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      Metaplastic Changes in Chronic Cholecystitis: Implications for Early Diagnosis and Surgical Intervention to Prevent the Gallbladder Metaplasia-Dysplasia-Carcinoma Sequence

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          Abstract

          Background

          Metaplastic features of the gallbladder epithelium are considered to be the precursors of gallbladder cancer. Considering the possible role of chronic inflammatory changes in the development of these lesions and the rationale for performing an early prophylactic cholecystectomy, we performed a retrospective study to assess the prevalence of gallbladder metaplasia in patients who underwent cholecystectomy due to underlying cholelithiasis.

          Methods

          We reviewed the routine histopathology reports of 86 patients with chronic cholecystitis, who underwent elective cholecystectomy, to assess the prevalence of gallbladder metaplasia in the course of chronic cholecystitis. We further attempted to evaluate the existence of any correlations between the presence of the gallbladder metaplasia and the type of lithiasis, as well as the gallbladder wall thickness.

          Results

          The overall prevalence of metaplastic features in the resected specimens was 25.6%. Dysplastic changes were more frequent in gallbladder specimens with concurrent metaplasia. Moreover, in presence of metaplastic changes, we observed an increase of the average gallbladder wall thickness. Finally, metaplastic and dysplastic changes were associated with the presence of micro-lithiasis rather than macro-lithiasis.

          Conclusions

          Gallbladder metaplastic changes appear to be more frequent in cases of micro-lithiasis and seem to be associated with a chronic thickening of the gallbladder wall. Taking into account the usually sub-clinical course of this group of patients, when compared to patients with macro-lithiasis, further studies are needed to evaluate a possible role of prophylactic cholecystectomy in this population to prevent the long term evolution of these early changes to cancerous lesions.

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          Most cited references11

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          Preneoplastic lesions in gallbladder cancer.

          Gallbladder cancer is an uncommon disease except in countries like Chile and areas of India and Japan. The knowledge regarding the etiology and mechanisms through which this neoplasia is developed is significantly less compared to other malignant tumors. The epithelial lesions involved in gallbladder carcinogenesis are dysplasia and adenomas that represent two biologically distinct carcinogenetic models. Dysplasia progresses to carcinoma in situ (CIS) and subsequently becomes invasive. Over 80% of invasive gallbladder cancers present areas adjacent to the CIS and epithelial dysplasia. Other authors have demonstrated adenomatous areas in carcinomas, or malignant transformation in an adenoma. The low incidence of gallbladder adenomas (0.14% of cholecystectomies) and the presence of adenomatous remnants in the neighboring mucosa to early carcinomas in less than 3% of the cases suggest the limited importance of this carcinogenic pathway. Epithelial dysplasia which is not associated with gallbladder cancer is observed in approximately 1% of cholecystectomies for symptomatic lithiasis. Metaplasia, dysplasia, and CIS are present in the mucosa adjacent to the cancer in 66%, 81.3%, and 69%, respectively. The average ages of patients with dysplasia not associated to cancer (51.9 years), early carcinomas (56.8 years), and advanced carcinomas (62.9 years) demonstrate a gradient which suggests the progression of these lesions. From the morphological point of view, the dysplasia-carcinoma sequence is the most plausible carcinogenic pathway for gallbladder cancer, a process which would require a period of approximately 10 years. Copyright 2006 Wiley-Liss, Inc.
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            Role of bacteria in carcinogenesis, with special reference to carcinoma of the gallbladder.

