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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of non-Hodgkin's lymphoma in individuals infected with HIV is approximately 60- to 100-fold increased over the general population. The majority of patients with AIDS-related lymphoma (ARL) present with stage III-IV disease and with B-symptoms. They often have multiple extranodal localisations, with a high incidence of central nervous system involvement. Histologically, most tumours are either diffuse large cell lymphomas or Burkitt lymphomas. Several factors, such as disrupted immune surveillance, Epstein-Barr virus infection, chronic antigenic stimulation, cytokine dysregulation and the acquisition of genetic lesions, are thought to contribute to the pathogenesis. Patients with ARL have a poor prognosis: overall survival ranges from 1.5 to 18 months. The most important adverse prognostic factors are poor performance status, a low CD4+ cell count and a history of opportunistic infections. Results of treatment with polychemotherapy compare unfavourably to results in patients without HIV infection. Since the advent of highly active antiretroviral therapy (HAART), there appears to be a decrease in the incidence of ARL. In addition, the use of HAART in combination with chemotherapy and the use of new treatment modalities may improve the outcome of this disease.
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PMID:Management of AIDS-related non-Hodgkin's lymphomas. 1151 Oct 24

The primary effusion lymphoma (PEL), commonly described in patients with AIDS, is a unique subset of diffuse large cell lymphoma in which the malignant lymphocytes proliferate exclusively in serous cavities. The cytologic, immunophenotypic, and molecular features of PEL are presented from findings of 2 patients coinfected with HIV and hepatitis C virus who presented with abdominal pain. Abdominal radiography in both patients displayed marked peritoneal effusions. Cytomorphologic examination of peritoneal fluid revealed a malignant lymphoma in both. Their immunophenotypic expression was CD30 (Ki-1) and epithelial membrane antigen. Molecular analysis demonstrated human herpesvirus 8 DNA in both patients and bcl-2 oncogene rearrangement within the major breakpoint region of t(14;18) chromosome translocation in Case B only. Clinical correlation supports the current concept that PEL represents a primary HIV/AIDS-related lymphoma in effusion. Cytomorphologic examination of body cavity fluid serves as a tool for the initial diagnosis of PEL.
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PMID:Primary effusion lymphoma with herpesvirus 8 DNA in patients coinfected with HIV and hepatitis C virus: a report of 2 cases. 1157 Feb 67

This review addresses various aspects of HIV infection pertinent to hematology, including the consequences of HIV infection on specific aspects of hematopoiesis and an update on the current biologic, epidemiologic and therapeutic aspects of AIDS-related lymphoma and Hodgkin's disease. The results of the expanding use of progenitor cell transplantation in HIV infected patients are also reviewed. In Section I, Dr. Scadden reviews the basis for HIV dysregulation of blood cell production, focusing on the role of the stem cell in HIV disease. T cell production and thymic function are discussed, with emphasis placed upon the mechanisms of immune restoration in HIV infected individuals. Results of clinical and correlative laboratory studies are presented. In Section II, Dr. Levine reviews the recent epidemiologic trends in the incidence of lymphoma, since the widespread availability of highly active anti-retroviral therapy (HAART). The biologic aspects of AIDS-lymphoma and Hodgkin's disease are discussed in terms of pathogenesis of disease. Various treatment options for these disorders and the role of concomitant anti-retroviral and chemotherapeutic intervention are addressed. Drs. Zaia and Krishnan will review the area of stem cell transplantation in patients with AIDS related lymphoma, presenting updated information on clinical results of this procedure. Additionally, they report on the use of gene therapy, with peripheral blood CD34+ cells genetically modified using a murine retrovirus, as a means to treat underlying HIV infection. Results of gene transfer experiments and subsequent gene marking in HIV infected patients are reviewed.
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PMID:Hematologic Aspects of HIV/AIDS. 1172 99

Non-Hodgkin's lymphoma (NHL) remains the second most common malignant complication in patients with human immunodeficiency virus (HIV) infection. As we enter the third decade of the acquired immunodeficiency syndrome (AIDS) epidemic, it is apparent that the evolution of antiretroviral therapy and the emergence of combination antiviral strategies have greatly affected the natural history of HIV infection and its neoplastic complications. For example, there may be a trend for declining incidence of AIDS-related lymphoma in the United States for the first time. However, in regions of the world where the burden of HIV infection is greatest, such as in East Africa, AIDS-related lymphoma is an increasing cause of morbidity and mortality. Treatment of lymphoma has evolved coincident with improvements in antiretroviral therapy. Infusional chemotherapy regimens may offer advantages over other regimens and schedules, but comparative trials have not been done. Clinical trial data are available on which to develop therapeutic strategies to treat this disease in East Africa where pragmatic approaches are needed. Both the differences in manifestations of HIV infection and the inherent difficulties in administering cytotoxic chemotherapy in this part of the world must be taken into consideration in planning therapeutic strategies. Improved understanding of the pathogenesis of HIV infection and lymphoma will likely yield improved therapeutic interventions as well.
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PMID:Therapeutic challenges of AIDS-related non-Hodgkin's lymphoma in the United States and East Africa. 1201 Dec 22

