Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of liposomal doxorubicin for treating Kaposi's sarcoma (KS) in patients infected with human immunodeficiency virus (HIV) was studied. Eight men with HIV infection and KS were to be given liposomal doxorubicin 20 mg/sq m i.v. monthly for six months and 10 mg/sq m i.v. monthly thereafter, depending on the response. They were assessed for the onset, extent, and duration of clinical response; relapse; adverse effects; development of new opportunistic infections; quality of life; and survival. Five patients had a clinical complete response (i.e., complete resolution of the manifestations of KS, as determined by physical examination but not confirmed by biopsy) and three patients had a partial response to the induction regimen of liposomal doxorubicin. Relapse occurred in all patients in whom therapy was stopped; reinstatement of therapy elicited a partial response. Neutropenia occurred in two patients; filgrastim therapy enabled the liposomal doxorubicin therapy to continue uninterrupted. Thromboembolic events developed or were suspected in three patients, although they may not have been caused by liposomal doxorubicin. Monthly i.v. administration of liposomal doxorubicin partially or completely eliminated the clinical manifestations of Kaposi's sarcoma in eight men infected with HIV.
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PMID:Treatment of Kaposi's sarcoma with liposomal doxorubicin. 852 67

Fluconazole is a triazole antifungal agent which is now an established part of therapy in patients with immune deficiencies. It is effective against oropharyngeal/oesophageal candidiasis (candidosis) when used orally once daily either as treatment or secondary prophylaxis in patients with AIDS or as treatment or primary prophylaxis in neutropenia associated with cancer therapy. Fluconazole also resolves symptoms in up to 60% of patients with cryptococcal meningitis and AIDS. However, in this infection its efficacy as treatment relative to that of amphotericin B is equivocal, and its major role is as the drug of choice for maintenance therapy following amphotericin B induction. In this regard, fluconazole has been proven superior to amphotericin B and to itraconazole 200 mg/day. Comparisons with other drugs used for the treatment of mucosal candidiasis in patients with AIDS show fluconazole to be superior to nystatin, similar to itraconazole and at least as effective as clotrimazole and ketoconazole; it was more so than the latter azole in 1 study. In patients undergoing chemotherapy or bone marrow transplantation, fluconazole as primary prophylaxis has produced greater clinical benefit than a clotrimazole regimen. The incidence of adverse events appears to be somewhat higher in patients with AIDS compared with HIV-negative cohorts, but the qualitative pattern of events is similar. The most frequent events are gastrointestinal complaints, headache and skin rash: rare exfoliative skin reactions and isolated instances of clinically overt hepatic dysfunction have occurred in patients with AIDS. Issues yet to be clarified include: the use of fluconazole in children with AIDS, in whom results have been promising; its efficacy against other fungal infections encountered in immunocompromised patients; whether the drug influences mortality, as has been suggested by one placebo-controlled trial in patients undergoing bone marrow transplant; and the appropriateness of its potential for use as primary prophylaxis against cryptococcal meningitis in patients with AIDS, where it shows efficacy but there is concern over increasing risk of development of secondary resistance. Notwithstanding these undefined aspects of its clinical profile, fluconazole is now confirmed as an important antifungal drug in the management of fungal infections in patients with immune deficiencies. In patients with AIDS it is the present drug of choice as maintenance therapy against cryptococcal meningitis and is a preferred agent for secondary prophylaxis against candidal infections; it is also a favoured agent for primary prophylaxis in patients at risk because of neutropenia associated with chemotherapy or bone marrow transplantation .
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PMID:Fluconazole. An update of its pharmacodynamic and pharmacokinetic properties and therapeutic use in major superficial and systemic mycoses in immunocompromised patients. 853 53

Analysis of the events that regulate development of red blood cells or granulocytes has led to therapies altering clinical conditions associated with anemia or neutropenia. The development of therapeutic approaches to target conditions associated with lymphopenia, such as AIDS, has been thwarted by limited techniques for studying T-lymphocyte development. We describe an in vitro system in which human bone marrow CD34+ cells proliferate, acquire the expression of the lymphoid-specific RAG-2 gene and a broad repertoire of rearranged T-cell receptor genes, develop the ability to produce T cell-specific interleukin-2 and achieve a range of T-cell immunophenotypes. The cells also become susceptible to infection with the T-lymphotropic strain of human immunodeficiency virus-1, HIV-1IIIB. This culture system induces human T lymphopoiesis and may permit further analysis of the events regulating human T-lineage differentiation. It provides a preclinical model for screening stem cell gene therapies directed toward AIDS.
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PMID:Generation of human T lymphocytes from bone marrow CD34+ cells in vitro. 856 38

