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

Current treatment options for acquired-immunodeficiency syndrome (AIDS)-related non-Hodgkin's lymphoma (NHL) are unsatisfactory because of excessive toxicity rates and frequent recurrence of lymphoma. In this phase II study, we evaluated a novel 12 week chemotherapy program with respect to feasibility, toxicity and therapeutic results. Thirty HIV-seropositive patients with intermediate grade or small non-cleaved cell NHL received a 12 week program of weekly intravenous and oral chemotherapy consisting of etoposide, adriamycin, cyclophosphamide, bleomycin, vincristine, methotrexate and prednisone as well as biweekly intrathecal cytosine arabinoside. Prophylaxis against Pneumocystis carinii pneumonia (PCP) and candida were given routinely. The overall objective response rate was 73% with 33% complete responders. The time to progression for those stable or responding was 9.4 months. Five of 10 complete responders are well and free of disease 13.2 to 24.5 months from diagnosis. Median survival for the 30 patients was 8.1 months. NHL was the most common cause of death (13/22); opportunistic infection caused only one death (cryptococcal meningitis). Only 1 case of PCP occurred. The major toxicity was neutropenia. In conclusion this regimen resulted in response rates similar to other reports with acceptable toxicity and a very low incidence of PCP. Relapse of NHL remains a major challenge, however, and further studies are needed. Routine PCP prophylaxis should be incorporated into new trials of therapy for AIDS-related NHL.
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PMID:Treatment of AIDS-related non-Hodgkin's lymphoma with a twelve week chemotherapy program. 128 56

The French-Italian Cooperative Study Group included patients with poor-prognosis AIDS-related non-Hodgkin's lymphoma (NHL), defined as those with performance status (PS) > or = 3 and/or opportunistic infections (OI), in a prospective study with a 50% reduced-dose combination chemotherapy regimen: CHVmP-Vincristine-bleo (cyclophosphamide 300 mg/m2 i.v. day 1, doxorubicin 25 mg/m2 i.v. day 1, teniposide 30 mg/m2 i.v. day 1, prednisone 20 mg/m2 per os days 1-5, vincristine 2 mg i.v. day 15, and bleomycin 10 mg i.v. day 15), given every 21 days for eight cycles, and concomitant zidovudine 500 mg per os per day. The aims of this combined treatment were to reduce bone marrow toxicity and infectious complications related to chemotherapy (with a low-dose chemotherapy regimen), and to control the HIV and related infectious complications (with zidovudine therapy). Thirty-seven patients entered this prospective study. At the time of the NHL diagnosis, 41% of the patients had asymptomatic HIV infection, 27% had ARC and 32% had already had CDC-defined diagnoses of AIDS. The median CD4+ cell count was 35 mm3. Only 29 patients are evaluable for response, since 8 received only one cycle of chemotherapy. Fifteen of 29 (52%) patients obtained objective responses, with only 4 (14%) achieving complete remissions (CR) of 1, 4, 14 and 29+ months. Three (16%) CRs were achieved in 19 evaluable patients included in the study because of poor PS, and only one CR was observed in 10 evaluable patients with histories of OI, either alone or with poor PS. The most common side effect was bone marrow toxicity with 2 related toxic deaths.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective study with combined low-dose chemotherapy and zidovudine in 37 patients with poor-prognosis AIDS-related non-Hodgkin's lymphoma. French-Italian Cooperative Study Group. 128 47

During the past 4 years, 122 patients with AIDS and 20 with thoracic lymphoma associated to AIDS were observed. There were 18 cases of non-Hodgkin's lymphoma, mostly at a high grade and a high b-cell stage (Burkitt's or Burkitt-like lymphoma) (16 cases). This prevalence reflects the general increase in the number of neoplasms secondary to immunosuppression, which goes along with the improvement of prevention and the control of opportunistic infections. Out of these 20 lymphomas in AIDS, 5 (25%) produced thoracic lesions; in 4 cases, the initial site of the disease was in a thoracic site. The frequency of such expressions is greater that reported in the literature. The radiological appearances are atypical relative to the classical signs of lymphoma in the general population, with predominantly nodular forms (60%) or peripheral, fast-growing masses that are likely to invade the thoracic wall. Isolate lymph node invasion is possible, as well as pleural effusion. Though not pathognomonic, this appearance is highly suggestive of lymphoma in AIDS (LDS) in HIV-positive patients. In all patients with pulmonary lymphoma, CT showed bilateral lesions in a greater number than plain radiography had shown, with morphological and CT appearances that allowed a correct approach of the diagnosis and an appropriate choice of the site of biopsy.
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PMID:[Thoracic lymphoma and AIDS]. 129 99