            Carcinoma of the gallbladder (CaGB) is the fifth commonest gastrointestinal tract cancer and is endemic in several countries. The interplay of genetic susceptibility, infections, and life style factors has been proposed to be responsible for carcinogenesis of gallbladder. Persistence of infection leading to chronic inflammation, and production of certain toxins and metabolites with carcinogenic potentials, by certain bacteria has been speculated to be involved in the transformation of the gallbladder epithelium. Therefore, any bacteria that have evolved to acquire both of the above carcinogenic mechanisms can cause cancer. Salmonella typhi has been found to be prominently associated with CaGB. Chronic typhoid carriage (persistence) and production of mediators of chronic inflammation and a genotoxic toxin (cytotoxic distending toxin, CdtB) are also known for this bacterium. Furthermore, the natural concentrating function of the gallbladder might amplify the carcinogenic effect of the mediators of carcinogenesis. In addition to S. typhi, certain species of Helicobacter (H. bilis and H. hepaticus) and Escherichia coli have also been implicated in carcinogenesis. As the isolation rate is very poor with the presently available culture techniques, the existence of bacteria in a viable but non-cultivable state is quite likely; therefore, sensitive and specific molecular techniques might reveal the etiological role of bacterial infection in gallbladder carcinogenesis. If bacteria are found to be causing cancers, then eradication of such infections might help in reducing the incidence of some cancers.
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              Prevalence and risk factors for gallbladder neoplasia in patients with primary sclerosing cholangitis: evidence for a metaplasia-dysplasia-carcinoma sequence.

              Primary sclerosing cholangitis (PSC) carries an increased risk (10% to 20%) of hepatobiliary malignancy, especially cholangiocarcinoma (CC). Dysplasia, adenomas, and carcinomas of the gallbladder have been described in PSC but are less common than bile duct carcinomas. However, the prevalence and risk factors for gallbladder neoplasia among patients with PSC undergoing orthotopic liver transplantation (OLT) have not been well studied. We evaluated 72 gallbladders from 100 consecutive liver explants for PSC, including 66 cholecystectomies performed at the time of OLT and 6 performed before OLT. All specimens were totally embedded for histologic examination. We evaluated the following histologic features: presence of diffuse lymphoplasmacytic chronic cholecystitis, pyloric metaplasia, intestinal metaplasia, dysplasia (low-grade or high-grade), and adenocarcinoma. Gallbladder dysplasia and adenocarcinoma were correlated with several clinicopathologic parameters using Fisher exact test and t test, including: (1) sex, (2) age, (3) PSC duration, (4) inflammatory bowel disease (IBD) at time of OLT, and (5) concomitant bile duct dysplasia or carcinoma. Lymphoplasmacytic chronic cholecystitis was present in 35 (49%), pyloric metaplasia in 69 (96%), intestinal metaplasia in 36 (50%), dysplasia in 27 (37%; low-grade in 12 and high-grade in 15), and adenocarcinoma in 10 (14%; 2 with lamina propria invasion and 8 with invasion into muscularis or adventitia). Gallbladder carcinoma was associated with intrahepatic bile duct dysplasia (P=0.001), CC (P=0.023), and IBD (P=0.03). Gallbladder dysplasia was associated with hilar/intrahepatic bile duct dysplasia (P=0.0006), CC (P=0.028), IBD (P=0.0014), and older age at OLT (P=0.007). Neither gallbladder carcinoma nor dysplasia had a significant association with sex or PSC duration. These results indicate that complete histologic evaluation of gallbladders in patients undergoing transplantation for PSC yields high frequencies of inflammatory, metaplastic, and neoplastic changes. The strong correlation between gallbladder dysplasia/adenocarcinoma and bile duct dysplasia/CC supports the concept of a neoplastic "field effect" along the intrahepatic and extrahepatic biliary tract in PSC.
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                Author and article information

                Journal
                J Clin Med Res
                J Clin Med Res
                Elmer Press
                Journal of Clinical Medicine Research
                Elmer Press
                1918-3003
                1918-3011
                February 2014
                13 December 2013
                : 6
                : 1
                : 26-29
                Affiliations
                [a ]Department of General Surgery, 401 General Army Hospital of Athens, Greece
                [b ]Medical School of Patras, Greece
                [c ]Department of Internal Medicine, Argos District Hospital, Greece
                Author notes
                [d ]Corresponding author: Charalampos Seretis, Department of General Surgery, 401 General Army Hospital of Athens, Greece. Email: babismed@ 123456gmail.com
                Article
                10.4021/jocmr1689w
                3881986
                24400028
                5d67c5b7-4944-4391-9436-807511161ed7
                Copyright 2013, Seretis et al.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 November 2013
                Categories
                Original Article

                Medicine
                cholecystectomy,gallbladder,cancer,metaplasia
                Medicine
                cholecystectomy, gallbladder, cancer, metaplasia

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