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

alpha-Interferon (IFN alpha) blocks replication of human immunodeficiency virus (HIV)-1 in vitro by interfering with the release of mature virions. Clinical trials have addressed the in vivo effects of IFN alpha, both alone and in combination with other agents, in a variety of patients at all stages of HIV-1 infection. Patients with late stages of HIV-1 infection (CD4 counts under 100) show few positive results following treatment with IFN alpha. Patients with earlier stages of HIV infection, however, may benefit from treatment with this agent. Several clinical trials have demonstrated the activity of interferon in the treatment of patients with acquired immunodeficiency syndrome, Kaposi's sarcoma, and CD4 counts over 200. In these trials, response rates of approximately 40% have been reported, with the probability of response directly correlated with the level of CD4 cells. These antitumor effects have been associated with declines in the circulating levels of the HIV-1 core antigen p24. alpha-Interferon activity has also been studied in patients concomitantly receiving zidovudine. In these studies, neutropenia, reversible with the concomitant administration of granulocyte macrophage colony-stimulating factor, has been the most common dose-limiting toxicity. Both the antitumor and antiviral activities of combination therapy appear to be at least as good as those observed when single agents are used. Controlled clinical trials are currently under way to evaluate the role of interferon therapy, both alone and in combination with zidovudine, in patients with early HIV infection.
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PMID:The role of alpha-interferon in patients with human immunodeficiency virus infection. 194 29

The incidence of bacterial pneumonia is increased in human immunodeficiency virus (HIV) infection, and bacteremia and recurrences occur frequently. Streptococcus pneumoniae and Haemophilus influenzae are the most common pathogens, but several other organisms have now been identified as etiologies. Several abnormalities in B-cells and humoral immunity, and possibly neutropenia and white blood cell dysfunction, predispose to bacterial pneumonia. Despite the severity of pneumonia in HIV infection, most patients respond well to specific antimicrobial chemotherapy. Potential preventive measures include vaccines, immunoglobulin therapy, and antimicrobial prophylaxis.
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PMID:Bacterial pneumonia in the HIV-infected patient. 195 96

Seven young cats were injected with feline leukemia virus (FeLV); six of them became viremic. All of the viremic cats developed AIDS-related symptoms, i.e. lymphopenia, neutropenia, thymic atrophy, and wasting syndrome, along with an altered pituitary and adrenocortical function. These symptoms closely resemble human AIDS induced by HIV. It was discovered that, after 2 weeks of infection, the average amount of plasma adrenocorticotropic hormone (ACTH) detected in the infected cats was reduced by 29% in comparison with that before the infection. In contrast to the second week, the fifth week of infection showed a 94% increase of plasma ACTH which then dropped back down to 38% after the sixth and seventh weeks. This opposing biphasic pattern of change was also observed in the plasma cortisol content of the infected cats. The amount of change in plasma cortisol did not correlate with the detected increase in plasma ACTH, indicating a weak adrenal response to pituitary action.
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PMID:Induction of feline immunodeficiency syndrome by feline leukemia virus: pituitary and adrenocortical dysfunctions. 196 24

Zidovudine (AZT) is a potent inhibitor of the replication of the human immunodeficiency virus (HIV), and it has been shown to improve survival in advanced HIV disease. We conducted a randomized, double-blind trial in adults with asymptomatic HIV infection who had CD4+ cell counts of fewer than 500 per cubic millimeter on entry into the study. The subjects (92 percent male) were randomly assigned to one of three treatment groups: placebo (428 subjects); zidovudine, 500 mg per day (453); or zidovudine, 1500 mg per day (457). After a mean follow-up of 55 weeks (range, 19 to 107), 33 of the subjects assigned to placebo had the acquired immunodeficiency syndrome (AIDS), as compared with 11 of those assigned to receive 500 mg of zidovudine (P = 0.002; relative risk, 2.8; 95 percent confidence interval, 1.4 to 5.6) and 14 of those assigned to receive 1500 mg of zidovudine (P = 0.05; relative risk, 1.9; 95 percent confidence interval, 1.0 to 3.5). In the three treatment groups, the rates of progression (per 100 person-years) to either AIDS or advanced AIDS-related complex were 7.6, 3.6, and 4.3, respectively. As compared with those assigned to placebo, the subjects in the zidovudine groups had significant increases in the number of CD4+ cells and significant declines in p24 antigen levels. In the 1500-mg zidovudine group, severe hematologic toxicity (anemia or neutropenia) was more frequent than in the other groups (P less than 0.0001). In the 500-mg zidovudine group, nausea was the only toxicity that was significantly more frequent (in 3.3 percent) than in the placebo group (P = 0.001). We conclude that zidovudine is safe and effective in persons with asymptomatic HIV infection and fewer than 500 CD4+ cells per cubic millimeter. Additional study will be required to determine whether such treatment will ultimately improve survival for persons infected with HIV.
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PMID:Zidovudine in asymptomatic human immunodeficiency virus infection. A controlled trial in persons with fewer than 500 CD4-positive cells per cubic millimeter. The AIDS Clinical Trials Group of the National Institute of Allergy and Infectious Diseases. 238 74

