, and the presence of H. pylori in the gallbladder and gastric mucosa was determined and recorded. The results were statistically analyzed by SPSS version 22. Results: Out of the 43 patients, 20 were male, and 23 were female. Recorded mean age was 54.8±9.9 years and 22 (51.2%) had acute cholecystitis and the remaining 21 (48.8%) had cholelithiasis. In the gastric mucosa, in 14 patients (32.6%) H. pylori was positive. Similarly, in the gall bladder; it was positive in 19 patients (44.2%). In 6 patients (13.9%) i.e. in 4 men and 2 women, H pylori was simultaneously present in both gallbladder and gastric mucosa. No particular relationship was observed in the H. pylori’s presence or absence in gallbladder and gastric mucosa. Conclusion: The presence of H. pylori in gallbladder plays a critical role in the gallbladder’s infection. However, its simultaneous presence in gastric mucosa is not a good standard to assess biliary diseases. Keywords: H. pylori, Cholecystitis, Cholelithiasis, Gallbladder, Gastric mucosa

IL-33 overexpression in gallbladder cancers associated with pancreatobiliary maljunction.

To investigate whether genetic or inflammatory pro-oncogenic factors are relevant to the increased risk of gallbladder cancers in patients with pancreaticobiliary maljunction (PBM). Mutations in KRAS exon 2 were examined by a highly sensitive, droplet digital PCR platform using surgically resected specimens of PBM-associated (n=31) and non-associated gallbladder cancers (n=49). The tissue expression of IL-6 and IL-33, which are suspected to promote biliary carcinogenesis, was analysed by quantitative real-time PCR and in-situ hybridisation. The incidence of KRAS mutations was similarly low in PBM-associated (five of 32 cases; 16%) and non-associated cancers (four of 49 cases; 8%) (P=0.272). The tissue expression of IL-33 mRNA, but not IL-6 mRNA, was significantly higher in PBM-associated gallbladder cancers than in gallbladder cancers without PBM (P=0.004). A similar degree of IL-33 overexpression was also observed in the background non-cancerous mucosa in cases of PBM-associated gallbladder cancers, and was significantly greater than that in PBM cases with cholecystitis alone (P<0.001). The results of in-situ hybridisation indicated that the source of IL-33 production in PBM-associated carcinomas was the endothelium, cancer cells and non-neoplastic biliary epithelium. In a combined PBM-associated and non-associated cohort, IL-33 overexpression in gallbladder cancers correlated with less aggressive features (e.g. a lower pT stage and longer overall survival), similar to recently reported findings on large-duct cholangiocarcinomas. KRAS mutations do not appear to be associated with a high risk of malignancy in PBM, while IL-33 overexpression may provide a pro-oncogenic microenvironment in the gallbladder mucosa of patients with PBM.

Factors Associated with Premalignant Epithelial Changes in Chronic Calculous Cholecystitis: A Case-Control Study.

Gallstones are known to be associated with premalignant changes in the gallbladder epithelium that range from atypical hyperplasia, metaplasia, dysplasia to carcinoma. Recognition of factors associated with these changes in patients with gallstones can potentially be helpful in identifying patients to whom prophylactic cholecystectomy can be offered to reduce the chances of developing carcinoma. To identify factors associated with premalignant epithelial changes including atypical hyperplasia, metaplasia, and dysplasia in gallbladder mucosa in patients with chronic calculus cholecystitis. This was retrospective case-control study conducted over a period of 10years from 2004 to 2014. Cases were patients with reported histopathological premalignant epithelial changes along with chronic calculus cholecystitis, and controls were patients without premalignant epithelial changes but chronic calculus cholecystitis. Controls were twice the number of the cases. Over study period, 92 patients were reported to have premalignant epithelial changes on gall bladder histopathology for whom 184 controls were selected. Of cases, 61 (66%) patients had atypical hyperplasia, while metaplasia and dysplasia were present in 26 (28%) and 5 (5%) cases, respectively. Mean age was 47.5±14.5years, and 74% of the study population were female. Wall thickness of more than 3mm (OR=4.14, p value<0.001) turned out to be statistically significant independent variables associated with premalignant lesions in gallbladder mucosa. Odds of premalignant epithelial change in gall bladder mucosa in patients with gall bladder wall thickness of more than 3mm is four times the odds of patients with wall thickness less than 3mm, and the effect is statistically significant. Prophylactic cholecystectomy should be considered for this group of patients.

