Vertebral osteomyelitis and epidural abscess in a patient receiving enfuvirtide.
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Biomedical subjects
Publications and source records attributed to V Boix.
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An immunosuppressed patient who presented with unusual clinical signs of cutaneous alternariosis, including papular, nodular and verrucous lesions of the forearms, is reported. In spite of continuous treatment with oral itraconazole for 6 months, a large, progressive, necrotic ulcer appeared on the patient's left leg. Liposomal amphotericin B was then administered (total dose, 750 mg) with excellent clinical results.
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OBJECTIVES: Rash is the most frequent adverse event associated with nevirapine. The use of prednisone has been controversial in this setting. A double-blind placebo-controlled study was performed to evaluate its efficacy in nevirapine-induced rash prevention. DESIGN: Multicentered, randomized, double-blind, placebo-controlled clinical trial with prednisone (30 mg/day x 2 weeks). INCLUSION CRITERIA: HIV-1 infection; CD4 count >200 cells/mm3; plasma viral load (PVL) <5 log10 copies/ml; nevirapine (200 mg/day x 2 weeks, followed by 200 mg twice daily) plus stavudine and didanosine. Clinical follow-up was performed at 15, 30, and 60 days and thereafter every 2 months. RESULTS: In all, 75 evaluable patients were enrolled (39 prednisone/36 placebo). Median baseline CD4 + cell count was 390 cells/mm3 and PVL, 20,200 copies/ml. Overall, nine cases of rash (12.5%) were detected, seven (18%) in the prednisone group and two (5.5%) in the placebo group (odds ratio [OR], 3.85; 95% confidence interval [CI], 0.65-29.3; p =.11). Incidence of moderate-to-severe rashes leading to nevirapine withdrawal was 13.5% (5 of 37) in the prednisone group and 3% (1 of 35) in the placebo group ( p =.2). Median time to rash in both groups was 16 days. Adverse events that motivated withdrawal of therapy appeared in 6 patients from the prednisone group (15.4%) and 3 from the placebo group (8.3%) ( p =.3). CONCLUSION: Short-term prednisone administration does not prevent nevirapine rash, but might even increase its incidence.
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Progressive multifocal leukoencephalopathy (PML) has been a devastating disease for HIV-1-infected patients since the beginning of the AIDS pandemic. Currently, highly active antiretroviral therapy (HAART) seems to improve the outcome of PML in many patients. We describe two cases of PML whose course worsened in spite of HAART, but had a good response to cidofovir.
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BACKGROUND: HIV-1 protease inhibitors (PI) have been recently associated with a syndrome of anomalous body fat distribution or lipodystrophy (LD), which sometimes is associated to hyperglycemia. Many aspects of this syndrome remain obscure. The objective of the study is to describe the prevalence, clinical patterns, derangement of glucose metabolism associated and follow-up. METHODS: Patients taking at least one PI during January 1998 were asked a questionnaire about any body change, and a physical exam looking for fat changes was performed. In patients found to have LD, basal plasma glucose, cholesterol, triglycerides and cortisol were studied, and an oral glucose tolerance test (OGTT) was performed. In those cases with breast enlargement, prolactin and estradiol were measured. RESULTS: Among 272 patients, five cases (1.8%) of LD were detected. The syndrome appeared associated with all the IP available at the time of the study, a medium of 4.2 months after the introduction of the drug. The most common pattern was fat accumulation in abdomen and breast, and fat loss in arms, legs and face. Basal glycemia was normal in all 5 patients, but OGTT showed carbohydrate intolerance in two (both of them had family antecedents of type 2 diabetes mellitus). Only one patient need treatment withdrawal because of progressive deforming changes. CONCLUSIONS: The LD can appear in patients taking any IP. Body changes are usually self limited and in many patients PI don't need to be stopped.
