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

Zidovudine is approved for administration in doses given every 4 hours. Less frequent dosing has been used in many clinical trials, but the toxicity and efficacy of such regimens have not been formally compared with the approved regimen. In this multicenter, randomized, double-blind, controlled trial, the safety, tolerance and efficacy of 600 mg of zidovudine given daily in two or six divided doses were compared. Three hundred and twenty patients with a CD4 lymphocyte count < 250 cells/mm3 (mean, 104 cells/mm3) or a prior AIDS-defining illness were treated with zidovudine 100 mg every 4 hours (regimen A) or 300 mg every 12 hours (regimen B). Eighty-eight patients (56%) and 94 patients (58%), assigned to regimens A and B, respectively, completed the planned 48 weeks of treatment. Serious anemia (hemoglobin < or = 7.5 g/dl) occurred in 13% and 7% of patients treated with regimens A and B, respectively (difference, 6%, 95% confidence interval [CI], 2, 12%; p = .13). The mean duration of treatment and the frequency of neutropenia and symptomatic complaints including nausea and headache were similar in the two treatment groups. The number of patients experiencing a new opportunistic infection (18% versus 20% for regimens A and B, respectively), and the number of deaths (five in each group) did not differ significantly between groups. The effect of treatment on CD4 lymphocyte counts and HIV p24 antigenemia also was similar for both regimens. Zidovudine given at the more convenient dose of 300 mg twice daily has similar safety, and tolerance and appears to have similar efficacy to the currently approved regimen. Use of this regimen should help simplify the treatment of HIV disease.
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PMID:A comparative trial of zidovudine administered every four versus every twelve hours for the treatment of advanced HIV disease. 929 87

Toxoplasma gondii is a frequent cause of subclinical latent human infection and an important opportunistic pathogen that may cause severe disease in immunocompromised patients. Patients with AIDS who have antibodies to T. gondii should be considered at high risk for development of clinical disease (toxoplasmosis). Reactivation of latent infection in the central nervous system is a common HIV/AIDS-related complication in these patients. Typical presenting symptoms are headache, confusion, fever, and focal neurologic deficits. Routine serologic tests cannot distinguish active from latent infection. Neuroradiologic studies may be highly suggestive of toxoplasmic encephalitis, but the definitive diagnosis can be made only by demonstration of toxoplasma in brain tissue. The unique pathogenesis of toxoplasmic encephalitis in patients with AIDS necessitates intensive primary therapy followed by life long suppressive therapy. Clinical and radiographic improvement is usually rapid with appropriate treatment.
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PMID:Recognition and management of toxoplasmosis. 931 66

Cerebral tuberculosis (TB) was diagnosed in 6 (4%) of 156 HIV-infected patients with TB seen at our institution over 6 years. We describe here the clinical and radiologic features of these cases and of 15 others reported in the literature. Of the 21 patients, 59% were intravenous drug users. Presenting symptoms were fever (76%), confusion (52%), seizures (38%), and headache (38%). Fourteen patients (66%) had previous or active extracerebral TB at presentation. Cranial CT scan showed ring-(62%) or nodular-(24%) enhancing lesions or mixed forms (14%). Among the 12 patients who underwent a brain biopsy, bacteriologic evidence of TB was found in 9. Four patients (19%) died during hospitalization. Among the 17 others who received antituberculous therapy, only 1 developed neurologic sequelae. Five patients also received steroid therapy to control cerebral edema or paradoxical growth of the cerebral mass lesions. TB should be considered as a cause of cerebral mass lesions in HIV-infected patients, especially if tuberculous infection is suspected at other sites.
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PMID:Cerebral tuberculosis in patients with the acquired immunodeficiency syndrome (AIDS). Report of 6 cases and review. 941 28

