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• W2087785382 abstract "Histoplasmosis, a dimorphic fungus, and sarcoidosis, a disease of unknown etiology, share many clinical features, including typical manifestations of granulomatous inflammation involving the lungs and mediastinal lymphatics in association with constitutional symptoms. As such, they are often difficult to distinguish based upon clinical presentation. Recent studies suggest that sarcoidosis may be triggered by infectious agents. Here we present a case of documented pulmonary histoplasmosis that evolved into sarcoidosis. This case supports the notion that infections promote sarcoidosis in predisposed hosts. Histoplasmosis, a dimorphic fungus, and sarcoidosis, a disease of unknown etiology, share many clinical features, including typical manifestations of granulomatous inflammation involving the lungs and mediastinal lymphatics in association with constitutional symptoms. As such, they are often difficult to distinguish based upon clinical presentation. Recent studies suggest that sarcoidosis may be triggered by infectious agents. Here we present a case of documented pulmonary histoplasmosis that evolved into sarcoidosis. This case supports the notion that infections promote sarcoidosis in predisposed hosts. First described in 1877 by Dr. Jonathan Hutchinson, sarcoidosis, a non-caseating granulomatous disease affecting multiple organs, remains a mystery in its etiology and pathogenesis. It is commonly believed that sarcoidosis arises when a genetically susceptible host is exposed to various environmental triggers.1Access Research GroupDesign of case controlled etiologic study of sarcoidosis (ACCESS).J Clin Epidemiol. 1999; 52: 1173-1186Abstract Full Text Full Text PDF PubMed Scopus (137) Google ScholarHistoplasma capsulatum, the pathogen responsible for pulmonary histoplasmosis, is a common cause of self-limited granulomatous inflammation in the lungs of residents of the Ohio and Mississippi Valleys, and is difficult to distinguish from sarcoidosis in the clinical setting.2Wheat L.J. French M.L. Wass J.L. Sarcoid manifestations of histoplasmosis.Arch Internal Med. 1989; 149: 2421-2426Crossref PubMed Google Scholar Here we describe a case of an individual with a documented pulmonary infection with histoplasmosis who subsequently developed pulmonary sarcoidosis. A 55-year-old previously healthy white male presented with several weeks of progressive shortness of breath, night sweats, weight loss and dry non-productive cough. His symptoms developed soon after the belfry of the church, of which he was the pastor, underwent a cleaning to remove copious amounts of bat guano. He and his secretary both developed pulmonary and constitutional symptoms, and were eventually referred to a local pulmonologist when their symptoms failed to improve with oral antibiotics. The Pastor's evaluation included a chest X-ray, which demonstrated patchy right middle and lower lobe infiltrates, and an elevated urine histoplamosis antigen. The patient was treated with itraconazole for 12 weeks with initial improvement in some of his symptoms, particularly the constitutional symptoms. However, the dyspnea and cough continued to progress despite antifungal therapy. He was then referred to a tertiary hospital for further evaluation. A CT scan of the chest showed prominent bilateral interstitial infiltrates with evidence of fibrosis at the lung bases, and pulmonary function tests demonstrated mild restrictive physiology. He was subsequently referred for an open lung biopsy, which demonstrated prominent granulomatous pneumonitis with moderate intra-alveolar septal fibrosis. Special stains and cultures for fungus and acid-fast bacilli were negative. He was treated with oral corticosteroids with good results, including subjective improvement of his pulmonary symptoms and objective improvements in his pulmonary function parameters over the next 6 months. Of note, his secretary recovered from her case of pulmonary histoplasmosis uneventfully. It is often difficult to distinguish sarcoidosis from pulmonary infections (mycobacterial, fungal) based solely on clinical presentation. Here we describe a case in which pulmonary histoplasmosis evolved into a chronic non-infectious pulmonary disease, which pathologically conformed to the diagnosis of sarcoidosis. It is unlikely that the onset of sarcoidosis preceded pulmonary histoplasmosis, because the patient had no symptoms even during jogging, prior to the cleaning of the belfry of his church. Although we can find no precedent for a case of documented pulmonary histoplasmosis transforming into sarcoidosis, there are plenty of cases wherein the diagnosis of sarcoidosis preceded the onset of histoplasmosis,3Abarquez C.A. Sharma O.P. Histoplasmosis in a patient with sarcoidosis.Sarcoidosis. 1991; 8: 69-71PubMed Google Scholar suggesting that the original diagnosis of sarcoidosis was erroneous or that sarcoidosis or associated treatment predisposes to fungal infection. In this case, it would appear that uncontrolled pulmonary granulomatous inflammation (sarcoidosis) evolved after the resolution of pulmonary histoplasmosis and, as such, may represent a persistent inflammatory response to fungal antigens. The putative relationship between environmental exposures and sarcoidosis was recently explored in A Case-Control Etiologic Study of Sarcoidosis (ACCESS), which showed positive correlations between certain environmental and occupational exposures and sarcoidosis.1Access Research GroupDesign of case controlled etiologic study of sarcoidosis (ACCESS).J Clin Epidemiol. 1999; 52: 1173-1186Abstract Full Text Full Text PDF PubMed Scopus (137) Google Scholar High risk exposures included agricultural employment and work environments associated with exposures to mold and mildew.4Newman L.S. Rose C.S. Bresnitz E.A. et al.A case control etiologic study of sarcoidosis, environmental and occupational risk factors.Am J Respir Crit Care Med. 2004; 107: 1324-1330Crossref Scopus (441) Google Scholar Other investigations suggest that exposure to certain infections, including mycobacteria, viruses, and propionobacteria, predispose to sarcoidosis.5Du Bois R.M. Goh N. McGrath D. Cullinan P. Is there a role for microorganisms in the pathogenesis of sarcoidosis (Minisymposium)?.J Internal Med. 2003; 253: 4Crossref Scopus (100) Google Scholar However, efforts to identify specific infectious agents have not consistently demonstrated an association with sarcoidosis. Moreover, a recent study revealed a strong association between a mutation of a gene located on chromosome six (butyrophilin-like 2), which is believed to regulate T-cell activity, and sarcoidosis in Germans,6Valentonyte R. Hampe J. Huse K. et al.Sarcoidosis is associated with a truncating splice site mutation in BTNL2.Nat Genet. 2005; 37: 357-364Crossref PubMed Scopus (372) Google Scholar and similar mutations appear to contribute to disease in North Americans.7Rybicki B.A. Walewski J.L. Maliarik M.J. et al.The BTNL2 gene and sarcoidosis susceptibility in African Americans and Whites.Am J Human Genet. 2005; 77: 491-499Abstract Full Text Full Text PDF PubMed Scopus (178) Google Scholar The current case, and other reports demonstrating retained byproducts of infectious agents in the tissues of patients with sarcoidosis,8Song Z. Marzilli L. Greenlee B.M. et al.Mycobacterial catalase-peroxidase is a tissue antigen and target of the adaptive immune response in systemic sarcoidosis.J Exp Med. 2005; 201: 755-767Crossref PubMed Scopus (267) Google Scholar supports the likelihood that sarcoidosis is a disease in which environmental factors, including infectious agents, together with a genetic predisposition of the host, combine to influence disease phenotype." @default.
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• W2087785382 title "Transformation of pulmonary histoplasmosis to sarcoidosis: A case report" @default.
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