Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty patients with AIDS-associated Kaposi's sarcoma (KS) treated with the combination of interferon alpha-2b (IFN-alpha) 10-20 MU day-1 and zidovudine (ZDV), 500-800 mg day-1, were evaluated for safety and efficacy. Eighteen patients (45%) had an overall response (CR+PR) at 3 months and a response persisting for a median of 14 (3-27) months. Patients with a CD4 count of less than 300 mm-3, prior to opportunistic infections or constitutional symptoms, were less likely to respond. However, between 28.5% and 36% of patients with a low CD4 count did respond to combined therapy. This is higher than would be predicted from single agent IFN-alpha therapy. Twelve of 28 patients (42.8%) receiving 10 MU day-1 of IFN-alpha (low dose) had an overall response. In addition, patients tolerated this dose of IFN-alpha better, presenting fewer flu-like symptoms and displayed a trend toward less anaemia. p24 antigen decreased in six out of nine evaluable cases, four of whom were treated with low-dose IFN-alpha. Low-dose IFN-alpha plus ZDV seems to be a useful and well-tolerated therapy for KS with antitumoral and antiviral activity. Patients without 'bad prognostic markers' are most likely to show improvement.
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PMID:Low-dose interferon alpha combined with zidovudine in patients with AIDS-associated Kaposi's sarcoma. 809 16

A pilot study was initiated to explore a sequential combination antiretroviral regimen in 21 patients with AIDS or advanced human immunodeficiency virus (HIV) infection, who had received little or no prior anti-HIV therapy. The mean entry CD4 cell count was 184/mm3. Patients received 3-week cycles consisting of zidovudine plus acyclovir, dideoxyinosine, and dideoxycytidine for 1 week each. Overall, the regimen was well tolerated for up to 3 years. The principal toxicities were anemia, nausea, and vomiting; 1 patient developed retinal lesions. The mean CD4 cell count reached a peak of 64 cells/mm3 above baseline at week 8 (P = .005 compared to baseline) and remained above baseline for > 40 weeks. Patients also gained weight and had decreases in serum HIV p24 antigen. Eight patients developed opportunistic infections or tumors. Only 4 patients died during 3 years of follow-up. This regimen appears to be generally tolerable and to have anti-HIV activity. Additional studies will be needed, however, to learn how to best combine the available agents in patients with HIV infection.
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PMID:A pilot study of sequential therapy with zidovudine plus acyclovir, dideoxyinosine, and dideoxycytidine in patients with severe human immunodeficiency virus infection. 839 67

Patients with the acquired immunodeficiency syndrome (AIDS) are characterized by a decrease in the number of T helper cells, a defect that is linked to the impaired immunologic competence. Vitamin A and its dietary precursor, beta-carotene, increase absolute T helper cell counts as well as indices of T cell function in both human and animal models. To determine if short-term beta-carotene treatment affects T lymphocyte subsets in patients with AIDS, a single-blind, non-randomized clinical trial of beta-carotene was performed in seven patients with AIDS. Enrollment criteria included no evidence of: a) active opportunistic infection: b) greater than 1 kilogram change in weight in the month preceding enrollment; c) chronic diarrhea or malabsorption; and d) hepatic disease or significant anemia. Beta-carotene was given with meals in two divided doses of 60 mg/day for four weeks; this was followed by no therapy for six weeks. Samples for total white blood cell, lymphocyte and T lymphocyte subset counts were measured at baseline, at the end of four weeks of treatment and another six weeks after treatment had stopped. P24 antigen, beta-2 microglobulin and liver function tests were also measured. All subjects tolerated the treatment well without evidence of toxicity. In response to beta-carotene, total lymphocyte counts rose by 66 percent (.05 < p < .10), and CD4+ cells rose slightly, but insignificantly, in the entire group. In all three of the patients who had baseline CD4+ cells greater than 10/microliters, however, the mean absolute increase in CD4+ cells in response to beta-carotene was 53 +/- 10 cells/microliters (p < .01). Six weeks off beta-carotene treatment, the absolute CD4+ cell count returned to pretreatment levels (p < .01). No change was observed in CD8+ cells. P24 antigen and beta-2 microglobulin did not change during treatment. These preliminary observations suggest that short-term treatment with beta-carotene may increase CD4+ cell counts in patients with AIDS who have greater than 10 cells/microliters.
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PMID:The effect of supplemental beta-carotene on immunologic indices in patients with AIDS: a pilot study. 874 63

We have previously demonstrated that the Gag p9 protein of equine infectious anemia virus (EIAV) is functionally homologous with Rous sarcoma virus (RSV) p2b and human immunodeficiency virus type 1 (HIV-1) p6 in providing a critical late assembly function in RSV Gag-mediated budding from transfected COS-1 cells (L. J. Parent et al., J. Virol. 69:5455-5460, 1995). In light of the absence of amino acid sequence homology between EIAV p9 and the functional homologs of RSV and HIV-1, we have now designed an EIAV Gag-mediated budding assay to define the late assembly (L) domain peptide sequences contained in the EIAV p9 protein. The results of these particle budding assays revealed that expression of EIAV Gag polyprotein in COS-1 cells yielded extracellular Gag particles with a characteristic density of 1.18 g/ml, while expression of EIAV Gag polyprotein lacking p9 resulted in a severe reduction in the release of extracellular Gag particles. The defect in EIAV Gag polyprotein particle assembly could be corrected by substituting either the RSV p2b or HIV-1 p6 protein for EIAV p9. These observations demonstrated that the L domains of EIAV, HIV-1, and RSV were interchangeable in mediating assembly of EIAV Gag particles in the COS-1 cell budding assay. To localize the L domain of EIAV p9, we next assayed the effects of deletions and site-specific mutations in the p9 protein on its ability to mediate budding of EIAV Gag particles. Analyses of EIAV Gag constructs with progressive N-terminal or C-terminal deletions of the p9 protein identified a minimum sequence of 11 amino acids (Q20N21L22Y23P24D25L26S27E28I29K30) capable of providing the late assembly function. Alanine scanning studies of this L-domain sequence demonstrated that mutations of residues Y23, P24, and L26 abrogated the p9 late budding function; mutations of other residues in the p9 L domain did not substantially affect the level of EIAV Gag particle assembly. These data indicate that the L domain in EIAV p9 utilizes a YXXL motif which we hypothesize may interact with cellular proteins to facilitate virus particle budding from infected cells.
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PMID:Equine infectious anemia virus utilizes a YXXL motif within the late assembly domain of the Gag p9 protein. 926 74