Telomere length of gallbladder epithelium is shortened in patients with congenital biliary dilatation: measurement by quantitative fluorescence in situ hybridization.

Congenital biliary dilatation (CBD) is a congenital malformation involving both dilatation of the extrahepatic bile duct and pancreaticobiliary maljunction. Persistent reflux of pancreatic juice injures the biliary tract mucosa, resulting in chronic inflammation and higher rates of carcinogenesis in the biliary tract, including the gallbladder. Telomeres are repetitive DNA sequences located at the ends of chromosomes. Chromosomal instability due to telomere dysfunction plays an important role in the carcinogenesis of many organs. This study was performed to determine whether excessive shortening of telomeres occurs in the gallbladder mucosa of patients with CBD. Resected gallbladders were obtained from 17 patients with CBD, ten patients with cholecystolithiasis without pancreatic juice reflux, and 17 patients with normal gallbladders (controls) (median age of each group of patients: 37, 50, and 53years, respectively). The telomere lengths of the gallbladder epithelium were measured by quantitative fluorescence in situ hybridization using tissue sections, and the normalized telomere-to-centromere ratio (NTCR) was calculated. The NTCRs in the CBD, cholecystolithiasis, and control groups were 1.24 [interquartile range (IQR) 1.125-1.52], 1.96 (IQR 1.56-2.295), and 1.77 (IQR 1.48-2.53), respectively. The NTCR in the CBD group was significantly smaller than that in the cholecystolithiasis and control groups (p=0.003 and 0.004, respectively), even in young patients. Our findings indicate that telomere shortening in the gallbladder mucosa plays an important role in the process of carcinogenesis in patients with CBD. These results support the recommendation of established guidelines for prophylactic surgery in patients with CBD because CBD is a premalignant condition with excessive telomere shortening.

Helicobacter pylori colonization of gallbladder in patients with symptomatic cholelithiasis

Background: The relation of Helicobacter pylori and its presence in gallbladder mucosa in patients with symptomatic cholelithiasis has been a topic of various studies. In order to establish this relation, this study has been performed so as to bring to light the capability of the organism to harbor in the gallbladder.Methods: The patients underwent gastroscopy for specimens of gastric mucosa followed by laparoscopic/open cholecystectomy and histopathological examination of gallbladder specimen.Results: The results showed H. pylori in 16 (40%) in gastric mucosa specimens and 4 (10%) in gallbladder mucosa specimens.Conclusions: This revealed a significant correlation of H. pylori colonization in gallbladder mucosa with respect to gastric mucosa colonization.

INCIDENCE OF PRESENCE OF H. PYLORI IN CASES OF CHOLECYSTITIS AND CHOLELITHIASIS IN A RURAL MEDICAL COLLEGE &amp; HOSPITAL

Cholecystitis is defined as inflammation of the gallbladder. Ninety percent of cases involve stones in the cystic duct and gall bladder, (i.e., calculus cholecystitis) with the other 10% of cases representing acalculus cholecystitis. (1) The association of gallstones with Helicobacter pylori has been investigated but not clearly demonstrated. In this study, the presence of H. pylori in the gallbladder mucosa of patients with symptomatic cholecystitis and cholelithiasis was investigated.The study included 50 cases of cholecystitis and cholelithiasis randomly selected who were admitted to the surgical wards of M.M.I.M.S.R, Mullana in last 2 years. All patients underwent cholecystectomy and gall bladder mucosa was histopathologically examined by giemsa staining (silver slide test). We concluded that no gall bladder mucosa exhibits presence of H. Pylori. Keywords: Cholelithiasis; Cholecystitis; H. pylori; Giemsa

An integrated analysis of differential miRNA and mRNA expressions in human gallstones.

