Comparison of two serological tests for the identification of recent HIV infection: Vironostika HIV-1 Microelisa and BED capture enzyme immunoassay.

A literature search with no date limits in PubMed using the keywords " lymphomatoid granulomatosis " and " larynx " found only two reported cases where LG affects the larynx, but in both of them, laryngeal disease was associated with pulmonary involvement. 2,3 The larynx has its own lymphatic structure called larynx-associated lymphoid tissue (LALT). In the subglottis, LALT is replaced throughout life by a diffuse infiltration of strong intensity consisting predominantly of CD3-positive T lymphocytes with scattered CD20-positive B cells, 4 therefore LG could be originated in subglottic tissues. LG pathogenesis is unclear, but it has been linked to EBV and immunodeficiency. As regards the close to 100% EBV association with LG and the presumed wide expression of EBV latent encoded proteins, it has been strongly inferred that EBV is not just an innocent bystander in the pathogenesis of LG. 5 When dealing with immunodeficiency, it has been proven that most patients with LG have defects in cytotoxic T cell function. That would explain how LG is less rare in many immunodeficiency states. 6 In our case, CD4 count cell was 124 cell/␮l due to a good treatment compliance with discordant response. Many studies have analyzed the connection between LG and AIDS. HIV infection is associated with an increased risk of lymp-homas by 60-165 fold even in the combined antiretroviral therapy era. Excellent outcomes with infusion therapy and concurrent ritu-ximab have been reported in the treatment of some of them. 7 We report that laryngeal LG can mimic Reinke's edema in its early stages. In our own experience, Reinke's edema should not be treated as a casual finding in patients with fever of unknown origin or immunodeficiency. Our current case was classified as grade III of LG, which is histo-logically considered as diffuse large B-cell malignant lymphoma, 8 but the first biopsy was reported as polymorph lymphoid proliferation related to a post-transplant lymphoproliferative disorder (PTLD), which can simulate a lower grade of LG. LG and PTLD are associated with immunodeficiency and are driven by EBV. Histo-pathologically, they present a morphological spectrum spanning polymorphic through monomorphic lymphoid proliferations. 9 The distinctness of LG and PTLD has been emphasized by the difference in the immune response. While LG has a large population of background T-cells, PTLD is recognized by a poor T-cell enviroment. 5 A better awareness of LG in recent years is at present allowing new therapeutic tools for this …