Immunodeficient individuals are prone to develop a number of opportunistic infections and unique neoplasms. Epstein-Barr virus-associated smooth muscle tumor is an uncommon neoplasm associated with immunodeficiency. It has been described in patients infected with human immunodeficiency virus, in the posttransplant setting, and in those with congenital immunodeficiency. Different anatomic sites can be involved by Epstein-Barr virus-associated smooth muscle tumor, and even multiple locations can contain these unique lesions within the same patient. The presence of variable numbers of intratumoral lymphocytes and primitive round cell areas are the unique defining features for this tumor. Histopathologic features may vary considerably in terms of cellular atypia, mitotic activity, and necrosis, with no correlation to the clinical behavior. Demonstration of Epstein-Barr virus infection by in situ hybridization within tumor cell remains critical for the diagnosis. The mechanism for Epstein-Barr virus infection of progenitor cells and neoplastic transformation has been an area of interest and conjecture. Different treatment strategies are proposed according to underlying disease status. This paper reviews the clinicopathologic features of this uncommon neoplasm with detailed discussion of the role of Epstein-Barr virus in the pathogenesis.
Histoplasma capsulatum, a dimorphic fungus often, is asymptomatic in the immunocompetent but can cause life threatening infection in immunocompromised patients. It is uncommon in the solid organ transplant recipients with an incidence of < 1%, majority occurring within 2 years of transplantation. It can be either endogenous reactivation of latent infection, de novo acquisition, or donor-derived infection. Disseminated infection is common, with non-specific symptoms, fever being the commonest. None of the available tests is 100% accurate. Modification of immunosuppression and anti-fungal can achieve 90% success rate. We report a liver transplant recipient, 3 months post-transplantation on everolimus, prednisolone, mycophenolate, and tacrolimus who had isolated hepatic histoplasmosis and responded to treatment. Liver biopsy revealed epithelioid granulomas with narrow-based budding yeast, suggesting histoplasma. Contrast CT abdomen revealed normal attenuation of graft liver few small non-enhancing hypodense lesions seen scattered in both lobes. And this patient was managed with just reduction of immunosuppressive doses as the patient was having renal dysfunction; starting itraconazole will lead to further deterioration in the clinical course and also interact with calcineurin inhibitors and mycophenolate mofetil.
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