Gallstone disease, including cholesterol precipitation in bile, increased bile salt hydrophobicity and gallbladder inflammation. Here, we investigated miRNA and mRNA involved in the formation of gallstones, and explored the molecular mechanisms in the development of gallstones. Differentially expressed 17 miRNAs and 525 mRNA were identified based on Illumina sequencing from gallbladder mucosa of patients with or without gallstones, and were validated by randomly selected 6 miRNAs and 8 genes using quantitative RT-PCR. 114 miRNA target genes were identified, whose functions and regulating pathways were related to gallstones. The differentially expressed genes were enriched upon lipoprotein binding and some metabolic pathways, and differentially expressed miRNAs enriched upon ABC transportation and cancer related pathways. A molecular regulatory network consisting of 17 differentially expressed miRNAs, inclusive of their target genes, was constructed. miR-210 and its potential target gene ATP11A were found to be differentially expressed in both miRNA and mRNA profiles. ATP11A was a direct target of miR-210, which was predicted to regulate the ABC-transporters pathway. The expression levels of ATP11A in the gallstone showed inverse correlation with miR-210 expression, and up-regulation of miR-210 could reduce ATP11A expression in HGBEC. This is the first report that indicates the existence of differences in miRNA and mRNA expression in patients with or without gallstones. Our data shed light on further investigating the mechanisms of gallstone formation.

Helicobacter Pylori Infection in Patients with Chronic Calcular Cholecystitis a Cross- Sectional Study

Aims: Helicobacter pylori was found in the bile and gallbladder, so we are aiming to examine the relationship between H. pylori-like bacteria and chronic calcular cholecystitis. METHODS: This cross-sectional study was conducted at our hospitals from May 2011 to January 2012. One hundred and forty patients with chronic calcular cholecystitis were enrolled in this study. Gastroscopy with gastric or duodenal H.pylori urease test and detection of H. pylori in serum were done before the surgical procedure for all patients. After cholecystectomy, the gallbladder tissue was investigated for H. pylori by rapid urease test and Geimsa stain. RESULTS: Of all 140 patients 62.1 % were females, mean age of our patients was 39.04 ± 7.3 years. H. pylori IgG antibody titre was positive in 32 patients with biliary duodenitis, in 43 patients with biliary gastritis, and in 18 patients with duodenal ulcer. The gastric rapid urease test was positive in 40.7 %. The gallbladder rapid urease test was positive in 25 %. In 24 patients both gastric and gallbladder mucosa tested positive for rapid urease test. In 28 patients, the gastric urease test was positive while the gallbladder mucosa tested negative. In 13 patients, the gallbladder mucosa tested positive while the gastric mucosa was negative. There was a significant correlation between the rapid urease test in the gallbladder and in the gastric or duodenal mucosa (P = 0.002). Modified Geimsa staining of gallbladder specimens revealed that H. pylori-like bacteria were detected in 63.6 %. There was a significant correlation between histopathological examination of gallbladder mucosa stained with Geimsa stain and the gallbladder rapid urease test (P < 0.001), but not correlated with the gastric urease test (P = 0.210). CONCLUSION: Our study demonstrates that H. pylori is present in the gallbladder mucosa in patients with chronic calcular cholecystitis and might be an etiological cause of chronic inflammation`.

Tissue expression of S100 proteins in gallbladder mucosa of the patients with calculous cholecystitis

Proteins of S100 group, produced by phagocytes represent endogenous activators of innate immune responses. Role of these proteins in the etiopathogenesis of cholelithiasis remains unknown. The studies aimed at the morphometric evaluation of S100A8 and S100A9 protein expression in gallbladder mucosa in patients with acute and chronic calculous cholecystitis (n = 71). The presence of proteins was detected by immunohistochemistry while quantitative analysis employed the spatial visualization technique. We found the immunopositive expression of the two studied S100 proteins in neutrophils and monocytes/macrophages of the gallbladder's wall and a higher expression in acute cholecystitis. Quantitative study revealed higher immunoexpression of S100A9 over S100A8 in both studied groups of patients. Moreover, a reciprocal linear relationship between the expression of the studied proteins and a positive correlation between expression of either S100A8 or S100A9 and inflammatory activity (grading) in the gallbladder wall were found. The expression of S100A8 protein in the chronic cholecystitis group and in older patients correlated with leukocytosis, which suggests the role of S100A8 particularly at the chronic stage of cholecystitis. The obtained results indicated close relationship between S100A8 and S100A9 proteins in their proinflammatory functions. The increased expression of only one of them can be recognized as a useful index of local inflammatory activity in calculous cholecystitis.

