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Query: UMLS:C0032285 (pneumonia)
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The full range and occurrence of medical conditions in persons infected with human immunodeficiency virus (HIV) before they develop illnesses that define acquired immunodeficiency syndrome (AIDS) have not been systematically or completely described. In a retrospective and prospective cohort study, 1,073 homosexual and bisexual men in three US cities were interviewed and examined twice per year from January 1988 to September 1992. Study participants were from San Francisco, California (273 HIV-seropositive and 432 HIV-seronegative men), Denver, Colorado (107 positive and 129 negative men), and Chicago, Illinois (54 positive and 78 negative men). A total of 305 HIV-positive men had specifiable dates of HIV seroconversion (mean of 15.3 months between the last negative and the first positive HIV antibody test). Besides much increased incidences of thrush (incidence relative risk (IRR) = 23.3) and hairy leukoplakia (IRR = 551), the following conditions also occurred significantly more frequently in HIV-positive men than in HIV-negative men: anal herpes (incidence density (ID) = 10.7/100 person-years; IRR = 7.7); sinusitis requiring antibiotics (ID = 6.2/100 person-years; IRR = 2.1); anal warts (ID = 5.8/100 person-years; IRR = 2.7); seborrhea (ID = 3.8/100 person-years; IRR = 6.6); community-acquired pneumonia (ID = 1.4/100 person-years; IRR = 2.7); skin cancers (ID = 1.0/100 person-years; IRR = 2.2); and seizures, often apparently "breaking through" prior anticonvulsant therapy (ID = 0.8/100 person-years; IRR = 5.6). First episodes of hairy leukoplakia, thrush, and skin cancer occurred at low mean CD4 counts (mean counts were less than 350 cells/microliters) and late in HIV infection (mean times were more than 8 years after HIV seroconversion). Many medical problems, some not widely appreciated, occur in HIV-infected men before they develop AIDS-defining illnesses, signifying considerable morbidity from pre-AIDS HIV infection.
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PMID:The spectrum of medical conditions and symptoms before acquired immunodeficiency syndrome in homosexual and bisexual men infected with the human immunodeficiency virus. 853 42

To determine if the use of corticosteroids for presumed Pneumocystis carinii pneumonia exacerbated undiagnosed tuberculosis or increased the likelihood of reactivation tuberculosis, we reviewed medical records of 144 hospitalized HIV-infected patients who received antipneumocystis therapy. Ninety-four patients (Group C) received corticosteroids and 50 patients (Group NC) did not. One hundred and thirty-seven patients (97%) had acid-fast stains and mycobacterial cultures performed. Group C and Group NC were similar in ethnicity, distribution of HIV risk factors and CD4 cell count. Eight (9%) Group C patients and seven (14%) Group NC patients had culture-proven tuberculosis during their hospitalization. After a median followup of 16 mo after discharge, one (2%) Group C patient and two (4%) Group NC patients developed tuberculosis. Only one patient in Group C died of tuberculosis, despite receiving antituberculosis therapy. We conclude that the use of corticosteroids for presumed P. carinii pneumonia does not increase morbidity from undiagnosed tuberculosis or increase the frequency of reactivation tuberculosis.
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PMID:Tuberculosis in patients with HIV infection who receive corticosteroids for presumed Pneumocystis carinii pneumonia. 791 9

Increasing evidence suggests an important role for cytokines in the regulation of eosinophilic inflammation. In the present study we investigated the distribution of leukocytes, lymphocyte subsets, their activation state, and the cytokine profile present in BAL fluid from patients with various lung diseases associated with eosinophilia. For this purpose, we analyzed the levels of IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-8, GM-CSF, TNF-alpha, and IFN-gamma, as well as soluble IL-2 and TNF receptors, in concentrated bronchoalveolar lavage (BAL) fluid obtained from clearly defined patients with allergic and nonallergic asthma, eosinophilic pneumonia, allergic bronchopulmonary aspergillosis (ABPA), hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis. BAL fluid from normal individuals and sarcoidosis patients was analyzed as noneosinophilic controls. BAL cytokine levels were compared with the cellular infiltrate and the activation state of CD4+ and CD8+ T cells as measured by the expression of IL-2 receptors (CD25), HLA-DR, and the very late activation antigen VLA-1. Beside the characteristic leukocyte infiltrate in the various lung diseases, all patients demonstrated significantly increased numbers of activated CD4 and CD8 T cells compared with normal individuals. The analysis of the cytokine profile present in BAL fluid revealed a T helper type 2 (Th2) cell cytokine pattern, with elevated IL-4 and IL-5 but normal levels of IL-2 or IFN-gamma in allergic asthma. ABPA patients demonstrated significantly increased levels of IL-4 and IL-5, with low but significantly elevated concentrations of IL-2 and IFN-gamma. In contrast, the analysis of the cytokine profile in sarcoidosis patients revealed a Th1 cell cytokine pattern characterized by increased concentrations of IL-2 and IFN-gamma but normal levels of IL-4 or IL-5. All other patient groups showed a cytokine pattern incompatible with a pure Th1 or Th2 cell response, because IL-5, IL-2, and IFN-gamma were found to be significantly increased. The BAL fluid analysis of the other, mainly non-T cell-derived cytokines and soluble receptors showed increased levels in all patients compared with normal individuals and may represent the ongoing inflammatory responses. In conclusion, whereas increased IL-4 levels were found only in diseases characterized by increased IgE production, IL-5 was elevated in all patients with increased numbers of eosinophils. The close correlation between IL-5 levels, number of eosinophils, and activated T cells further supports a role for IL-5 in causing tissue eosinophilia.
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PMID:Activated T cells and cytokines in bronchoalveolar lavages from patients with various lung diseases associated with eosinophilia. 792 34