Toxoplasmosis of the central nervous system (CNS) is the most common cause of intracerebral lesions in patients with AIDS. It is now standard clinical practice to treat empirically, based on clinical and radiographic findings, and to perform a biopsy of the lesion only in those patients who fail to have a clinical and radiographic response after two weeks of therapy. This study describes the presentation and response to therapy of central nervous system toxoplasmosis in patients with AIDS at a private practice in Mexico City. A retrospective chart and radiology review of all patients with AIDS treated empirically for toxoplasmosis between 1988 and 1993 was performed. A total of 177 patients with AIDS were seen, nine (5.1%) had toxoplasmosis. Patients with toxoplasmosis were males with a median age of 39 years (range 26 - 65). In two patients, toxoplamosis of the CNS was the initial manifestation of HIV infection, all others had a prior diagnosis of AIDS with a mean of 10 months between their first AIDS defining event and the diagnosis of toxoplasmosis. The median CD4+ T-cell count at the time of the diagnosis of toxoplamsosis was 78 cells/microL. Most patients had headache associated with other focal neurological symptoms such as hemiplegia (2), hemiparesis (2) or seizures (4). Only 4 out of 9 patients had fever as part of their initial clinical presentation. Serum IgG antibodies against Toxoplasma gondii were positive in 6 out of 7 patients tested, while IgM antibodies were negative in all patients. On imaging studies (Computerized Tomography or Magnetic Resonance Imaging), 4 patients had a single lesion while the rest had two or more lesions. Two patients were initially treated with pyrimethamine/sulfadiazine and were later changed to pyrimethamine/clindamycin, which was the treatment given from the beginning to all other patients. One patient died of an intralesional hemorrhage two weeks after the diagnosis despite adequate therapy. The probability of surviving 6 months after the diagnosis of toxoplasmosis was 60%. The findings of these authors are similar to those reported in other series where toxoplasmosis of the CNS is a late complication of HIV infection associated with a CD4+ cell count of < 100 cells/microL. However, survival was short in spite of a good response to therapy.
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PMID:Toxoplasmosis of the central nervous system in patients with AIDS in Mexico. 942 78

This study was carried out in 60 AIDS patients who presented toxoplasma encephalitis in Martinique (French West Indies). Diagnosis was based on a combination of fever, neurologic signs, and characteristic CT-scan images in patients with positive HIV serology. There were 46 males and 14 females with a mean age of 40 years. The mode of transmission was heterosexual in most cases (68.3%). The incidence of drug-related transmission was low (6.7%). Neurotoxoplasmosis was the most frequent presenting symptom of AIDS (53.3%) followed by esophageal candidosis (20%) and pneumocystosis (10%). Clinical symptoms were headache (56.5%), fever (48.3%), hemiparesia (36.6%), and confusion (36.6%). CT-scan showed most lesions to be multiple (70%), hypodense (89%), and subject to contrast uptake (93%). Mean lymphocyte level was 1128/mm3 with 88 CD4/mm3 and a CD4-to-CD8 ratio of 0.14. Conventional treatment using a combination of pyrimethamine and sulfadiazine led to skin rash and neutropenia and had to be discontinued in 30% of cases. Clinical symptoms and mean survival (327 days) were the same as comparable findings from Europe and North America.
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PMID:[Cerebral toxoplasmosis and AIDS in Martinique]. 951 53

Abacavir is a nucleoside analogue reverse transcriptase inhibitor that inhibits clinical isolates of HIV in vitro with a potency similar to that of zidovudine. Resistance to abacavir develops relatively slowly. Cross-resistance between abacavir and didanosine, zalcitabine or lamivudine, but not zidovudine or stavudine, has been reported in vitro. Abacavir has good oral bioavailability, as demonstrated in animals, and penetrates the CNS. Treatment with abacavir, alone or in combination with other anti-HIV agents (zidovudine, lamivudine, nevirapine, amprenavir and/or other protease inhibitors), decreased viral load and increased CD4+ cell count in patients with HIV infection. Effectiveness was maintained for at least 48 weeks. In early phase I/II trials, headache, gastrointestinal disturbances, rash, malaise, fatigue and/or asthenia were the most common adverse events reported with abacavir alone or in combination with other anti-HIV agents. Hypersensitivity reactions lead to discontinuation of therapy in 2 to 3% of patients.
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PMID:Abacavir. 958 69