Helicobacter pylori in gallbladder mucosa in patients with gallbladder disease

Helicobacter species have been found to be associated with biliary tract diseases. This prospective study was done to determine the prevalence of H. pylori in the biliary tract of patients suffering from gallbladder disease. Forty-nine patients undergoing laparoscopic/open cholecystectomy for benign biliary tract diseases were investigated with urea breath test for H. pylori infection of gastric antrum. Bile and gallbladder tissues were studied for presence of H. pylori by rapid urease test, histopathological examination, culture and PCR analysis. Gallbladder specimens from two patients who underwent Whipple's operation and from 10 cadavers were studied as controls. The mean (SD) age of patients was 42.4 (11.1) years. Urea breath test was positive in 17 (34.6%) cases. Rapid urease test was negative in all the cases. There was no evidence of H. pylori infection of gallbladder on histopathological examination using H&E, Giemsa and Warthin Starry stains. H. pylori DNA were detected in 16 patients (32.6%) and none of the 12 controls by PCR analysis (p = 0.025). The presence of H. pylori DNA in bile and/or gallbladder was associated with positive urea breath test, (p < 0.0001). Other factors like age, gender, jaundice and cholestasis were not associated with H. pylori infection of bile and gallbladder. Nearly three quarters of patients with positive urea breath test have detectable H. pylori DNA in gallbladder tissue. The significance of these findings needs to be further evaluated.

Hepcidin Is an Antibacterial, Stress-Inducible Peptide of the Biliary System

Background/AimsHepcidin (gene name HAMP), an IL-6-inducible acute phase peptide with antimicrobial properties, is the key negative regulator of iron metabolism. Liver is the primary source of HAMP synthesis, but it is also produced by other tissues such as kidney or heart and is found in body fluids such as urine or cerebrospinal fluid. While the role of hepcidin in biliary system is unknown, a recent study demonstrated that conditional gp130-knockout mice display diminished hepcidin levels and increased rate of biliary infections.MethodsExpression and localization of HAMP in biliary system was analyzed by real time RT-PCR, in-situ hybridization, immunostaining and –blotting, while prohepcidin levels in human bile were determined by ELISA.ResultsHepcidin was detected in mouse/human gallbladder and bile duct epithelia. Biliary HAMP is stress-inducible, in that it is increased in biliary cell lines upon IL-6 stimulation and in gallbladder mucosa of patients with acute cholecystitis. Hepcidin is also present in the bile and elevated prohepcidin levels were observed in bile of primary sclerosing cholangitis (PSC) patients with concurrent bacterial cholangitis compared to PSC subjects without bacterial infection (median values 22.3 vs. 8.9; p = 0.03). In PSC-cholangitis subjects, bile prohepcidin levels positively correlated with C-reactive protein and bilirubin levels (r = 0.48 and r = 0.71, respectively). In vitro, hepcidin enhanced the antimicrobial capacity of human bile (p<0.05).ConclusionHepcidin is a stress-inducible peptide of the biliary epithelia and a potential marker of biliary stress. In the bile, hepcidin may serve local functions such as protection from bacterial infections.

H pyloriexist in the gallbladder mucosa of patients with chronic cholecystitis

To study whether H pylori locate in the gallbladder mucosa of patients with chronic cholecystitis. Using Warthy-Starry (W-S) silver stain and immunohistochemistry stain with anti-H pylori antibodies, we screened paraffin specimens in 524 cases of cholecystitis. H pylori urease gene A (HPUA) and H pylori urease gene B (HPUB) were analyzed by polymerase chain reaction (PCR) in the fresh tissue specimens from 81 cases of cholecystitis. H pylori-like bacteria were found in 13.55% of the gallbladders of the cholecystitis patients using W-S stain. Meanwhile, bacteria positive for H pylori antibodies were also found in 7.1% of the gallbladders of patients with cholecystitis by immunohistochemistry. Of 81 gallbladders, 11 were positive for both HPUA and HPUB, 4 were positive for HPUA only and 7 were positive for HPUB only. H pylori exist in the gallbladders of patients with chronic cholecystitis.