Based on our prior data suggesting a therapeutic advantage for infusional administration of cyclophosphamide (C), doxorubicin (D), and etoposide (E) in patients with relapsed and resistant non-Hodgkin's lymphoma (NHL), we administered C (750 mg/m2), D (50 mg/m2), and E (240 mg/m2) via continuous intravenous infusion over 96 hours as first line therapy for 21 patients with intermediate- or high-grade non-Hodgkin's lymphoma associated with human immunodeficiency virus (HIV) infection. Treatment was repeated every 28 or more days. The median CD4 count of the study group was 87/ul, and the median serum lactate dehydrogenase was 383 IU/L. Extranodal disease, lymphomatous marrow involvement, and lymphomatous meningitis were present at diagnosis in 90%, 33%, and 10% of patients, respectively. Complete response (CR) occurred in 13 patients (62%, 95% confidence intervals 41%, 81%) and partial response occurred in five patients (24%). The estimated median survival of the study group was 18.0 months. Hematologic toxicity required dose reduction for 47% of cycles and for 79% of patients who received at least two cycles. The mean dose intensity for C, D, and E were 73%, 70%, and 73% of the intended dose intensity, respectively. Opportunistic infection included oral/esophageal candidiasis (N = 7), herpes labialis (N = 3), pulmonary Mycobacterium avium-intracellulare (N = 1), candidemia (N = 1), pneumonitis (N = 1), and disseminated aspergillosis than resulted in a single treatment-related death (5%). Treatment resulted in a significant decrease in the CD4+ lymphocytes, as well as total lymphocytes, T lymphocytes, and CD8+ lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infusional cyclophosphamide, doxorubicin and etoposide in HIV-related non-Hodgkin's lymphoma: a follow-up report of a highly active regimen. 795 Sep 15

Bronchoalveolar lavage (BAL) populations recovered from mice with secondary influenza pneumonia contain gamma delta T cell receptor (TCR)+NK1.1- lymphocytes and gamma delta TCR-NK1.1+ natural killer (NK) cell populations. Stimulating the CD4-8- component of the BAL with a monoclonal antibody to CD3 epsilon and rIL-2 leads to the emergence of substantial numbers of CD4-8- gamma delta TCR+NK1.1+ and CD4-8- alpha beta TCR+NK1.1+ lymphocytes. The NK1.1+ gamma delta T cells are potent cytotoxic effectors, causing much higher lysis of YAC-1 target cells than the gamma delta TCR+NK1.1- lymphocytes that are present concurrently. CD4+ and CD8+ alpha beta T cells cultured in the same way express little (if any) NK1.1. The possible functional role of NK1.1+ gamma delta T cells is discussed.
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PMID:Gamma delta T cells from influenza-infected mice develop a natural killer cell phenotype following culture. 795 44

Incidence rates of AIDS illnesses are described among patients with < or = 100 CD4 cells/mm3 grouped by use of antiretrovirals and chemoprophylaxis. Data were obtained from 2646 homosexual men infected with human immunodeficiency virus type 1. Participants were in the Multicenter AIDS Cohort Study during 1985-1993. The incidence rates per 100 person-years for Pneumocystis carinii pneumonia were 47.4 without treatment, 21.5 with antiretrovirals alone, and 12.8 with antiretrovirals combined with chemoprophylaxis. For Kaposi's sarcoma these rates were 23.2, 11.3, and 15.1, respectively. The incidence of some opportunistic infections, including Mycobacterium avium complex, nonretinitis cytomegalovirus disease, and cytomegalovirus retinitis, increased among persons receiving P. carinii pneumonia prophylaxis, because of reduction of this pneumonia and extension of life span. The incidence pattern of AIDS-defining illnesses in patients receiving treatment points to the changing AIDS epidemic and the need for new therapies. The data are particularly relevant to the development and planning of clinical trials and to health care providers.
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PMID:Incidence of clinical AIDS conditions in a cohort of homosexual men with CD4+ cell counts < 100/mm3. Multicenter AIDS Cohort Study. 796 28

