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

The aim of the present was to study the possible clinical histological correlations in the cases of lymphomatoid granulomatosis (LG) diagnosed in the last 10 years. Clinic evolutive data were collected in 7 patients diagnosed LG. The histological samples related to the same were revised and an immunohistochemical study was carried out with the oxidase/antiperoxidase technique. Seven patients (5 females and 2 men) with a mean age of 47 years (limit 23-47) were studied. The form of presentation was alteration of the general state in 5 cases accompanied by respiratory symptoms in 4. In 2 cases lung involvement was not found. In 7 biopsies performed at the initiation of the disease, 3 presented characteristics of lymphoma. Three patients are presently alive with a mean follow up time of 31 months and 4 have died (mean survival 17 months). Immunohistochemistry demonstrated T lymphocyte predominance in most of the cases (5 out of 6). The first case of LG in a patient simultaneously infected with the HIV and HTLV-1 is presented. Lymphomatoid granulomatosis possesses a symptomatology which is very inspecific and has histological features which may be superposed to other lymphoproliferative disorders, specially those of the T strain. Given the known relation between HTLV-1 and T lymphomas the role of HTLV-1 in the genesis of LG should be studied in these patients specially in those with the HIV.
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PMID:[Lymphomatoid granulomatosis: clinicopathologic analysis of 7 cases]. 160 54

Malignant lymphoma with meningeal involvement was detected in 7 patients with stage IV HIV infection. The diagnosis of lymphoma was made at a maximum of four months before discovery of meningeal involvement. In our seven cases the lymphoma was B-cell type, one case expressed Kappa chains, four cases demonstrated Lambda chains and in two cases differentiation was not possible. A review of findings in all HIV positive patients treated in the same period revealed 10 non-Hodgkin lymphomas of the B-cell type, though meningeal and cerebral involvement was observed only in B-cell lymphoma of the Burkitt type.
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PMID:Meningitis with Burkitt like B-cell lymphoma in HIV infection. 161 39

Chronically immunosuppressed individuals are susceptible to lymphoreticular tumors. Up to 15% of patients with congenital deficiencies such as ataxia=telangiectasia may develop malignancies, mainly high-grade B cell non=Hodgkin's lymphomas (NHLs). AIDS lymphomas are comprised of NHLs including Burkitt's lymphoma (BL) and primary cerebral lymphomas (PCLs). Almost 3% of all AIDS patients (2824 of 97,258 cases) developed NHL. Epstein-Barr virus (EBV) as a co-factor in AIDS lymphomagenesis has been studied: in 12 cases of 24 AIDS lymphomas EBV by DNA in situ hybridization was found. In an analysis of 6 primary cerebral lymphomas, .5 were positive for EBV DNA by Southern blotting. In Burkitt's lymphoma the characteristic genetic alteration affects the c-myc oncogene. In 1/3 of BL p53 mutations were found but none in the 43 NHLs suggesting that p53 mutations and c-myc activation act synergistically in the pathogenesis of these tumors. Cytotoxic agents dideoxyinosine, dideoxycytosine, and zidovudine may cause secondary neoplasia. 8 of 55 AIDS patients under zidovudine treatment developed high-grade lymphoma 23.8 months subsequently; recently doses were reduced. PCL was found in 21 of 90 patients. A 5.2 months survival was associated with combined treatment with cyclophosphamide, Oncovin (vincristine), methotrexate, etoposide, and cytosine arabinoside compared with 11.3 months with chemotherapy. Colony-stimulating factors (CSFs) alleviate drug-induced myelotoxicity and zidovudine-induced neutropenia, however, l8 of 11 patients receiving granulocyte-macrophage CSF developed hematological toxicity. Interleukine-2 produced by T-helper cells enhancing tumor cells cytotoxicity has been used in AIDS-associated cryptosporidial diarrhea and in 4 patients with AIDS lymphoma with modest response, but its stimulation of the HIV-infected substrate may increase viral proliferation.
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PMID:AIDS lymphomas. 161 63

