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      Mycobacterium tuberculosis como agente etiológico potencial de sarcoidosis Translated title: Mycobacterium tuberculosis as a potential etiologic agent of sarcoidosis

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          Abstract

          La etiología de la sarcoidosis es aún desconocida; sin embargo, se ha encontrado una fuerte asociación con tuberculosis dadas sus similitudes clínicas e histológicas. A continuación se presenta un caso clínico que muestra la coexistencia de las dos entidades y su posible asociación etiológica. (Acta Med Colomb 2013; 38: 36-39).

          Translated abstract

          The etiology of sarcoidosis is still unknown; however, a strong association with tuberculosis has been found, given its clinical and histological similarities. We present a clinical case that shows the coexistence of the two entities and their possible etiologi-cal association. (Acta Med Colomb 2013; 38: 36-39).

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          Most cited references17

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          Molecular evidence for the role of mycobacteria in sarcoidosis: a meta-analysis.

          The aetiology of sarcoidosis is currently unknown. Due to the clinical and histological similarities between sarcoidosis and tuberculosis, the role of mycobacteria has been repeatedly investigated as an aetiological agent for sarcoidosis. The current meta-analysis aimed to evaluate the available molecular evidence on the possible role of mycobacteria in the development of sarcoidosis. The MEDLINE, EMBASE, CINAHL, DARE and CENTRAL databases were searched for relevant studies published from 1980 to 2006, and studies evaluating the presence of mycobacteria using molecular techniques in biological samples of patients with sarcoidosis were included in the current analysis. The 95% confidence intervals (CI) were calculated for the expected proportion (of individual studies); the data was then pooled to obtain a summary success rate with 95% CI. The odds ratio (95% CI) was also calculated in order to assess the presence of mycobacteria in samples of patients with sarcoidosis versus those from nonsarcoidosis control samples. The database search yielded 31 studies. All studies used polymerase chain reaction for nucleic acid amplification followed by identification of nucleic acid sequences specific for different types of mycobacteria. Overall, 231 out of the 874 patients were positive for mycobacteria with a positive signal rate of 26.4 (23.6-29.5%), and the odds of finding mycobacteria in samples of patients with sarcoidosis versus controls were 9.67 (4.56-20.5%) using the random effects model and 19.49 (11.21-35.54%) using the exact method. There was methodological and statistical heterogeneity and evidence of publication bias. The results of the current study illustrate a demonstrable mycobacterial presence in sarcoidosis lesions suggesting an association between mycobacteria and some cases of sarcoidosis. To avoid methodological diversity, larger multicentre trials with a central laboratory for sample testing should be designed.
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            The immunology of sarcoidosis.

            Sarcoidosis continues to be a disease of research interest because of its complicated immune mechanisms and elusive etiology. So far, it has been established that granulomatous inflammation in sarcoidosis is predominantly a T-helper 1 immune response mediated by a complex network of lymphocytes, macrophages, and cytokines. The cause of progression to a chronic and potentially fibrotic form is unclear but may involve loss of apoptotic mechanisms, loss of regulatory response, or a persistent antigen that cannot be cleared. Recent genomic and proteomic technology has emphasized the importance of host susceptibility and gene-environment interaction in the expression of the disease.
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              Etiology of sarcoidosis.

              Research over the past decade has advanced our understanding of the pathogenesis of sarcoidosis and provided new insights into potential causes of this disease. It is important to remember that any etiologic agent of sarcoidosis must be capable of causing the pathologic hallmark of systemic noncaseating granulomas and the heterogeneous clinical features of sarcoidosis. In addition, etiologic agents must be compatible with immunologic features, including polarized T-helper 1 cytokine profiles and oligoclonal T cell expansions consistent with antigen driven processes. Yet, even with studies conducted in this disease, there remains a lack of consensus on the etiology of sarcoidosis. This challenge is likely to be overcome only with additional research that incorporates clinical, genetic, immunologic, environmental, and microbiologic profiles in groups of patients, supplemented with testing of candidate pathogenic agents in experimental models that recapitulate critical features of this disease.
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                Author and article information

                Journal
                amc
                Acta Medica Colombiana
                Acta Med Colomb
                Asociacion Colombiana de Medicina Interna (Bogotá, Distrito Capital, Colombia )
                0120-2448
                January 2013
                : 38
                : 1
                : 36-39
                Affiliations
                [01] Bogotá D.C. orgnameFundación Neumológica Colombiana
                Article
                S0120-24482013000100010 S0120-2448(13)03800110
                c807ef15-6ccf-4d5e-863f-2a814649e636

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 24 January 2013
                : 16 February 2012
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 18, Pages: 4
                Product

                SciELO Colombia

                Self URI: Texto completo solamente en formato PDF (ES)
                Categories
                Presentación de casos

                sarcoidosis,mycobacterium tuberculosis,reacción en cadena de la polimerasa,polymerase chain reaction

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