Bacterial infections are common in persons with symptomatic disease caused by human immunodeficiency virus (HIV). Colonisation and infection with Staphylococcus aureus is present in 30% to 50% of persons with HIV disease. Risk factors for bacteraemia due to S. aureus include nasal colonisation, advanced HIV disease with CD4+ lymphocyte count < 100/mm3, prior hospitalisations, neutropenia, skin lesions, intravenous drug use, and the presence of invasive devices, such as intravenous catheters. Some antibiotics may increase the risk of S. aureus nasal colonisation, and others such as trimethoprim-sulphamethoxazole and rifabutin may reduce colonisation and disease. Preliminary data suggest that mupirocin may decrease nasal colonisation with S. aureus, but the optimal regimen, duration of effect, use, and concerns about resistance, need further evaluation. Recent data suggest that bacterial infection may accelerate the progression of HIV disease. The presence of bacterial superantigens or cytokines, such as the exotoxins present in many strains of S. aureus have been shown to induce HIV production in human peripheral blood mononuclear leukocyte cultures in vitro, although the precise mechanism is unclear. Thus, HIV infection may increase the risk of S. aureus colonisation and disease and, in turn, infection or colonisation with S. aureus may accelerate the progression of HIV disease to AIDS.
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PMID:Staphylococcus aureus colonisation and bacteraemia in persons infected with human immunodeficiency virus: a dynamic interaction with the host. 860 35

Patients with HIV infection may present with symptoms and/or signs of anaemia, neutropenia or thrombocytopenia at all stages, including seroconversion.
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PMID:Managing HIV. Part 5: Treating secondary outcomes. 5.12 HIV and haematological disease. 861 43

Recombinant human granulocyte colony-stimulating factor (G-CSF) has been used to treat neutropenia in patients with cancer and HIV disease. Since lymphocyte counts have been reported to increase with G-CSF therapy, we studied the effect of G-CSF on lymphocyte subsets in HIV-infected patients. Six patients with HIV-associated neutropenia were treated with G-CSF and had significant increases in white blood cell counts. G-CSF induced a significant rise in total lymphocytes, total T-cells, CD8 T-cells, and natural killer cells. A smaller but statistically significant increase in CD4 T-cells and cytotoxic CD8 T-cells was also noted. We conclude that G-CSF has the ability to raise lymphocyte subset levels in patients with HIV disease. The potential immunologic benefit of G-CSF therapy merits further investigation.
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PMID:Increase in lymphocyte subsets following treatment of HIV-associated neutropenia with granulocyte colony-stimulating factor. 862 Jun 26

The object of this case control study was to evaluate the frequency, the risk factors, the microbiological spectrum and the outcome of 249 cases of bacteraemia observed in 209 HIV-infected patients, most them affected by AIDS. The rate of bacteraemia in the total yearly HIV-related admissions increased from 4% in 1985 to 13% in 1993. The more common aetiological agents of bacteraemia were: Staphylococcus aureus (29.7%), non-typhoidal species of Salmonella (14.1%), Staphylococcus epidermidis (10.9%), Streptococcus pneumoniae (8.4%) and Pseudomonas aeruginosa (7.6%). A mixed flora was found in 14% of the episodes. Multivariate analysis of predisposing factors indicated that a low CD4+T-cell count (<0.2 x 10(9)/l) (P=0.01), use of central venous catheters (CVC) (P=0.01) and neutropenia (polymorphonuclear neutrophils <1.0 x 10(9)/l) (P=0.04) were independent risk factors for the development of bacteraemia. Logistic regression did not reveal any association of bacteraemia with intravenous drug abuse (on univariate analysis P=0.04). The response (31.8%). Recurrences to specific therapy was favourable in 170 episodes (68.2%); death occurred in 79 (31.8%). Recurrences arose in 40 patients, 17 (42.5%) of them died. The outcome of bacteraemia was influenced by a low number of CD4+T-cells (P<0.001) but not of polymorphonuclear cells. Our findings suggest that bacteraemia is a relatively common event in HIV-infected patients, especially under particular conditions (e.g. intravenous drug abuse, use of CVC, neutropenia and a low CD4-T-cell count). It requires special attention from physicians who must recognise and treat the condition promptly at an early stage.
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PMID:The impact of bacteraemia on HIV infection. Nine years experience in a large Italian university hospital. 866 42