Increased acylcoa-cholesterol ester acyltransferase activity in gallbladder mucosa in patients with gallbladder cholesterolosis

Objective: Although cholesterolosis of the human gallbladder is a relatively common disease, its etiology has not been fully understood. The aim of this study was to determine this etiology. Methods: The lipid composition of the gallbladder mucosa and gallbladder bile and the enzyme activities (acylCoA-cholesterol ester acyltransferase [ACAT] and cholesterol ester hydrolase [CEH]) of the gallbladder mucosa were measured in control subjects, patients with cholesterolosis, and patients with cholesterol gallstone disease. Results: Levels of cholesterol ester in gallbladder mucosa in patients with cholesterolosis (n = 12) were higher than those in control subjects (n = 8). With regard to the lipid content in gallbladder bile, no differences were found in concentrations of cholesterol, phospholipids, and bile acids among control subjects (n = 11), patients with cholesterolosis (n = 13), and those with cholesterol gallstone disease (n = 15). In gallbladder mucosa, ACAT activity was significantly higher in patients with cholesterolosis (n = 10) than in control subjects (n = 8), whereas CEH activity did not differ between the two groups. As a result, the ACAT/CEH activity ratio was higher in patients with cholesterolosis than in control subjects. Conclusions: It would be suggested that cholesterol ester synthesis of gallbladder mucosa might play an etiological role in the development of cholesterolosis.

Increased acylcoa-cholesterol ester acyltransferase activity in gallbladder mucosa in patients with gallbladder cholesterolosis

Objective: Although cholesterolosis of the human gallbladder is a relatively common disease, its etiology has not been fully understood. The aim of this study was to determine this etiology. Methods: The lipid composition of the gallbladder mucosa and gallbladder bile and the enzyme activities (acylCoA-cholesterol ester acyltransferase [ACAT] and cholesterol ester hydrolase [CEH]) of the gallbladder mucosa were measured in control subjects, patients with cholesterolosis, and patients with cholesterol gallstone disease. Results: Levels of cholesterol ester in gallbladder mucosa in patients with cholesterolosis (n = 12) were higher than those in control subjects (n = 8). With regard to the lipid content in gallbladder bile, no differences were found in concentrations of cholesterol, phospholipids, and bile acids among control subjects (n = 11), patients with cholesterolosis (n = 13), and those with cholesterol gallstone disease (n = 15). In gallbladder mucosa, ACAT activity was significantly higher in patients with cholesterolosis (n = 10) than in control subjects (n = 8), whereas CEH activity did not differ between the two groups. As a result, the ACAT/CEH activity ratio was higher in patients with cholesterolosis than in control subjects. Conclusions: It would be suggested that cholesterol ester synthesis of gallbladder mucosa might play an etiological role in the development of cholesterolosis.

Cholesterol metabolism in liver and gallbladder mucosa of patients with cholesterolosis

The objective of this study was to investigate possible pathogenetic factors for cholesterolosis. Liver tissue, gallbladder mucosa, and gallbladder bile were collected in patients with cholesterol gallstones (GS) (14 patients with and 14 patients without cholesterolosis) and gallstone-free (GSF) subjects (11 with and 21 without cholesterolosis) undergoing cholecystectomy. In cholesterolosis, the gallbladder mucosa was characterized by a fivefold increase in esterified cholesterol and normal content of free cholesterol. The hepatic levels of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, governing cholesterol synthesis, and acyl coenzyme A: acyltransferase activity, catalyzing the esterification of cholesterol, were similar in patients with and without cholesterolosis. Also in the gallbladder mucosa, the 3-hydroxy-3-methylglutaryl coenzyme A reductase activity was similar in patients with and without cholesterolosis. The acyl coenzyme A: acyltransferase activity of the gallbladder mucosa was increased in the GSF subjects with cholesterolosis. The nucleation time of gallbladder bile was shorter in the GSF subjects with cholesterolosis compared with the time of those without cholesterolosis. Occurrence of cholesterol crystals, lipid composition, and cholesterol saturation of gallbladder bile were not significantly influenced by the absence or presence of cholesterolosis. The study has confirmed that cholesterolosis is associated with a several-fold increased level of esterified cholesterol. The data suggest that patients with cholesterolosis have normal hepatic cholesterol formation and esterification. The local synthesis of cholesterol in the gallbladder mucosa seems to be normal. A positive correlation was obtained between the cholesterol saturation of bile and the content of esterified cholesterol in the gallbladder mucosa in the whole series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholesterol metabolism in liver and gallbladder mucosa of patients with cholesterolosis