PML affects 4% of patients with AIDS and there is no effective treatment. Five cases of PML-AIDS have been described, showing clinical and radiological improvement after treatment with C-ara. We describe the case of a 33-year-old woman, addict to heroin, her clinical record including VIH infection, pneumonia by P. carinii, milliary tuberculosis, infection by virus B and C and treatment with AZT and tuberculostatics since January, 1992. In May, she began to develop a cerebellar syndrome. Images obtained with nuclear magnetic resonance were typical of PML. Subsequently, treatment with C-ara (2 mg/kg/day IV during 5 days each 4-6 weeks) was begun. From the third month of treatment on, the patient showed a clinical improvement and as of the sixth month, the affected areas of white substance were reduced in size. In addition, CD4 improved. Although in this patient a positive effect was observed after treatment with C-area, it should be verified in a controlled clinical trial.
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PMID:[Progressive multifocal leukoencephalopathy and AIDS. Response to cytarabine]. 806 Nov 41

AIDS-related lymphoma was not apparent until 1985, when a statistically significant increase in the frequency of lymphoma had occurred. Over 50% are high-grade lymphoma, either immunoblastic or small, noncleaved cells (Burkitt's-like lymphoma), with involvement of extranodal sites such as the central nervous system (> one-third of patients), gastrointestinal tract, skin and bone marrow. Optimal therapy for AIDS-associated lymphoma has not yet been defined. Using intensive chemotherapy protocols, high response rates, albeit of brief duration, have been demonstrated. The majority of patients succumbed to intercurrent opportunistic infections. Poor prognosis has been particularly noted in debilitated patients, patients with a CD4 cell count of < 200/dl, bone marrow and brain involvement and a history of AIDS before diagnosing the lymphoma. New strategies in the management of patients with AIDS-lymphoma should include cytotoxic therapy, antiretroviral therapy, anti-pneumocystic Carini pneumonia, prophylaxis of CNS spread and marrow protective therapy (haematopoietic growth factors).
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PMID:Biology of disease and clinical aspects of AIDS-associated lymphoma: a review. 806 66

The effects of depleting CD4+ and CD8+ T cells on macrophage recruitment have been analyzed for bronchoalveolar lavage (BAL) populations from mice with primary or secondary influenza pneumonia. Macrophages were characterized by both the capacity to engulf latex particles and the expression of mRNA for a 65 kD heat shock protein (hsp65). The localization of hsp65 mRNA+ cells to the pneumonic lung was greatly enhanced in the secondary response. Eliminating the CD4+ and CD8+ T cells decreased the prevalence of hsp65 mRNA+latex+ macrophages as much as seven-fold, though the frequency of latex+ cells was higher in the residual inflammatory process. The CD4-8- gamma delta T cells were also relatively enriched in the BAL from the depleted mice. However, the localization of gamma delta T cells to the pneumonic lung does not compensate either quantitatively or qualitatively for the lack of the CD4+ and CD8+ alpha beta T-cell subsets, which are responsible for activating a substantial proportion of the phagocytic cells to express transcripts of an endogenous hsp65 gene.
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PMID:hsp65 mRNA+ macrophages and gamma delta T cells in influenza virus-infected mice depleted of the CD4+ and CD8+ lymphocyte subsets. 810 Jun 10

In a 62-year old man who consulted for dyspnoea, clinical, radiological and functional examinations led to the diagnosis of immunoallergic lung disease caused by gold salt therapy. Regression of the symptoms when gold salt therapy was withdrawn supported this diagnosis. Contrary to previously published cases concerning treatment with gold salts, the study of bronchoalveolar lavage (BAL) fluid yielded a lymphocytic alveolitis with a very high CD4/CD8 ratio, as already reported with methotrexate, cyclothiazide and nitrofurantoin. This case can be added to the list of drugs that may induce CD4 alveolitis; it also reminds the existence of gold salt pneumonia and permits to discuss the value of a lymphocyte subpopulation study in the BAL fluid in patients with drug-induced immunoallergic lung diseases.
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PMID:[Gold salt-induced pneumonia and CD4 alveolitis]. 810 58


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