I.v. pentamidine is well known to cause severe multiorgan adverse effects and is usually given to hospitalized patients under close monitoring. The primary purpose of this retrospective quality assurance study is to assess the safety of administering i.v. pentamidine in the medical daycare unit (MDCU) for outpatients. Thirty-five outpatients infected with the HIV made 306 visits to the MDCU from January 1991 to December 1993. They received i.v. pentamidine in a dosage of either 300 mg once a month for prophylaxis or 4 mg/kg/d 5 days a week for treatment of Pneumocystis carinii pneumonia (PCP). BP was monitored every 15 to 30 min over 3 to 4 h and clinical side effects were noted. CBC count, BUN, creatinine, amylase, and blood glucose values were taken twice a week. The records were reviewed retrospectively and analyzed for clinical and biochemical derangement. GI side effects occurred in 59 of 306 (19%) visits; 43 (73%) of the side effects were nausea. Routine normal saline solution boluses before and after pentamidine infusion prevented the drop in BP and actually significantly elevated BP after i.v. pentamidine. The most common biochemical derangement was elevated BUN level in eight patients and creatinine in nine patients, but they were mild and required no intervention. Significant neutropenia occurred in three, anemia in two, hyponatremia in two, hyperamylasemia in two, and hyperglycemia in two patients. No palpitation or irregular pulse was encountered. No death was associated with the administration of i.v. pentamidine. Three patients required hospital admission. Only one hospital admission was definitely related to adverse drug effects. In conclusion, the side effects of i.v. pentamidine are common but minor. We conclude that it is safe to administer i.v. pentamidine in carefully selected patients with appropriate monitoring in an ambulatory setting. This has a major health economic implication, because ambulatory i.v. pentamidine can result in significant cost savings and can also enhance quality of life. Further studies regarding the feasibility of home administration of i.v. pentamidine is warranted as even further cost savings and improvement in the quality of life of HIV-infected patients may be achieved.
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PMID:The safety of i.v. pentamidine administered in an ambulatory setting. 868 17

Neutropenia occurs in approximately 17% of symptomatic patients infected with HIV. Results of studies have failed to demonstrate a consistent relationship between HIV-related neutropenia and the subsequent development of bacterial infections. This was a case control study to determine if HIV-related neutropenia was associated with increased rates of bacteremia. The experimental group was comprised of 29 patients infected with HIV that had an absolute neutrophil count less than 1000 cells/mm3 and were paired with 29 control subjects infected with HIV that had been matched for age, sex, CD4 count, and month and year of entry. The frequency of bacteremia was 12.6 per 100 patient months among the experimental group compared to a frequency of 0.87 per 100 patient months among the control group (relative risk [RR] = 14.9, P = 0.0027). Other independent risks for the development of bacteremia included central venous catheters (RR = 3.9, P = 0.03), with a trend toward increased risk for bacteremia in those patients who were intravenous drug users (RR = 3.8, P = 0.11), or who had infiltrative bone marrow disease (RR = 3.1, P = 0.11). Multivariate analysis demonstrated that neutropenia (odds ratio [OR] = 22.6, P = 0.028) and the presence of a central venous catheter (OR = 8.5, P = 0.026) were significant risks for bacteremia. These data suggest that neutropenia is a significant risk for the development of bacteremia in patients infected with HIV.
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PMID:Neutropenia is associated with bacteremia in patients infected with the human immunodeficiency virus. 878 77

Despite the frequent occurrence of mucosal candidiasis in patients infected with HIV, systemic candidiasis is uncommon and usually associated with intravenous catheters, parenteral nutrition, or antibiotics and neutropenia. Most of the fungal isolates are usually Candida albicans, Candida tropicalis or Candida parapsilosis. The authors report a case of infective endocarditis due to Candida zeylanoides that occurred in a patient infected with HIV in the absence of the usual risk factors for systemic candidiasis.
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PMID:Case report: Candida zeylanoides infective endocarditis complicating infection with the human immunodeficiency virus. 878 83


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