We describe a case of cytomegaloviral laryngitis and probable primary laryngeal malignant non-Hodgkin's lymphoma in a man with acquired immunodeficiency syndrome who presented to an otolaryngology clinic with odynophagia and hoarseness. While both of these disease processes have a known association with human immunodeficiency virus infection, laryngeal presentation is extremely rare. We stress the need for thorough clinical and pathologic otolaryngologic evaluation of patients with human immunodeficiency virus infection who have upper aerodigestive complaints.
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PMID:Cytomegaloviral laryngitis and probable malignant lymphoma of the larynx in a patient with acquired immunodeficiency syndrome. 131 14

Excesses of non-Hodgkin's lymphoma have been observed among farmers exposed to phenoxyacetic acid herbicides and, less persuasively, among workers exposed to insecticides. Exposure to organic solvents (particularly chlorinated hydrocarbons) has also been associated with an increased risk of NHL. TCDD (which is a contaminant of phenoxy herbicides), DDT, and chlorinated solvents have all been reported to induce impairment or suppression of cell-mediated immunity. We hypothesize that NHL is caused by common viruses, such as the Epstein-Barr virus, that induce proliferation and immortalization of B-cells, followed by T-cell impairment entailing cell-mediated immunodeficiency. The increased risk of NHL with HIV infection and heart or kidney transplantation, in which immunodeficiency also occurs, is consistent with this hypothesis.
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PMID:The role of occupational exposure and immunodeficiency in B-cell malignancies. Working Group on the Epidemiology of Hematolymphopoietic Malignancies in Italy. 131 21

Herein we have provided a panorama of the clinical, histopathologic, and molecular biologic mechanisms of EBV-induced LPD particularly in immunosuppressed individuals. A listing of EBV-related diseases is shown in Table 4. We have stressed the frequent need to use multiple diagnostic methods for detecting EBV genome, particularly in immunodeficient patients who may fail to mount antibody responses to EBV. Given that we now recognize some of the immunocompromised patient populations at high risk for EBV-induced LPD, and have developed techniques for detecting EBV genome and early LPD, we may eventually prevent the occurrence of some of these life-threatening diseases. For example, we have learned to recognize and distinguish hepatic allograft rejection from EBV-induced LPD in hepatic biopsies (154). A periportal and sinusoidal infiltrate of small and large lymphoid cells, immunoblasts, and plasma cells, alert us to stain frozen liver sections for EBNA. Finding EBV guides the clinicians to reducing immunosuppression which then allows the restoration of immunosurveillance against the EBV-infected B cells. Whether an EBV vaccine can be successful in immunosuppressed individuals remains to be seen. As for other vaccines, many logistical problems prevail, such as the early occurrence of EBV infection during infancy in regions where BL is endemic. Surely, with the menacing threat that approximately 10% of patients with AIDS will develop NHL, new anti-viral therapy against EBV and the causative agent of AIDS and HIV, will be developed. The pathologist and virologist play essential roles in the recognition of EBV infection by performing clinical laboratory determinations. The characteristic histopathologic features of EBV-induced LPD are now recognized and when confirmed with molecular hybridization and immunofluorescent techniques will provide a solid diagnostic approach and, thus, a foundation for developing a sound therapeutic strategy.
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PMID:Epstein-Barr virus-associated lymphoproliferative disorders. 132 Jul 11

