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HIV associated lymphomas: problems with the histopathologic classification

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HIV associated lymphomas: problems with the histopathologic classification

Helenemarie Schaer Barbosa

The incidence of B-cells lymphoma in HIV infected individuals is increased up to 100 times. These lymphomas are usually aggressive, of high grade, disseminated and frequently extranodal. The most frequent histological types are diffuse large B cell and Burkitt's lymphomas. Recently, two new histological types were described almost exclusively in AIDS patients: Primary Effusion Lymphoma (PEL) and Plasmablastic Lymphoma. Typically Primary Effusion Lymphomas present as a cavitary effusion containing malignant neoplastic cells. Occasionally they present solid tumors simultaneously with the effusion or during the course of disease. Almost 100% of these cases are HIV+, the tumor cells are HHV8+, and more than 2/3 of the cases are EBV+. The malignant cells resemble immunoblasts and sometimes they show plasmacytoid differentiation. Half of the patients express CD45R (LCA) and 20% express CD20 (pan-B). They can also express CD38, a marker of plamocytes. The present discussion about PEL is the finding of several solid tumors with similar characteristics, HHV8+, but without effusion during the whole course of disease. Knowles, Chadburn and Cesarman's group support the idea that these cases are inside the PEL spectrum and that they should be classified as extra-cavitary variant of the PEL. On the other hand, the plasmablastic lymphoma, EBV+ and HHV8- described originally from the oral mucosa, which is a solid tumor with no effusion, has been found in other sites like nasal and paranasal sinuses, testicle, bone and anorectal regions and a few are HHV8+. Morphologically, the plasmablastic lymphoma is very similar to PEL. The malignant cells have plasmablastic differentiation (an immunoblast with plasmacytoid differentiation), in other terms they are similar to immunoblasts, large cells with vesicular nucleus and a prominent nucleolus that usually do not express normal B cell markers such as CD20, but express plasmacytoid differentiation markers such as CD38. Even the immunocytochemical profile is similar to PEL. The situation is complicated by a recent publication of HIV patients with multiple mieloma developing extramedular solid tumors with plasmablasts of similar morphology to PEL and plasmablastic lymphoma. In conclusion, patients with AIDS can present lymphomas with plasmablastic differentiation, associated or not to HHV8, generally EBV+ that sometimes present with cavitary effusion, some other times are solid tumors or even mixed. If they are part of the spectrum of the same lymphoma or distinct entities, it is not quite clear. With the present knowledge, I believe that it is too soon to classify these lymphomas, before more is known about them. To designate a solid tumor as a solid variant of effusion primary lymphoma, looks to me farfetched and does not contribute to clarify the disease. The role of HHV8 and EBV in the genesis of these lymphomas with plasmablastic differentiation need further studies.

Publication Dates

  • Publication in this collection
    06 Jan 2006
  • Date of issue
    Oct 2005
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