Eighteen asymptomatic men with persistent human immunodeficiency virus type 1 (HIV-1) p24 antigenemia were treated with zidovudine 250-500 mg (+/- acyclovir 800 mg) 6-hourly for 4-12 weeks, and thereafter with zidovudine 500 mg (+/- acyclovir 1600 mg) 12-hourly for 92 weeks. Six additional HIV-1 p24 antigenemic subjects were treated with zidovudine 500 mg 12-hourly for 76 weeks. Disease progression occurred in 4 subjects, despite sustained reduction of serum HIV-1 p24 antigen levels: Pneumocystis carinii pneumonia was diagnosed after 60, 80, 90 and 93 weeks, respectively. The median CD4+ cell count of these 4 men at study entry was 0.2 x 10(9)/l, and it declined to 0.07 x 10(9)/l at the moment AIDS was diagnosed. In 20 subjects no disease progression occurred. The median CD4+ cell count of these 20 men at study entry was 0.4 x 10(9)/l and it was 0.45 x 10(9)/l at the end of the study period. Median serum HIV-1 p24 antigen levels at the end of the study period were 42% lower than at study entry in these 20 subjects. In 5/20 men, an initial decline was followed by a rise in antigen levels to above pretreatment value. Treatment with zidovudine was well tolerated. Anemia caused symptoms in 3/24 men, but prolonged leucopenia or neutropenia did not occur. None developed clinical or convincing biochemical evidence of zidovudine-associated myopathy.
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PMID:Long-term zidovudine treatment of asymptomatic HIV-1-infected subjects. 197 21

The presence of platelet- and neutrophil-bound immunoglobulin (PBIg and NBIg) in thrombocytopenic or neutropenic HIV-infected individuals has led to the concept that in HIV infection thrombocytopenia and neutropenia are mediated by autoimmunity. However, PBIg and NBIg were also demonstrated in non-cytopenic HIV-infected individuals. We determined the prevalence of autoantibodies against neutrophils and platelets by immunofluorescence in randomly chosen persons in different stages of asymptomatic and symptomatic HIV infection. Platelet and neutrophil autoantibodies already appeared in the asymptomatic stage and their prevalence further increased in the symptomatic stages. No correlation was found between the presence of either platelet or neutrophil antibodies and the occurrence of circulating immune complexes in the blood or the serum immunoglobulin level. There was no significant difference in neutrophil counts in HIV-infected persons with or without neutrophil autoantibodies. In addition, no significant difference in neutrophil count was found between HIV-infected and non-HIV-infected persons. HIV-infected individuals with platelet autoantibodies tended to have a lower platelet count than HIV-infected individuals without these antibodies. However, the platelet count in HIV-infected individuals without platelet antibodies was significantly lower than in the non-HIV infected persons. Thus, autoantibodies against platelets and neutrophils occur early in HIV infection and their prevalence is correlated with disease progression. Their presence is associated with cytopenia only in a limited number of persons. Non-immune mechanisms also mediate thrombocytopenia in HIV infection.
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PMID:Autoantibodies against peripheral blood cells appear early in HIV infection and their prevalence increases with disease progression. 197 74