The data presented here indicate that the pathogenesis of AIDS-NHL is variably associated with multiple genetic alterations including monoclonal EBV infection, oncogene activation (c-myc, N-, Ki-ras) and tumor suppressor gene (p53) inactivation. Up to three (3 cases) or four (1 case) different lesions have been observed in the same tumor. The distribution of these lesions among the various histotypes is heterogeneous, although some preferential associations have been found either between lesion and histotype or between lesions. The most notable case involves p53 mutations/loss that is exclusively associated with the SNCC lymphoma subtype. Since alterations of the c-myc gene occur at very high frequency in this same histotype it is possible that both lesions may be required for the pathogenesis of the BL phenotype. The consistent negativity of p53 lesions in other NHLs associated or non associated with HIV infection (18) reinforces this hypothesis. Finally, we note that the frequency of p53 mutations is significantly higher in AIDS-BL than in non HIV-related BL (18), although the significancy of this difference remains to be assessed. This study confirms the relatively low frequency of EBV infection in systemic AIDS-NHL in general, but reinforces the notion that EBV may be required for the pathogenesis of AIDS-LC-IBP, as recently suggested by the high frequency of EBV positivity in primary CNS AIDS-NHL which are mostly represented by LC-IBP (2). Conversely, the low frequency of EBV sequences in the AIDS-SNCC lymphomas appears similar to that observed in sBL. Only in a small minority of cases were ras oncogene mutations found, mostly associated with the BL type.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular pathogenesis of HIV-associated lymphomas. 132 69

HIV-1-related neurological diseases, excluding opportunistic infections and HIV encephalitis, are considered here. Most occur in severely immunosuppressed patients, with CD4 counts of under 200 x 10(6) l-1. Primary brain lymphoma and metastases from systemic non-Hodgkin's lymphoma, the second commonest cause of cerebral mass lesions in AIDS, are usually aggressive B cell tumours. Their poor median survival after treatment, compared with that of lymphomas in non-AIDS patients, seems related to systemic complications, particularly opportunistic infections. Kaposi's sarcoma produces neurological symptoms exceptionally. Cerebral infarction is often unrecognized clinically but large vessel arteritic occlusions may occur. Intracranial haemorrhages occur mostly in thrombocytopenic patients. Seizures are frequently referred to the neurologist; investigation may lead to a diagnosis of AIDS. Nearly 50% of patients with seizures have cerebral toxoplasmosis or cryptococcal meningitis; HIV-1 encephalitis is presumed to be the cause in 30%. A subacute or chronic vacuolar myelopathy with pyramidal and posterior column signs is the commonest form of spinal cord involvement in AIDS; its cause remains unknown. Peripheral nerve syndromes occur at all stages of HIV-1 infection. Distal symmetrical peripheral neuropathies are the most frequent, particularly a painful form with axonal atrophy, associated with CMV infection, and seen during ARC or AIDS. Mononeuritis multiplex due to vasculitis, CMV, or lymphoma and a serious lumbosacral polyradiculopathy due to CMV are infrequent. The commonest myopathy is due to zidovudine (AZT); it usually responds to drug withdrawal. The nature, prognosis and optimal management of most other myopathies is yet to be determined.
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PMID:Other neurological diseases in HIV-1 infection: clinical aspects. 134 49

Immunosuppressed persons are at greater risk of developing malignancies. In human immunodeficiency virus (HIV) immunosuppression the most common oral cancers are Kaposi's sarcoma and non-Hodgkin's lymphoma. Squamous cell carcinoma has also been reported to be associated with HIV disease. Kaposi's sarcoma is the most frequent neoplastic disease in acquired immunodeficiency syndrome and is by far the most common in the head and neck area. This article reviews the prevalence, clinical features, and management of these diseases in HIV infection.
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PMID:Head and neck malignancies associated with HIV infection. 137 99

The majority of lymphomas in the setting of acquired, iatrogenic, or congenital immunodeficiencies are B-cell lymphoproliferations. We describe a rare T-cell lymphoma in a fulminantly ill patient infected with human immunodeficiency virus type 1 (HIV-1). The T-cell nature of the process was defined genotypically (monoclonal T-cell receptor beta-chain [CT beta] rearrangement) and phenotypically (CD45RO+, CD4+, CD5+, CD25+, CD8-, CD3- and negative for a variety of B-cell and monocyte markers). The CD4+, CD25+ (interleukin-2 receptor [IL-2R]) phenotype with production of IL-2 and IL-2R RNA is analogous to human T-lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma (ATLL); however, no HTLV-1 could be detected. Southern blot analysis did demonstrate monoclonally integrated HIV-1 within the tumor genome. Furthermore, the tumor cells were producing HIV p24 antigen as shown by immunohistochemistry. This is the first case of acquired immunodeficiency syndrome (AIDS)-associated non-Hodgkin's lymphoma in which HIV-1 infection may have played a central role in the lymphocyte transformation process.
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PMID:Acquired immunodeficiency syndrome-associated T-cell lymphoma: evidence for human immunodeficiency virus type 1-associated T-cell transformation. 137 87


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