Cases reported "HIV Infections"

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1/97. Minimizing HIV/AIDS malnutrition.

    HIV/AIDS malnutrition influences immune function, disease progression, and quality of life. Changes in dietary intake, altered metabolism, and malabsorption are among the mechanisms that contribute to the nutritional alterations seen in HIV/AIDS. Medical-surgical nurses can help their patients minimize HIV/AIDS malnutrition through early and ongoing assessment, which guides nutritional and pharmacologic interventions.
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2/97. CD4 depletion in HIV-infected haemophilia patients is associated with rapid clearance of immune complex-coated CD4 lymphocytes.

    The predominant immunological finding in HIV haemophilia patients is a decrease of CD4 lymphocytes during progression of the disease. Depletion of CD4 lymphocytes is paralleled by an increase in the proportion of immune complex-coated CD4 cells. We examined the hypothesis that the formation of immune complexes on CD4 lymphocytes is followed by rapid clearance of immune complex-coated CD4 lymphocytes from the circulation. In this study, the relationship of relative to absolute numbers of immune complex-loaded CD4 blood lymphocytes and their association with viral load were studied. Two measurements of relative and absolute numbers of gp120-, IgG- and/or IgM-loaded CD4 lymphocytes were analysed in HIV and HIV- haemophilia patients, with a median interval of approx. 3 years. Immune complexes on CD4 lymphocytes were determined using double-fluorescence flow cytometry and whole blood samples. viral load was assessed using NASBA and Nuclisens kits. Whereas the proportion of immune complex-coated CD4 lymphocytes increased with progression of the disease, absolute numbers of immune complex-coated CD4 lymphocytes in the blood were consistently low. Relative increases of immune complex-coated CD4 blood lymphocytes were significantly associated with decreases of absolute numbers of circulating CD4 lymphocytes. The gp120 load on CD4 blood lymphocytes increased in parallel with the viral load in the blood. These results indicate that immune complex-coated CD4 lymphocytes are rapidly cleared from the circulation, suggesting that CD4 reactive autoantibodies and immune complexes are relevant factors in the pathogenesis of AIDS. Relative increases of immune complex-positive cells seem to be a consequence of both an increasing retroviral activity as well as a stronger loading with immune complexes of the reduced number of CD4 cells remaining during the process of CD4 depletion. The two mechanisms seem to enhance each other and contribute to the progressive CD4 decrease during the course of the disease.
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keywords = progression
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3/97. Highly active antiretroviral therapy used to treat concurrent hepatitis B and human immunodeficiency virus infections.

    We report a case of simultaneous infection with hepatitis b virus (HBV) and human immunodeficiency virus type 1 (hiv-1) in a 26-year-old Japanese homosexual man. He was admitted to our hospital for acute hepatitis caused by HBV. At that time, HIV-1antibody (Ab) was not detected in his serum. After 6 months, he was readmitted to our hospital for further examination of his liver because of confined liver enzyme abnormalities. Anti-HIV- Ab was detected in his serum by both enzyme immunosorbent assay (EIA) and particle agglutination (PA). His serum hiv-1 rna level was 50 x 10(4) copies/ml and serum levels of HBV dna polymerase (dna-P) and HBV dna were 6535cpm and 3 plus (>1000 copies/ml). His clinical course and laboratory data suggested progression from acute to chronic hepatitis related to coinfection with hiv-1. The diagnosis was chronic active hepatitis caused by HBV as an opportunistic infection due to coinfection with hiv-1. We began highly active antiretroviral therapy (HAART) because interferon (IFN) therapy was ineffective. HAART was started at an initial dosage of 600 mg zidovudine (AZT), 300 mg lamivudine (3TC), and 2400 mg indinavir (IDV) daily. After 4 weeks, the serum level of HBV dna-polymerase (p) had decreased markedly to 37cpm and that of hiv-1 rna had decreased to below the sensitivity threshold, indicating considerable suppression of the replication of these viruses by the treatment. But HBV dna remained at low levels. Although the incidence of HBV infection in patients with hiv-1 infection has been reported to be high in the united states and europe, simultaneous HBV and hiv-1 infection leading to persistent HBV infection is rare.
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4/97. Moyamoya syndrome in a patient with congenital human immunodeficiency virus infection.

    A 10-year-old boy with congenital human immunodeficiency virus (HIV) infection developed recurrent episodes of left hemiparesis at age 7 years. The progression of his disease was followed by computed tomography, magnetic resonance imaging, magnetic resonance angiography, and cerebral angiography. The series of images showed progressive stenosis of both carotid arteries at the suprasellar origin with involvement of his anterior and middle cerebral arteries, while prominent collateral vessels developed from his external carotid supply through ophthalmic and middle meningeal arteries. The pattern of cerebrovascular disease is consistent with moyamoya syndrome. We suggest that further studies on the pathophysiology of cerebrovascular disease in patients with HIV could be helpful in understanding the cause of moyamoya disease as well. Also, with the various advances in treatment of HIV, neurovascular complications could be seen more frequently as the long-term survival in these patients improves.
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5/97. Management of liver failure in a haemophilic patient co-infected with human immunodeficiency and hepatitis c viruses.

    We present a case of liver failure in a haemophilic patient coinfected with transfusion acquired human immunodeficiency (HIV) and hepatitis c (HCV) viruses. The case illustrates the interaction of multiple viruses with accelerated progression to end stage liver disease and ultimately death. We report the impact on the patient management of two liver biopsies, which diagnosed an initial drug induced hepatitis and subsequently an atypical HCV related hepatitis.
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6/97. Lack of viral escape and defective in vivo activation of human immunodeficiency virus type 1-specific cytotoxic T lymphocytes in rapidly progressive infection.