Duration of the AIDS-free period after HIV-infection and survival time vary to a wide extent. About 50 percent of the patients develop AIDS within 10 years. The most important prognostic factor is the CD4-lymphocyte count. The risk of AIDS increases significantly after CD4-lymphocyte counts drop below 400/microliters. Another prognostic factor is age. In older patients disease progresses more rapidly. AIDS often is preceded by an AIDS-Related-Complex characterized for example by Oral Candidiasis, Hairy Leukoplakia or Zoster of more than one dermatome. AIDS mostly develops 1/2 to 1 year after AIDS-Related-Complex. After AIDS is diagnosed the median survival time is not longer than 1 1/2 years. Single patients live much longer. Prognosis is influenced by the disease defining AIDS. Kaposi's Sarcoma often occurs early in the course of immunodeficiency and median survival is longer than after other opportunistic diseases. Survival also is longer after Pneumocystis Carinii Pneumonia since it is well treatable. A very short survival has been noticed after Non-Hodgkin-Lymphoma. During the last few years survival after HIV-infection and AIDS has been prolonged a little by sufficient prophylaxis of Pneumocystis Carinii Pneumonia which is the most frequent opportunistic disease, by antiretroviral treatment with Zidovudine and by increase of knowledge which makes early diagnosis and treatment of opportunistic diseases possible.
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PMID:[Survival in HIV infection and AIDS]. 162 24

The incidence of non-Hodgkin's lymphoma (NHL) has increased by over 50% in the United States since 1973. There is epidemiologic evidence that some of this increase is the result of AIDS-related lymphoma and that this component is increasing. Prolonged survival in the setting of a variety of immunodeficiency states is associated with an increased incidence of NHL. The development of antiretroviral therapy and improved therapy for the complications of AIDS has resulted in prolonged survival of patients with AIDS. As these patients survive longer with profound immunodeficiency, they have an increased cumulative risk of developing NHL. This may result in even more AIDS-related NHL in the future than predicted from current epidemiological studies. An increased understanding of the pathogenesis of AIDS-related NHL may lead to means of preventing their occurrence. Also, therapies that may prevent immunodeficiency from developing in HIV-infected patients may reduce the likelihood of NHL developing. Current efforts at treating these lymphomas are aimed at preventing the myelosuppression and immunosuppression associated with current regimens, lymphoma relapses within the central nervous system, and the opportunistic infections associated with treatment of these tumors. Ultimately, the best means of preventing the development of these lymphomas is by preventing infection with HIV.
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PMID:The occurrence of opportunistic non-Hodgkin's lymphomas in the setting of infection with the human immunodeficiency virus. 164 22

The pathogenesis of the HIV-associated lymphomas is not well understood. In order to begin characterizing this class of lymphoma, we initiated a molecular genetic study of DNA extracted from 31 diagnostic biopsy specimens from patients diagnosed with AIDS-associated non-Hodgkin's lymphoma. Analysis of 25 peripheral lymphomas showed that 14 were monoclonal B-cell processes, while 11 appeared to be of polyclonal origin. Five of the 14 monoclonal lymphomas were found to have rearrangements of the c-myc gene. Epstein-Barr virus (EBV) genomes were found in seven out of 14 monoclonal samples, but only two out of nine polyclonal samples. The six primary central nervous system (CNS) lymphoma samples were more homogeneous than the peripheral samples and all were monoclonal, positive for EBV and lacked detectable c-myc gene rearrangements. This study allows us to subdivide the HIV-associated lymphomas into three major molecular subtypes: (1) monoclonal B-cell process frequently associated with c-myc rearrangement or detectable EBV genomes, (2) polyclonal B-cell process typically without evidence of EBV, and (3) monoclonal primary CNS process associated with EBV genomes and lacking detectable c-myc rearrangement.
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PMID:Evidence for molecular subtypes of HIV-associated lymphoma: division into peripheral monoclonal, polyclonal and central nervous system lymphoma. 165 78

A 50 year old patient with non-diagnosed HIV-infection at onset of his illness developed impairment of vision and temporary double vision combined with severe hemianopsia. With normal fundus and suspicious Herpes simplex iritis therapy with Acyclovir was started. Primarily the patient showed a good response to the therapy and loss of vision could be prevented. After 4 weeks CMV-retinitis developed. In spite of Gancyclovir therapy manifestation of total loss of vision after 6 weeks. Autopsy demonstrated signs of simultaneous a CMV-infection of the retina and a herpes simplex-infection of the optic nerve combined with a Non-Hodgkin-Lymphoma of the optic tract.
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PMID:[Sudden blindness in an AIDS patient. Simultaneous infection with cytomegalovirus and herpes simplex viruses and development of malignant non-Hodgkin lymphoma]. 165 79