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An observational cohort study was performed to assess the effectiveness of a cytomegalovirus antigenemia (CMV-Ag) assay designed to predict clinical CMV disease in patients with AIDS. Eighty-six HIV-infected patients with CD4+ cell counts of < 100/mm3, positive CMV IgG, and no previous CMV disease were enrolled. Thirty-eight (44%) patients had at least one positive CMV antigenemia test, ten of whom eventually developed CMV focal disease. CMV disease was diagnosed in 13 (15%) patients. The CMV antigenemia assay was positive in ten of these 13 patients. Using a cut-off value of five positive cells in every 150,000 leukocytes sampled, the CMV antigenemia assay had a positive predictive value of 89% and a negative predictive value of 94%. The median time from the first positive CMV antigenemia test to the onset of CMV disease was 102 days. CMV disease probability at 6 months in patients with a CMV antigenemia value > or = 5 was 77.8% versus 6% in patients with CMV antigenemia value < 5 (log-rank test = 48.345; P < 0.001). Several independent factors were associated with the development of CMV disease: CMV antigenemia > or = 5 cells (hazard ratio: 20.44), CD4+ count < or = 25/mm3 (HR: 3.12), and sexual transmission of HIV infection (hazard ratio, 3.15). CMV antigenemia seems to be a good predictor of CMV disease in patients with AIDS.
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BACKGROUND: The changes that HIV coinfection can induce in clinical symptoms, response to treatment and prognosis of visceral Leishmaniasis (VL) are not well known. METHOD: We retrospectively describe the characteristics of VL in patients with and without HIV infection, between 1988-1998. RESULTS: Fifty episodes of VL were diagnosed in 40 patients. Nineteen (47.5%) were HIV coinfected, 57.8% of them have had an aids defining illness, and the median of CD4+ lymphocytes was 50/mm3. Clinical and laboratory data were similar to patients non HIV infected, except for lower levels of LDH (437 vs 578 U/ml; p = 0.02) and total lymphocytes (665 vs 1.500/mm3; p = 0.004) and higher levels of hemoglobin (9.8 vs 8.7 gr/dl; p = 0.01) and ESR (85 vs 44 mm; p = 0.01). The first episode of VL was diagnosed in 87.5% patients through bone marrow aspirate, and the other cases were diagnosed by biopsies of gum (2), lymph node (1) or liver (1). One patient was diagnosed clinically: he had a positive serology and a good response to antileishmanial therapy. Treatment failed in nine patients (22.5%), 7 HIV-coinfected. Eight patients died (20%), 6 HIV-coinfected. Five deaths were directly attributed to VL. Six coinfected patients (31.5%) relapsed and only one (4.7%) in the other group. CONCLUSIONS: We did not find major differences in clinical manifestations or laboratory data between the two groups. Biopsies of several tissues can be particularly helpful for diagnosis in immunocompromised patients with negative bone marrow aspirates. Failures, mortality and relapses are more common in HIV infected patients. VL coinfection usually affects HIV infected patients when they develop severe immunodepression.
Liver failure with hepatic encephalopathy during an acute viral hepatitis carries a very high mortality. Liver transplantation is the usual treatment, but for poor candidates for transplantation only supportive therapy is available. Two patients with HIV infection developed an acute B hepatitis with liver insufficiency and hepatic encephalopathy. After an alprostadil infusion was begun they improved quickly and made a full recovery. This drug merits further investigation.
OBJECTIVES: To describe the clinical presentation of HIV disease in older patients. METHODS: In the period 1989-1996 we reviewed the medical records of 100 patients with human immunodeficiency virus (HIV) infection aged 50 years or older and, 197 controls among HIV-infected patients aged 15-40 years, who attended six institutions in the autonomous community of Valencia (Spain). RESULTS: Older patients were mostly males (86%), men who have sex with men (42%) or unknown (20%) as exposure categories. Older patients had lower CD4 cell counts/mm3 (163+/-136 vs. 450+/-373, P= 0.008), and had AIDS at first evaluation (49% vs. 29%, P = 0.0006) compared with younger patients. For patients presenting with AIDS at HIV infection diagnosis, type and frequency of AIDS indicator diseases did not differ between older and younger patients. CONCLUSION: Studies on clues for early detection of HIV infection in patients aged 50 years or older are urgently needed to improve the health care in this population.