Prevalence of gallbladder disease among persons with hepatitis C virus infection in the United States†

Bini, Edmund J.; McGready, John

doi:10.1002/hep.20647

Cited by 34 publications

(32 citation statements)

References 40 publications

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“…We were unable to demonstrate the correlation between GSD and hepatitis B or C virus infection, although hepatitis C infection has been reported to be related to GSD in men. 57 There are some limitations to our study. The major limitation is the low overall response rate, as well as the preponderance of older people and women among those who did respond.…”

Section: Discussionmentioning

confidence: 94%

Prevalence and risk factors of gallstone disease in an adult population of Taiwan: an epidemiological survey

Chen

Huang

Yang

et al. 2006

J of Gastro and Hepatol

142

118

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Section: Discussionmentioning

confidence: 94%

Prevalence and risk factors of gallstone disease in an adult population of Taiwan: an epidemiological survey

Chen

Huang

Yang

et al. 2006

J of Gastro and Hepatol

142

118

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“…Chronic hepatitis C virus (HCV) infection is associated with cholesterol and pigment gallstone formation 153–156. Chronic hepatic damage might be responsible for this effect, leading to deranged liver function and cirrhosis 155,156.…”

Section: Role Of Infection Inflammation and The Immune System In Fomentioning

confidence: 99%

Roles of Infection, Inflammation, and the Immune System in Cholesterol Gallstone Formation

2009

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Cholesterol gallstone formation is a complex process mediated by genetic and environmental factors. Until recently, the role of the immune system in the pathogenesis of cholesterol gallstones was not considered a valid topic of research interest. This review collates and interprets an extensive body of basic literature, some of which is not customarily considered to be related to cholelithogenesis, describing the multiple facets of the immune system that appear to be involved in cholesterol cholelithogenesis. A thorough understanding of the immune interactions with biliary lipids and cholecystocytes should modify current views of the pathogenesis of cholesterol gallstones, promote further research on the pathways involved, and lead to novel diagnostic tools, treatments, and preventive measures.Bile is a complex aqueous colloidal system that is essential for a wide range of physiologic functions, including the excretion of lipids from the organism and intestinal fat absorption. 1,2 Bile is formed primarily in hepatic canaliculi, small (1-2 μm) spaces formed between the tight junctions of hepatocytes. It is composed of water, electrolytes, and a variety of lipid solutes dispersed in mixed micelles and vesicles including bile salts, phospholipids (>96% being mixed phosphatidylcholines), and cholesterol, as well as proteins and bilirubin conjugates. 3 Phospholipids and bile salts are essential for the removal from the organism of otherwise insoluble cholesterol molecules in an aqueous environment by solubilizing the sterol in mixed micelles, composed of the catabolic product bile salts, and unilamellar vesicles. [2][3][4] Bile is transported from the canaliculi along tubules of increasingly greater diameter until it egresses into the gut at the midduodenum. In health, about half the secreted bile is stored, concentrated, and slightly acidified in the gallbladder during the interdigestive interval. The gallbladder is connected to the biliary tree via the cystic duct, which functions simultaneously as a gallbladder filling and emptying conduit. 3 Alterations in the relative or absolute proportions of cholesterol, phospholipids, and bile salts can lead to phase separation of cholesterol from solution in bile. Most frequently these changes Address requests for reprints to: Kirk J. Maurer, DVM, PhD, Cornell Center for Animal Resources and Education, College of Veterinary Medicine, Cornell University, Ithaca, New York. e-mail: km429@cornell.edu; fax: (607) 253-3527. M.C.C. and J.G.F. contributed equally to this work. John P. Lynch and David C. Metz, Section EditorsThe authors disclose no conflicts. NIH Public Access Author ManuscriptGastroenterology. Author manuscript; available in PMC 2010 February 1. Published in final edited form as:Gastroenterology. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript result from excess secretion of cholesterol from the liver. [1][2][3] As the absolute cholesterol concentration increases, the excess cholesterol phase separates, forming unilamellar vesicle...

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“…A US cohort comprising of 13,465 people from the National Health and Nutrition Examination Survey (NHANES) III cohort found an increased risk of gallstones (OR 3.2, 95% CI 1.08–9.45) and cholecystectomy (OR 4.57, 95% CI 1.57–13.27) in men with HCV compared to HCV-negative men [113]. The above association was not reported in women in this study, however the increased risk of gallstones in both genders with HCV has been supported by others [114,115].…”

Section: Environmental Factorsmentioning

confidence: 99%

Gallstones: Environment, Lifestyle and Genes

Stokes

Krawczyk

Lammert³

2011

Dig Dis

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Gallstone disease represents one of the most common and costly gastroenterological disorders. In Germany, 0.25% of the population undergo cholecystectomy per year, and cholelithiasis incurs annual medical expenses of more than USD 6.5 billion in the United States. The paradigm of environmental risk factors for gallstones has lately been challenged by genetic studies in experimental models and humans. The analysis of more than 40,000 Swedish twin pairs with gallstones demonstrated that genetic factors account for 25% of the phenotypic variance. Since then, studies employing genome-wide association analysis, case-control cohorts and analysis of sib-pairs in families with gallstones have expanded our knowledge of ‘gallstone genes’. Indeed, gallstone disease phenotypes are likely to result from the complex interaction of genetic factors, chronic overnutrition with carbohydrates, depletion of dietary fibre and other not fully defined environmental factors including physical inactivity and infections. This hypothesis is supported by the profound increases of cholesterol gallstone prevalence rates in Native Americans, post-war European countries and current urban centres in East Asia, all of which were associated with ‘westernized’ nutrition. Herein, we summarise the spectrum of environmental and genetic risk factors which should pave the way to ‘personalised’ strategies for the prevention and therapy of gallstones.

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Prevalence of gallbladder disease among persons with hepatitis C virus infection in the United States†

Cited by 34 publications

References 40 publications

Prevalence and risk factors of gallstone disease in an adult population of Taiwan: an epidemiological survey

Prevalence and risk factors of gallstone disease in an adult population of Taiwan: an epidemiological survey

Roles of Infection, Inflammation, and the Immune System in Cholesterol Gallstone Formation

Gallstones: Environment, Lifestyle and Genes

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