Lymphoma In HIV-infected Patients Research Articles

Lymphoid infiltrates of the salivary glands

Lymphoid infiltrates of the salivary glands are common to a variety of pathologic conditions including autoimmune disorders, malignant lymphomas, and immunoregulatory responses to parenchymal neoplasms. Clearly, the correct identification of these salivary gland lymphoid infiltrates has important implications regarding patient prognosis and management. Immunophenotypic and molecular analyses have demonstrated that many lesions formerly regarded as myoepithelial sialadentis or benign lymphoepithelial lesion in fact represent neoplastic lymphoid proliferations with the potential for extrasalivary dissemination. In the most recent classification scheme of non-Hodgkin's lymphomas, these neoplasms fall within the spectrum of low-grade B-cell lymphoma of mucosa-associated lymphoid tissue. In the early stages of HIV infection, patients may develop salivary gland enlargement resulting from cystic lymphoepithelial lesions. These lesions are thought to reflect a localized manifestation of persistent generalized lymphadenopathy. Although HIV-associated salivary gland disease is regarded as a benign condition, malignant lymphoma has been described in association with some of these lesions, and further work is required to define more precisely the risk of salivary gland lymphoma in HIV-infected patients. Tumor-associated lymphoid proliferation refers to a prominent lymphoid reaction accompanying certain epithelial tumors of the salivary glands. Although tumor-associated lymphoid proliferation has not received as much attention as other types of salivary lymphoid infiltrates, it is a common phenomenon that is sometimes mistaken for an intraparotid lymph node harboring metastatic carcinoma.

Epstein-Barr Virus-Associated Non-Hodgkin's Lymphoma in HIV-infected Patients

Epstein-Barr virus (EBV) has been implicated in the pathogenesis of many lymphoproliferations arising in diverse settings, including HIV-infection. The precise roles of EBV may differ between these settings. For example, both the frequencies of EBV-association and the specific c-MYC translocations differ between sporadic and African Burkitt's lymphoma. Similarly, the frequencies of EBV-association in HIV-infected patients differs between anatomical sites, types of NHL, and geographic locations. HIV-related NHL have genetic alterations similar to NHL arising in the general population, and have less in common with the lymphoproliferations which arise in the setting of transplantation. However, the patterns of latent EBV transcription in systemic HIV-related NHL is unique among NHL, suggesting that EBV may contribute differently to their pathogenesis.

Clinical and biological characteristics of malignant lymphomas in HIV-infected patients

THE ACQUIRED IMMUNODE~~CIENCY SYNDROME (AIDS) was described at the beginning of the last decade with the observation of opportunistic infections (especially Pneumocystis pneumonia) and Kaposi’s sarcoma within homosexual men with marked acquired immunosuppression [ 1, 21. Besides homosexual men, other groups (intravenous drug users, haemophiliacs) presented a similar syndrome in the USA and Europe. In Africa, AIDS spread rapidly in young adults of both sexes as well as in infants of infected mothers. In 1983-84, the pathogenic virus was first isolated in France and then in the USA [3, 41. The main targets of the human immunodeficiency virus (HIV) are the T-helper lymphocytes, which are infected through the surface CD4 receptor that is recognised by the viral envelope glycoprotein gp120 [5-71. Some monocytes and macrophages also express the CD4 receptor and may also be infected by HIV [8, 91. The virus causes the destruction of CD4 lymphocytes by direct cytolysis, syncitia formation, as well as by other immune and auto-immune mechanisms [ 10-131. The result is progressive and severe impairment of cellular immunity. In addition to the T-cell deficit, HIV causes important disorders in humoral immunity. HIV proteins trigger B-cell proliferation either in a mitogenic or an antigen-specific manner [14, 151. The mitogenic response may be directly caused by the virus (independently of accessory cells), and also by the release of cytokine, such as interleukin 6 [16, 171. B-cell activation is characteristic of patients with mild as well as severe manifestations of HIV infection [ 181. Infected subjects display increasing serum levels of irnmunoglobulins, circulating immunocomplexes and also an increased number of peripheral lymphocytes spontaneously secreting immunoglobulin [ 19, 201. In addition, seropositive individuals develop a persistent generalised lymphadenopathy (PGL) in approximately 30% of the cases. This lymphadenopathic syndrome is characterised by an exuberant hyperplasia of the germinative centres, where B-cell maturation occurs, with polyclonal B-cell proliferation [21, 221. Severe immunodeficiency together with chronic antigenicimitogenic stimulation has been associated with lymphoid malignancies [23-271. Thus, HIV infection may be considered as a prelymphomatous state. The first cases of Burkitt’s lymphomas (BL) in homosexual men were reported in 1982 [28, 291. In 1983, with the observation of several cases of aggressive non-Hodgkin lymphomas (NHL) in risk groups for AIDS, a definitive relation between NHL and AIDS was established [30]. This association was further confirmed epidemiologically [3 1, 321. In 1985, the inci

Oral manifestations of non-Hodgkin's lymphoma in HIV-infected patients

The incidence of non-Hodgkin's lymphomas (NHL) in patients infected with human immunodeficiency virus (HIV) is relatively high. However, there have been few reports on the clinical and histopathological features of oral manifestations of NHL in these patients. The lesions reported so far were all tumorous swellings with or without ulceration, as in non-HIV-infected patients. In this report 3 cases are presented of HIV-infected patients with solitary, primary oral NHL. These lesions showed a striking resemblance to acute, necrotizing gingivitis, a common finding in these patients, thus making the diagnosis more difficult.

Oral lymphomas in HIV-infected patients: Association with Epstein-Barr virus DNA

Nine instances of oral non-Hodgkin's lymphoma occurring in homosexual male patients infected with the human immunodeficiency virus were evaluated for clinical features, histopathologic features, lymphocyte phenotypic markers, and Epstein-Barr virus (EBV) DNA. Histologically, the tumors represented immunoblastic sarcoma and small noncleaved cell lymphomas, some manifesting Burkitt-like features. Five cases exhibited positive staining with monoclonal antibody L26, a B-cell marker; none of the tumors showed evidence of a T-cell lineage with the use of monoclonal antibody UCHL 1. DNA in situ hybridization studies disclosed the presence of EBV DNA sequences in seven instances. These findings indicate that most oral lymphomas among patients with AIDS, similar to extraoral lymphomas in this population, are of B-cell lineage and harbor EBV DNA.