Human herpesvirus type 8 (HHV-8; Kaposi's sarcoma-associated herpesvirus) is frequently identified in tumor tissue obtained from human immunodeficiency virus (HIV)-infected patients with Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), or multicentric Castleman's disease. The association between HHV-8 and acquired immunodeficiency syndrome (AIDS)-associated solid lymphomas is less clear. Herein, I describe the case of a man with a CD4+ count of 30 cells/microL, and HIV viral load of 90,000 copies/mL, multi-drug resistant HIV infection, and limited stage KS. Biopsy of a progressive dorsal foot rash revealed a dense, deep, lymphoid infiltrate that extended into papillary dermis but without epidermotrophism. Microscopy showed a homogeneous population of anaplastic large B cells that stained positive for CD20 (L26), CD30, and lambda light chain. In situ hybridization of tumor tissue identified Epstein-Barr virus (EBV)-encoded RNA, and polymerase chain reaction amplification yielded HHV-8-specific gene products. Staging studies did not reveal lymphoma elsewhere, and the patient began chemotherapy, but died from septic complications. Autopsy was notable only for the presence of a consolidative pneumonia. Although extranodal presentations are common in the setting of immunodeficiency, reports of AIDS-associated lymphoma presenting as a nonepidermotrophic foot lesion are rare. Such a presentation serves to broaden the differential of skin and foot lesions in the setting of HIV infection. More importantly, this case provides further support that HHV-8 can be associated with solid lymphomas that have an anaplastic large cell morphology.
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PMID:HHV-8- and EBV-associated nonepidermotrophic large B-cell lymphoma presenting as a foot rash in a man with AIDS. 1201 67

Two forms of acquired immunodeficiency have dominated the last quarter of the twentieth century and are responsible for the majority of lymphomas in the immunosuppressed: post-transplantation lymphoproliferative disorders (PTLD) and AIDS-related lymphomas (ARL). The central role of Epstein-Barr virus in PTLD has led to novel treatment strategies designed to enhance immunity to this virus both as prevention and therapy. This is achieved by reducing iatrogenic immunosuppression and adoptive immunotherapy with allogeneic cytotoxic T-lymphocytes. Improved immune function in HIV seropositive patients treated with highly active antiretroviral therapy appears to be reducing the relative risk of AIDS-related lymphoma. However, ARL will remain a frequent diagnosis with the rapidly rising incidence of HIV throughout the world. The clinical management requires expertise in both the lymphoma chemotherapy and the treatment of HIV, including antiretroviral therapy and opportunistic infection management. Modest improvements in survival have been achieved recently for ARL.
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PMID:The management of lymphoma in the immunosuppressed patient. 1246 3

The development of high-grade B-cell lymphoma in Acquired Immunodeficiency Syndrome (AIDS) patients is a relatively late manifestation induced by Human Immunodeficiency Virus-1 (HIV) infection and is considered to be an AIDS-defining condition. Multiple, ongoing molecular and cytogenetic aberrations appear necessary for the development of AIDS-related lymphoma. Studying a panel of human B-cell lines derived from patients with Burkitt's lymphoma (BL) and AIDS-associated Burkitt's lymphoma (AIDS-BL) we had described constitutive expression and secretion of large amounts of Interleukin-16 (IL-16), Macrophage Inflammatory Protein-1alpha (MIP-1alpha), Macrophage Inflammatory Protein-1beta (MIP-1beta), Interleukin-12 (IL-12), Interleukin-10 (IL-10), and Interleukin-7 (IL-7). Some of these cytokines like IL-16, MIP-1beta, MIP-1alpha and Regulated upon activation normal T expressed and secreted (RANTES) are shown to have inhibitory effect on HIV replication. Interestingly, we identified a novel transcription factor family, Macrophage Inflammatory Protein-1alpha Nuclear Protein (MNP), which is suggested as a potential target for anti-retroviral therapy based on the implication of its role and involvement as a key regulator of MIP-1alpha. It is apparent, that HIV induces the production of a cascade of cytokines and cytokine receptors. Some of these molecules serve to increase the infection and replication of HIV per se, and some others serve to induce a state of B-cell growth, activation, and differentiation. This review attempts to delineate the complex mechanisms of viral, B-cell, oncogene, cytokine/cytokine receptor and transcription factor interactions that are involved in AIDS associated lymphomagenesis. Unfolding the relationship between cytokines and the underlying mechanisms of the disease will not only help in understanding the pathophysiology but also will facilitate focusing on the development of new diagnostic and therapeutic strategies.
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PMID:Current perspectives on cytokines for anti-retroviral therapy in AIDS related B-cell lymphomas. 1276 91