The objective of this study was to investigate possible pathogenetic factors for cholesterolosis. Liver tissue, gallbladder mucosa, and gallbladder bile were collected in patients with cholesterol gallstones (GS) (14 patients with and 14 patients without cholesterolosis) and gallstone-free (GSF) subjects (11 with and 21 without cholesterolosis) undergoing cholecystectomy. In cholesterolosis, the gallbladder mucosa was characterized by a fivefold increase in esterified cholesterol and normal content of free cholesterol. The hepatic levels of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, governing cholesterol synthesis, and acyl coenzyme A: acyltransferase activity, catalyzing the esterification of cholesterol, were similar in patients with and without cholesterolosis. Also in the gallbladder mucosa, the 3-hydroxy-3-methylglutaryl coenzyme A reductase activity was similar in patients with and without cholesterolosis. The acyl coenzyme A: acyltransferase activity of the gallbladder mucosa was increased in the GSF subjects with cholesterolosis. The nucleation time of gallbladder bile was shorter in the GSF subjects with cholesterolosis compared with the time of those without cholesterolosis. Occurrence of cholesterol crystals, lipid composition, and cholesterol saturation of gallbladder bile were not significantly influenced by the absence or presence of cholesterolosis. The study has confirmed that cholesterolosis is associated with a several-fold increased level of esterified cholesterol. The data suggest that patients with cholesterolosis have normal hepatic cholesterol formation and esterification. The local synthesis of cholesterol in the gallbladder mucosa seems to be normal. A positive correlation was obtained between the cholesterol saturation of bile and the content of esterified cholesterol in the gallbladder mucosa in the whole series of patients. However, because cholesterolosis may occur in both GSF subjects and patients with cholesterol GS with or without cholesterol-saturated bile, the uptake of cholesterol from the gallbladder bile may not be the only mechanism for the development of cholesterolosis.

Evidence of impaired acidification in vitro by human gall bladder mucosa in patients with gallstone disease

Objective: To study the capacity of the human gall bladder with and without gallstones to secrete H + ions. Design: Human gall bladders were studied in vitro which permitted the measurement of the electrical potential difference and secretion of H + ions. Results: Thirty-three gall bladders were studied (five normal, 20 with cholesterol and eight with pigment gallstones). The normal gall bladder group secreted 14.53 ± 1.04 nmol (mean ± SEM), the mildly inflamed group 8.27 ± 1.71 nmol and the moderately inflamed group 4.03 ± 0.94 H + over 60 min in the mucosal bathing fluid. H + secretion was significantly different when the mildly and moderately inflamed groups were compared with the normal group (P < 0.002 and P < 0.009, respectively)

Lipid composition of bile and gallbladder mucosa in patients with acalculous cholesterolosis

To investigate pathogenetic factors of cholesterolosis of the gallbladder, the lipid composition of both the hepatic and gallbladder bile and gallbladder mucosa were compared with each other in 6 patients with and 5 patients without acalculous cholesterolosis. The molar percentage of biliary cholesterol and total bile acid pattern were similar in the two groups. Of the biliary cholesterol precursors, methyl sterols, but not squalene, correlated closely with cholesterol both in the hepatic (r = 0.901) and gallbladder bile (r = 0.747). Methyl sterols, expressed either per cholesterol or bile acids, were higher and squalene was lower in the gallbladder bile than in the hepatic bile. In addition, methyl sterols were increased in the hepatic and gallbladder bile of the patients with cholesterolosis, as if the hepatic production of these precursors had been enhanced—probably as a consequence of altered hepatic cholesterol synthesis. In cholesterolosis the gallbladder mucosa was characterized by a marked increase in triglycerides and significant elevations of the esterified sterols and free methyl sterols. The esterification degrees of sterols, which were consistently higher for methyl sterols than for cholesterol, were closely correlated with the respective mucosal sterol concentrations. The methyl sterols/cholesterol ratio in the bile correlated significantly with mucosal free and esterified methyl sterols, esterified cholesterol, and the methyl sterols/cholesterol ratio. The data suggest that free sterols can be transferred from the bile to the gallbladder mucosa, and that altered hepatic cholesterol synthesis is associated with the development of the cholesterolosis of human gallbladder.