    Human immunodeficiency virus type 1 (hiv-1)-specific immune responses over the course of rapidly progressive infection are not well defined. Detailed longitudinal analyses of neutralizing antibodies, lymphocyte proliferation, in vivo-activated and memory cytotoxic T-lymphocyte (CTL) responses, and viral sequence variation were performed on a patient who presented with acute hiv-1 infection, developed an AIDS-defining illness 13 months later, and died 45 months after presentation. Neutralizing-antibody responses remained weak throughout, and no hiv-1-specific lymphocyte proliferative responses were seen even early in the disease course. Strong in vivo-activated CTL directed against Env and Pol epitopes were present at the time of the initial drop in viremia but were quickly lost. memory CTL against Env and Pol epitopes were detected throughout the course of infection; however, these CTL were not activated in vivo. Despite an initially narrow CTL response, new epitopes were not targeted as the disease progressed. Viral sequencing showed the emergence of variants within the two targeted CTL epitopes; however, viral variants within the immunodominant Env epitope were well recognized by CTL, and there was no evidence of viral escape from immune system detection within this epitope. These data demonstrate a narrowly directed, static CTL response in a patient with rapidly progressive disease. We also show that disease progression can occur in the presence of persistent memory CTL recognition of autologous epitopes and in the absence of detectable escape from CTL responses, consistent with an in vivo defect in activation of CTL.
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7/97. Identification of a new recipient in the Sydney blood Bank Cohort: a long-term HIV type 1-infected seroindeterminate individual.

    We have reported previously a cohort of long-term survivors of hiv-1 infection, known as the Sydney blood Bank Cohort, who received hiv-1-positive blood from a common infected donor. A new recipient, C135, has been identified. This recipient became infected after receiving blood donated during the presumed time of seroconversion of the donor in February 1981. C135 has been infected for more than 18 years without signs of disease progression. The virus load in this recipient has remained below the detectable level (<20 rna copies/ml of plasma) and repeated Western blot analyses have given an indeterminate result. By booster PCR techniques we have demonstrated that this individual is infected with hiv-1 and have characterized the viral nef and nef/LTR region sequences present. The strain of hiv-1 identified contains deletions of 88 bp from the nef alone region and a total of 139 bp deleted from the nef/LTR overlap and LTR regions. The LTR contains three wild-type sp1 transcription factor-binding sites, the 3' wildtype NF-kappaB site, and a duplicated Sp1 and NF-kappaB region. A truncated Nef protein of only 19 amino acids is encoded. The deletions and rearrangements in the nef gene and LTR sequences are characteristic of Sydney blood Bank Cohort strains of virus. The identification of C135 increases the Sydney blood Bank Cohort size to nine individuals and represents a rare example of a genuine, long-term hiv-1 infection accompanied by indeterminate anti-hiv-1 serology.
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keywords = disease progression, progression
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8/97. The use of paclitaxel and cisplatin in a patient with epithelial ovarian cancer and human immunodeficiency virus.

    OBJECTIVE: Several spots exist of human immunodeficiency virus (HIV)-positive patients developing epithelial ovarian cancer. The optimal chemotherapeutic regimen has been unclear due to potential immunotoxicity from chemotherapy in these already immunocompromised patients. This is the first report of paclitaxel-based combination chemotherapy in an HIV-positive patient with ovarian cancer. METHOD: A 39-year-old woman with HIV was diagnosed with poorly differentiated serous carcinoma. She underwent optimal cytoreductive surgery and received six courses of paclitaxel and cisplatin. RESULTS: The patient experienced a complete clinical response to therapy with no adverse effect on surrogate markers for human immunodeficiency virus (CD4 count, beta2 microglobulin, neopterin, p24 antigen, and viral load). CONCLUSION: paclitaxel- and platinum-based chemotherapy, the standard of care for adjuvant chemotherapy in advanced ovarian carcinoma, is appropriate therapy for ovarian cancer patients with HIV. There is no evidence that the paclitaxel/cisplatin regimen is associated with progression of HIV or increased chemotherapy-associated morbidity.
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keywords = progression
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9/97. Multiple drug resistance mutations in human immunodeficiency virus in semen but not blood of a man on antiretroviral therapy.

    The concept that the male reproductive tract harbors isolated reservoirs of human immunodeficiency virus (HIV) infection has now been widely accepted. The significance of semen viral burden to sexual transmission of HIV is obvious; however, its contribution to disease progression is unknown. We report a case study that demonstrates the emergence of resistance-conferring mutations to antiviral therapy in infected seminal leukocytes from a man with asymptomatic prostatitis associated with leukospermia. This finding demonstrates the potential importance of male reproductive tract organs to the development of therapy resistance in HIV-infected men.
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10/97. The natural history of hepatitis c viral infection.

    Although early data suggested that chronic hepatitis c virus infection carried little risk, studies with longer duration of infection have reported concerning results. Of patients with acute infection, approximately 80% will develop chronic infection. The greatest risk of morbidity comes with cirrhosis and the resulting increased risk of hepatocellular carcinoma. The true risk of progression to cirrhosis, however, has emerged as an area of controversy. Both host and viral factors seem to impact susceptibility to chronic infection, cirrhosis, and hepatocellular carcinoma. hepatitis c virus has become the most common indication for liver transplantation, but the infection routinely recurs and may have a more aggressive course after transplantation. Given that current treatment options for hepatitis c virus infection are clearly not optimal, informed decisions regarding treatment require an in depth understanding of the natural history.
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keywords = progression
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