Interleukin-10 (IL10) may contribute to the development of non-Hodgkin's B cell lymphoma, especially in the context of acquired immunodeficiency syndrome (AIDS), where lymphoma incidence is greatly increased. Utilizing specimens from the Multicenter AIDS Cohort Study (MACS) obtained prior to diagnosis of AIDS-associated lymphoma, detectable serum human IL10 was seen much more frequently in lymphoma cases (n = 61, 26%) compared to CD4-matched AIDS controls (5%, P = 0.004), or to HIV-infected (2%, P = 0.002) or HIV uninfected subjects (0%, P = 0.0003). In longitudinal studies, detectable IL10 occurred at times closest to but preceding lymphoma diagnosis (P = 0.01). In an independent genetic analysis of single-nucleotide polymorphisms within the promoter region of the IL10 gene in 1157 MACS subjects, a high IL10-expressing genotype (-592 C/C) was overrepresented among lymphoma subjects (P = 0.009), even when controlling for race (P = 0.006). These results suggest that elevated serum IL10 or the IL10 promoter -592 C/C genotype are associated with development of AIDS lymphoma.
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PMID:Non-Hodgkin's B cell lymphoma in persons with acquired immunodeficiency syndrome is associated with increased serum levels of IL10, or the IL10 promoter -592 C/C genotype. 1459 10

In contrast to the situation in the post-transplant setting, in HIV-infected individuals an elevated EBV load is not predictive of EBV-related malignancies. To study whether a high EBV load is already a normal situation early in HIV infection and is not related to a decrease in immune function over time, we investigated EBV load and EBV-specific CD8(+) T cells approximately 1 year before and 1 year after HIV seroconversion. EBV load significantly increased after HIV seroconversion from 205 to 1002 copies/10(6) PBMC (p < 0.001), whereas no further increase in EBV load was observed between 1 and 5 years after HIV seroconversion (median, 1827-2478 copies/10(6) PBMC; p = 0.530). Interestingly, the absolute number of EBV lytic epitope, RAKFKQLL-specific CD8(+) T cells increased over HIV seroconversion (4.78 to 9.54/ micro l; p = 0.011). Furthermore, the fraction of CD27-negative effector, RAK-specific CD8(+) T cells tended to increase (from 12.2 to 17.31% CD27(-); p = 0.051), in accordance with Ag-driven differentiation. In conclusion, both virological and immunological data support the idea that a new EBV viral setpoint is reached early in HIV infection, probably by EBV reactivation, as suggested by the preferential increase in EBV lytic epitope-specific CD8(+) T cells. These data may thus help to explain the lack of predictive value of EBV load for the occurrence of AIDS-related lymphoma.
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PMID:Altered EBV viral load setpoint after HIV seroconversion is in accordance with lack of predictive value of EBV load for the occurrence of AIDS-related non-Hodgkin lymphoma. 1515 12

Linkage of AIDS and cancer registries has indicated an increase in T-cell lymphomas among individuals infected with the HIV. The characteristics of T-cell versus B-cell lymphoma in HIV-infected patients are not well described. Retrospectively, 11 cases of T-cell lymphoma were identified from the AIDS-Lymphoma Registry at the University of Southern California. These patients were compared with 418 consecutive HIV-seropositive patients with B-cell lymphoma diagnosed and treated within the same time period. T-cell lymphomas comprised 3% of all AIDS lymphomas. Pathologic types included peripheral T-cell lymphoma in 5; anaplastic large cell lymphoma in 3; and angioimmunoblastic, enteropathy type, and human T-cell lymphotropic virus-I-related adult T-cell lymphoma/leukemia in 1 case each. No differences in demographic characteristics, history of prior opportunistic infection, or immunologic characteristics were observed between T-cell and B-cell cases. Extranodal involvement of the skin (36% vs. 2%, P < 0.001) and bone marrow (45% vs. 15%, P = 0.019) was significantly more common in T-cell lymphomas. The median survival of patients with T-cell lymphomas was not significantly different from that of B-cell lymphoma patients (10.6 vs. 6.6 months, P = 0.13). T-cell lymphomas in HIV-infected patients represent a spectrum of pathologic types. T-cell lymphomas differ from B-cell cases in terms of a higher propensity for skin and bone marrow involvement. The median survival of patients with T-cell lymphoma is comparable to that of patients with B-cell AIDS-related lymphoma.
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PMID:T-cell lymphoma in HIV-infected patients. 1524 54


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