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      Epidemiology of gallbladder cancer

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          Abstract

          According to GLOBOCAN 2018 data, gallbladder cancer (GBC) accounts for 1.2% of all global cancer diagnoses, but 1.7% of all cancer deaths. Only 1 in 5 GBC cases in the United States is diagnosed at an early stage, and median survival for advanced stage cancer is no more than about a year. The incidence of the disease is increasing in the developed world. Gallstones, biliary cysts, carcinogen exposure, typhoid, and Helicobacter pylori infection, and abnormal pancreaticobiliary duct junctions are all risk factors, many of which account for its geographical, ethnic and sex distribution. Genetics also plays a strong role, as about a quarter of GBC cases are considered familial, and certain ethnicities, such as Native Americans, are at far higher risk for the neoplasm. Prevention includes weight loss, vaccination against and treatment of bacterial infections, early detection and elimination of polyps and cysts, and avoidance of oral estrogen replacement therapy.

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          Gallstone disease: Epidemiology of gallbladder stone disease.

          Thomas E. Shaffer (2005)
          Gallstone disease is common: >700,000 cholecystectomies and costs of approximately 6.5 billion dollars annually in the U.S. The burden of disease is epidemic in American Indians (60-70%); a corresponding decrease occurs in Hispanics of mixed Indian origin. Ten to fifteen per cent of white adults in developed countries harbour gallstones. Frequency is further reduced in Black Americans, East Asia and sub-Saharan Africa. In developed countries, cholesterol gallstones predominate; 15% are black pigment. East Asians develop brown pigment stones in bile ducts, associated with biliary infection or parasites, or in intrahepatic ducts (hepatolithiasis). Certain risk factors for gallstones are immutable: female gender, increasing age and ethnicity/family (genetic traits). Others are modifiable: obesity, the metabolic syndrome, rapid weight loss, certain diseases (cirrhosis, Crohn's disease) and gallbladder stasis (from spinal cord injury or drugs like somatostatin). The only established dietary risk is a high caloric intake. Protective factors include diets containing fibre, vegetable protein, nuts, calcium, vitamin C, coffee and alcohol, plus physical activity.
          Article 0 comments Cited 188 times – based on 0 reviews     Review now
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            Systematic population-based assessment of cancer risk in first-degree relatives of cancer probands.

            D Easton, D Goldgar, Cheryl Albright … (1994)
            Cancer has long been recognized to have a familial component. Elevated risks for cancers at the same site for relatives of cancer probands have been reported for both common cancers and a number of the rarer cancer sites. For a particular cancer site, however, the estimated risks to relatives have varied considerably depending on criteria for selection of probands, how cancers were determined in relatives, and overall study design. Not surprisingly, the estimated risks of other cancers in relatives of probands with cancer at a given site have been subject to even more variation. The aim of this study was to use the Utah Population Database resource to systematically study familial clustering of 28 distinct cancer site definitions among first-degree relatives (parents, siblings, and off-spring) of cancer probands. We estimated familial relative risks from the Utah Population Database by identifying all cases of cancer in these first-degree relatives. These observed values were compared with those expected based on cohort-specific internal rates calculated from 399,786 relatives of all individuals in the Utah Population Database known to have died in Utah. All sites showed an excess of cancers of the same site among relatives, with thyroid and colon cancers and lymphocytic leukemia showing the highest familial risks. When the analyses were restricted to cases with early ages at diagnosis, increased familial components for most cancer sites became evident. A significant difference in familial relative risk (FRR) between male (FRR = 4.04; 95% confidence interval [CI] = 3.13-5.07) and female (FRR = 2.24; 95% CI = 1.54-3.08) probands was found for colon cancer. Highly significant familial associations (one-sided; P < .001) were found among breast, colon, and prostate cancers and between breast and thyroid cancers. Statistically significant (one-sided, P < .01) associations were also found between tobacco-associated sites (lung, larynx, lip, and cervix). This study represents a unique comprehensive population-based study of familial cancer. The familial associations reported here will be useful in generating hypotheses about specific genetic and environmental factors that can be tested in genetic linkage and case-control studies.
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              Chronic and acute infection of the gall bladder by Salmonella Typhi: understanding the carrier state.

              Geoffrey Gonzalez-Escobedo, Joanna Marshall, John Gunn (2011)
              Despite major treatment and prevention efforts, millions of new typhoid infections occur worldwide each year. For a subset of infected individuals, Salmonella enterica subsp. enterica serovar Typhi colonizes the gall bladder and remains there long after symptoms subside, serving as a reservoir for the further spread of the disease. In this Progress article, we explore recent advances in our understanding of the mechanisms by which Salmonella spp.--predominantly S. Typhi--colonize and persist in the human gall bladder.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Exp Hepatol
                Journal ID (iso-abbrev): Clin Exp Hepatol
                Journal ID (publisher-id): CEH
                Title: Clinical and Experimental Hepatology
                Publisher: Termedia Publishing House
                ISSN (Print): 2392-1099
                ISSN (Electronic): 2449-8238
                Publication date (Electronic): 23 May 2019
                Publication date (Print): May 2019
                Volume: 5
                Issue: 2
                Pages: 93-102
                Affiliations
                [1 ]Department of Internal Medicine/Hospitalist, Sovah Health, Martinsville, VA, United States
                [2 ]Division of Gastroenterology and Hepatology, Mercy Medical Center, Des Moines, IA, United States
                [3 ]Department of Pulmonary and Critical Care Medicine, Sentara Virginia Beach General Hospital, Virginia Beach, VA, United States
                [4 ]Hillman Cancer Center, University of Pittsburgh, PA, United States
                Author notes
                Address for correspondence Dr. Prashanth Rawla, Department of Internal Medicine/Hospitalist, Sovah Health, 24112, Martinsville, VA, United States. e-mail: rawlap@ 123456gmail.com
                Article
                Publisher ID: 36699
                DOI: 10.5114/ceh.2019.85166
                PMC ID: 6728871
                PubMed ID: 31501784
                SO-VID: bf166dc3-a5b3-4568-9b8d-a061214ff732
                Copyright © Copyright: © 2019 Clinical and Experimental Hepatology
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                History
                Date received : 25 December 2018
                Date accepted : 28 January 2019
                Categories
                Subject: Review Paper

                Keywords: risk factor,survival,incidence,etiology,mortality
                Data availability:
                Keywords: risk factor, survival, incidence, etiology, mortality

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