Patients with human immunodeficiency virus infection are predisposed to fungal, parasitic, and viral infections. Bacterial infection can also be seen, although ocular bacterial infections have not been reported in patients with acquired immunodeficiency syndrome until recently. We present two cases of Pseudomonas corneoscleritis and one case of Pseudomonas keratitis in patients with human immunodeficiency virus infection that failed to respond to antibiotic treatment. Predisposing factors included extended-wear soft contact lens use in one patient and exposure secondary to Bell's palsy in another patient. All three patients had neutropenia that may have contributed to their poor response to treatment. Enucleation was required to treat two patients with overwhelming infection. Enucleation has been rarely required for treatment of corneoscleritis in immunocompetent patients treated at our institution. Pseudomonas keratitis in human immunodeficiency virus-infected patients represents a serious ocular infection requiring early diagnosis and aggressive treatment.
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PMID:Fulminant pseudomonal keratitis and scleritis in human immunodeficiency virus-infected patients. 201 49

A number of studies have illustrated the effectiveness of hematopoietic growth factors in managing treatment-related cytopenias in patients with human immunodeficiency virus (HIV) infection. One of these factors, granulocyte-macrophage colony-stimulating factor, has been shown to restore absolute neutrophil counts in patients with acquired immunodeficiency syndrome (AIDS) and Kaposi's sarcoma receiving a combination of zidovudine (AZT) and interferon alfa. A combination of granulocyte colony-stimulating factor and erythropoietin has also been demonstrated to alleviate both neutropenia and anemia in patients with advanced AIDS or AIDS-related complex receiving zidovudine. Hematopoietic growth factors, in combination with each other and with antiretroviral agents, thus have an important supportive role to play in the treatment of patients with HIV disease.
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PMID:Antiretroviral therapy and immunomodulators in patients with AIDS. 201 46

Combined zidovudine (ZDV) and interferon-alpha (IFN) is an appealing therapy for AIDS-associated Kaposi's sarcoma because of the antiretroviral as well as antitumor potential of this combination. Overlapping myelotoxicity of these agents, however, frequently complicates their clinical use. This phase I/II study was undertaken to test the safety and efficacy of granulocyte-macrophage colony stimulating factor (GM-CSF) in those patients who became neutropenic while receiving ZDV (1,200 mg/day) and IFN (9 MU/day). Despite a "high-risk" population of patients, the tumor response rate among evaluable patients was 50% (33% overall). Sixty-four percent of patients required GM-CSF and all patients receiving GM-CSF had a prompt improvement in their absolute neutrophil count (ANC). The use of GM-CSF was associated with an improved end of study ANC (p less than 0.05), but was not associated with tumor response, CD4 count improvement, or improved change in hemoglobin concentration. GM-CSF/ZDV/IFN was not associated with increased toxicity over ZDV/IFN; however, two unusual events occurred in the GM-CSF/ZDV/IFN group: erythema multiforme and glucose intolerance. Dose-limiting thrombocytopenia and anemia were seen in two patients and anemia in one patient on GM-CSF/ZDV/IFN. No consistent alterations in serum HIV p24 antigenemia were noted in either group. The use of GM-CSF mitigated the neutropenia of combined ZDV and IFN. Further study evaluating the utility of this hematopoietic growth factor in combination therapies for AIDS patients is warranted.
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PMID:GM-CSF as an alternative to dose modification of the combination zidovudine and interferon-alpha in the treatment of AIDS-associated Kaposi's sarcoma. 204 63

Invasive pulmonary aspergillosis was diagnosed in two patients with HIV infection, one with prolonged neutropenia and another receiving corticosteroid therapy. We found 17 additional cases in the literature. A known predisposing risk factor for invasive aspergillosis, eg, neutropenia, corticosteroid use, or intravenous drug abuse, was present in 79% of the cases. That the known immunologic defect of AIDS is not a major host defense against Aspergillus is supported by the empiric observation of the relative rarity of aspergillosis in patients with AIDS. The lung was the most common site of Aspergillus infection (75%), and transbronchial biopsy is diagnostically useful. Central nervous system involvement was seen in 55% and appears to be more frequent in HIV-infected patients than in other immunosuppressed patients with invasive aspergillosis. Prognosis is grim. Despite early institution of amphotericin B therapy in a few cases, the disease was uniformly fatal. Efficacy of therapy with amphotericin B plus rifampin or itraconazole remains to be evaluated. We conclude that aspergillosis is not an AIDS-related opportunistic infection.
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PMID:Invasive aspergillosis in AIDS. 206 21


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