The paper presents multiorgan manifestations of AIDS syndrome in an infant at the age of 8 months. The child was admitted to the Clinic with enteric disorder, anaemia, hepatosplenomegaly and pneumonia. The diagnosis of those anomalies and the treatment of pneumonia took much time. Infection with CMV was recognized but, despite the treatment and elimination of the virus, the child's condition did not improve and general emaciation progressed. The diagnosis of AIDS syndrome was based upon indicator illnesses: chronic recurrent pneumonia, cytomegaly and emaciation syndrome as well as upon the results of additional examinations, first of all including the presence of p24 antigen in the serum. In children with chronic diseases and manifesting non-specific multiorgan symptoms we should take into consideration AIDS syndrome in the differential diagnosis.
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PMID:[AIDS syndrome in an eight-month-old infant]. 1080 May 76

The purpose of this study was to assess the population pharmacokinetics (PK) and pharmacodynamics (PD) of zidovudine (ZDV) in infants and children. This evaluation includes 394 subjects who participated in Pediatric AIDS Clinical Trials Group (PACTG) Study 152 and received either ZDV alone or in combination with didanosine. The most significant PK covariate was age, with infants < 2 years of age having reduced size-adjusted clearance. ZDV exposure was weakly related to maximal reduction in immune complex-dissociated (ICD) p24 antigen but not to reduction at 6 months. Mild chronic anemia occurred in 7.6% of subjects with ZDV average concentration < 1.3 microM (350 ng/mL) versus in 23.4% subjects with higher ZDV concentrations (p < 0.001). There was a direct linear relationship between hemoglobin and ZDV levels. It was concluded that ZDV oral clearance is reduced in infants compared to older children. This lower clearance leads to higher ZDV exposure in infants and contributes to increased hematologic toxicity.
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PMID:Population pharmacokinetics and pharmacodynamics of zidovudine in HIV-infected infants and children. 1261 65

Untreated tropical parasitic co-infections appear to speed the progression of HIV-1 disease. However, to date, there have been few studies conducted in resource limited settings to ascertain the interaction of parasitic co-infection where HIV/AIDS management largely depends on CD4+ T lymphocyte cells counts and WHO clinical staging. This study aimed to determine the prevalence of parasites, their association with CD4+ T lymphocyte cells changes and clinical manifestation of HIV-infection in patients attending HIV/AIDS management clinics in Tanzania. Adult HIV-infected patients registering for the first time at HIV/AIDS management clinics were recruited; with physical examination and laboratory tests performed at baseline and after 6 months. Patients were assigned a clinical stage and scr.eened for helminths and Plasmodium sp. co-infection, CD4+ T lymphocyte cells, haemoglobin and HIV-1 p24 antigen. Of the 421 HIV-1 infected patients studied, 198 (47.0%) were co-infected with one or more parasites. Of those studied, 93/421(22.1%) had helminth only co-infection, and 50/421 (12.9%) had Plasmodium sp only co-infection. Mixed Plasmodium sp and helminth co-inf6ction was diagnosed in 55/421 (13.0%) patients. Helminths frequently diagnosed included: hookworm 65/421(15.4%), Schistosomiasis 49/421(11.6%), Strongyloides stercoralis 57/421(13.5%), and Ascaris lumbricoides 54/421(12.8%). No statistical association was found between CD4+ T lymphocyte cells < 200/ 1, or WHO clinical stage III/ IV with parasite co-infections (AOR 1.2, 95%CI 0.8-1.8). Anaemia was common in parasite co-infected patients (32.8% vs. 18.8%). Parasite co-infection was associated with risk of anaemia (AOR 2.1, 95%CI 1.3-3.2). In multivariable logistic regression analysis, baseline CD4+ T lymphocyte cells <200/V1 was significantly associated with CD4+ T lymphocyte cells <20041 (AOR 2.4, 95%CI 1.3-4.7) at six months. HIV-1 P24 antigen mean concentration was higher in parasite co- infected patients (ranges 47.6 to 56.9) as compared to patients without parasite co-infection (5.5). We have looked at one set of parasites and found high prevalence of malaria and helminth co-infection in HIV-infected individuals. Given the available reports on health impacts of helminth co-infection in HIV/AIDS patients and the anecdotal reports of helminths health effects in HIV-uninfected persons, helminths and other prevalent parasites should not be ignored in HIV/AIDS programs. Based on local helminth epidemiology and HIV-infected cohort specific helminths co-infection prevalence data, mass treatment of soil transmitted helminths can be incorporated into HIV/AIDS management programmes.
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PMID:HIV and parasitic co-infections among patients seeking care at health facilities in Tanzania. 2659 51


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