The authors studied all patients with serologic evidence of human immunodeficiency virus (HIV) infection and malignant non-Hodgkin's lymphoma (NHL) that presented at a single hospital from 1982 to 1989. Sixteen patients were identified, all white homosexual men with a mean age of 38.2 years. Lymphoma was the initial presentation of HIV infection in 37.5%. Sixty-two percent of the cases had a high-grade NHL, 31% had intermediate-grade, and 6% (one patient) had a low-grade lymphoplasmacytoid lymphoma. Extranodal involvement was present in 43.7%, with the gastrointestinal tract and liver being the most common sites. Actuarial survival was increased by treatment with methotrexate, doxorubicin, cyclophosphamide, vincristine, prednisone, and bleomycin (MACOP-B). Colorimetric in situ hybridization identified Epstein-Barr virus (EBV) in nine of the 14 cases hybridized. A statistically significant association of EBV with diffuse small noncleaved type (i.e., Burkitt's-like) (six of six) compared with other morphologic types (three of eight) was found (P = 0.025).
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PMID:Non-Hodgkin's lymphomas in patients with human immunodeficiency virus infection. Presence of Epstein-Barr virus by in situ hybridization, clinical presentation, and follow-up. 165 57

All 51 cases of HIV-related malignant lymphoma in Denmark diagnosed from 1983 to 1989 were reviewed. There were 12 Burkitt-type lymphomas, 30 immunoblast-rich lymphomas and 9 other lymphomas. Patients with immunoblast-rich lymphomas had significantly lower CD4 cell counts (median 60 vs. 188 x 10(6)/l, P less than 0.05), and more often a history of previous AIDS-defining illnesses (50% vs. 0%, P less than 0.005), compared with patients with Burkitt-type lymphomas. Epstein-Barr virus (EBV) DNA was demonstrated in 14 of 19 immunoblast-rich tumours, and in 2 of 7 Burkitt-type lymphomas (P = 0.10). Compared with EBV DNA-negative tumours EBV DNA-positive tumours were associated with lower CD4 cell counts (median 39 vs. 188 x 10(6)/l, P = 0.01). It is concluded that two main types of HIV-related malignant lymphoma exist. One is associated with severe immunosuppression, is often of immunoblast-rich morphology, and may be linked to EBV, whereas the other may occur in the absence of immunosuppression, is often of Burkitt-type morphology, and is probably not linked to EBV. In addition to these two main types, other non-Hodgkin lymphomas and Hodgkin's disease do occur.
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PMID:HIV-associated lymphoma: histopathology and association with Epstein-Barr virus genome related to clinical, immunological and prognostic features. 166 Feb 93

This is a clarification of the nomenclature for the human retroviruses, now know as HIV-1, HIV-2, HTLV-I, HTLV-II, and HTLV-V. HIV-1 is the accepted cause of AIDS. It was formerly know as HTLV-III, LAV and ARV. HIV-2 is know to cause AIDS, was first reported in West Africa, but is now found in Europe, North and South America. Special EIA, Western Blot, polymerase chain reaction or virus isolation tests are needed to diagnose it, and it is not being screened in the U.S. Blood supply. HTLV-I was the 1st retrovirus shown to cause human disease, a T-cell leukemia/lymphoma and a myelopathy also known as tropical spastic paraparesis. It can be diagnosed by enzyme immunoassay (EIA), Western blot, radioimmunoprecipitation assay and the definitive tests, polymerase chain reaction or virus isolation. Most infected persons do not have clinical illness. HTLV-II has been found in 2 patients with hairy cell leukemia, but the etiologic relationship is uncertain. HTLV-IV is now known to be a non-human primate virus, probably a laboratory contaminant from West Africa, and does not cause any known human disease. HTLV-V is another virus that targets the CD4+ T-lymphocyte; HTLV-V is thought to cause a cutaneous T-cell leukemia/lymphoma.
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PMID:The first decade of human retroviruses: a nomenclature for the clinician. 166 Sep 67


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