Amprenavir is a viral protease inhibitor with specificity for the HIV protease enzyme. The resistance profile of amprenavir appears to differ from that of other protease inhibitors such as saquinavir and indinavir. Twelve hours after single-dose administration of amprenavir 1200mg to HIV-infected individuals, the mean plasma concentration of the drug was more than 10-fold greater than the 50% inhibitory concentration for HIV-1IIIB in peripheral blood lymphocytes. In a small nonblind study, amprenavir monotherapy increased CD4+ cell count and decreased viral load in 37 patients with HIV infection and no previous exposure to protease inhibitor therapy. Combination therapy comprising amprenavir and other antiretroviral agents (abacavir, zidovudine, lamivudine, indinavir, saquinavir or nelfinavir) decreased viral load and increased CD4+ cell counts in patients with HIV infection. Antiviral efficacy was maintained during up to 24 weeks' follow-up. Available data suggest that rash, headache and diarrhoea or loose stools are the most frequent adverse events associated with amprenavir therapy.
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PMID:Amprenavir. 961 98

In immunocompetent patients the postnatally acquired toxoplasmosis is usually a mild or asymptomatic disease. CNS manifestations are rare, e.g. in patients with HIV infection or in patients with other types of immunosuppression. We report on a 9-year old healthy boy, who was hospitalized after one week with subfebrile temperatures and headache with clinical signs of encephalitis and unilateral deafness. We diagnosed a toxoplasmosis and treated the patient with pyrimethamine and sulfadiazine. While most of the signs and symptoms disappeared rapidly the deafness persisted.
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PMID:[Acquired toxoplasmosis with cerebral involvement and subsequent hearing loss]. 962 46

A study was undertaken to determine the role of typhoid in febrile illness. It was found that in 1992, Salmonella typhi, the causative agent of typhoid, played a 2.3% role in 25404 diagnostic specimens sent to Mulago Hospital, Kampala, the largest hospital in Uganda. The rates of isolation fell gradually from 2.3% in 1992 to 0.3% by 1995. Instead malaria was found to play a major role in febrile illnesses. Out of 355 patients attending a private clinic in Kampala, whose blood was examined for both malaria and typhoid, 97% were positive for malaria parasites compared to 0.84% with significant O and H Salmonella typhi antibody titres of > 1:80. Also malaria parasites were found in 60% (out of 105) of patients who had had persistent fevers and in whom doctors had also requested for HIV antibodies. Those who had HIV antibodies alone were six per cent and the ones with both were 28%, a finding which showed relatively low association of malaria and HIV. Where multiple tests were requested on one patient having general malaise or body joint pains and/or constant headaches, malaria was found to play a major role (73%) compared to syphilis (4.3%) and brucellosis (13.3%). Malaria parasites were seen in normal sizes and in somehow young or stunted forms. The latter were found more often in patients who had experienced one or a combination of the following: intermittent fevers, backache, headache, tiredness, joint and/or neck pains, and who had already received treatment for malaria.
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PMID:Selected laboratory tests in febrile patients in Kampala, Uganda. 964 Aug 25

A 38-year-old homosexual male with AIDS suffered four neurological episodes including headaches, confusion, visual impairment, memory disturbances, and dysarthria which resolved spontaneously in a few days. He was admitted to hospital during a fifth episode. Neurological examination revealed a cerebellar syndrome. General examination was normal. CD4 count was 90. CSF contained two WBCs/mm(3) and 12.30 mg/dL protein. MRI revealed diffuse ill defined increased signal on T2-weighted images in the white matter. His condition worsened rapidly with vomiting and he died 1 month after admission. Neuropathological examination revealed diffuse brain oedema with ventricular compression, central diencephalic herniation and bilateral tonsilar herniation in the absence of a focal lesion. Microscopical examination revealed predominant involvement of the white matter with diffuse myelin pallor and massive perivascular dilatation containing an exudate expressing serum proteins and occasional macrophages. The same exudate was also diffuse in the leptomeninges. Parenchymal damage predominated around the perivascular spaces and included loosening of tissue, axonal damage with spheroids and reactive astrocytosis. There was no evidence of productive HIV encephalitis, no multinucleated giant cells; p24 immunostaining and RT-PCR for HIV genome were negative. There was neither significant inflammation nor microglial activation. In this illustrative case, the relapsing course of the neurological signs, the diffuse topography of the blood-brain barrier breakdown and the absence of local cause make it likely that the diffuse leak and axonal damage could be related to circulating factors.
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PMID:Acute, relapsing brain oedema with diffuse blood-brain barrier alteration and axonal damage in the acquired immunodeficiency syndrome. 971 86


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