ABSTRACT
INTRODUCTION: Highly active antiviral therapy (HAART) results in a sharp decrease in HIV-related morbidity and mortality, but also induces adverse effects such as dyslipidemia, which is difficult treat because of drug interactions. Guidelines recommend lipid-lowering therapy with pravastatin or atorvastatin to reduce LDL cholesterol in these patients, and gemfibrozil or fenofibrate for treating hypertriglyceridemia. The use of statins in the management of dyslipidemia is complicated by drug interactions with some of the components of HAART. Rosuvastatin, a statin with minimal cytochrome P-450-mediated metabolism, could be an alternative option for this population. METHODS: Retrospective study to evaluate the efficacy and safety of rosuvastatin (10 mg/day) for 16 weeks in HAART-treated HIV-infected patients with dyslipidemia, and moderate to high cardiovascular risk. Results were analyzed with the Shapiro-Wilks, K-S Lilliefors, and sign tests. Percentages were analyzed with the chi-square test. RESULTS: Seventy-eight patients were started on rosuvastatin for dyslipidemia, 60 as single therapy. After 16 weeks of treatment, a significant median decrease was seen in both LDL-cholesterol and non-HDL cholesterol (31.3% reduction in LDL and 29.9% in non-HDL). The therapeutic goal for non-HDL was achieved in 65.8% of patients. The decrease in triglyceride levels was also significant (34.1%); 35% of subjects achieved the therapeutic goal. The drug was withdrawn in 2 patients because of myositis, and in 1 because of gastrointestinal intolerance. There were no differences in efficacy or toxicity between patients receiving protease inhibitors, non-nucleoside reverse transcriptase inhibitors, or fibrates. CONCLUSION: Rosuvastatin was safe and effective for treating dyslipidemia in HAART-treated HIV-infected patients. Results were similar to those observed in the HIV-uninfected population.
Subject(s)
Antiretroviral Therapy, Highly Active/adverse effects , Dyslipidemias/chemically induced , Dyslipidemias/drug therapy , Fluorobenzenes/therapeutic use , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Pyrimidines/therapeutic use , Sulfonamides/therapeutic use , Adult , Aged , Female , HIV Infections/drug therapy , Humans , Male , Middle Aged , Retrospective Studies , Rosuvastatin CalciumABSTRACT
INTRODUCCIÓN. El tratamiento antirretroviral combinado de gran actividad (TARGA) redujo la morbimortalidad por la infección por el virus de la inmunodeficiencia humana(VIH), pero indujo efectos adversos como la dislipidemia, cuyo tratamiento se dificulta por interacciones farmacológicas. En las guías para su tratamiento sepropuso usar pravastatina o atorvastatina para reducir el colesterol de las lipoproteínas de baja densidad (c-LDL), y gemfibrozil o fenofibrato para tratar la hipertrigliceridemia. Rosuvastatina, una estatina con escaso metabolismo hepático, podría ser una nueva alternativa. MÉTODOS. Estudio retrospectivo para evaluar la efectividad y la toxicidad del uso de rosuvastatina (10 mg/día) por 16 semanas en pacientes con dislipidemia, portadores del VIH con TARGA y riesgo cardiovascular de moderado a muy elevado. Los resultados se analizaron mediante las pruebas de Shapiro-Wilks, K-S Lilliefors y el test del signo; los porcentajes se compararon mediante la prueba de chi al cuadrado. RESULTADOS. Setenta y ocho pacientes recibieron rosuvastatina, 60 como único hipolipemiante. Tras16 semanas, el descenso mediano del c-LDL y del colesterol no ligado a las lipoproteínas de alta densidad(c-no-HDL) fue significativo (31,3 y 29,9%,respectivamente); el 65,8% de los pacientes lograron la meta para c-no-HDL. La reducción de la trigliceridemia también fue significativa (34,1%); el 35% de los pacientes alcanzaron la meta terapéutica para trigliceridemia. Dos individuos suspendieron la droga por toxicidad muscular y uno por intolerancia digestiva. No hubo diferencia en la toxicidad y la eficacia de acuerdo a si los pacientes recibían concomitantemente inhibidores de proteasa, inhibidores de transcriptasa inversa no nucleosídicos o fibratos. CONCLUSIÓN. Rosuvastatina fue efectiva y segura para tratar la dislipidemia de pacientes VIH con TARGA, logrando resultados similares a los descritos en población no infectada por VIH (AU)
INTRODUCTION. Highly active antiviral therapy (HAART)results in a sharp decrease in HIV-related morbidity and mortality, but also induces adverse effects such as dyslipidemia, which is difficult treat because of drug interactions. Guidelines recommend lipid-lowering therapy with pravastatin or atorvastatin to reduce LDL cholesterol in these patients, and gemfibrozil or fenofibrate for treating hypertriglyceridemia. The use of statins in the management of dyslipidemia is complicated by drug interactions with some of the components of HAART. Rosuvastatin, a statin with minimal cytochrome P-450-mediated metabolism, could be an alternative option for this population. METHODS. Retrospective study to evaluate the efficacy and safety of rosuvastatin (10 mg/day) for 16 weeks in HAART-treated HIV-infected patients with dyslipidemia, and moderate to high cardiovascular risk. Results were analyzed with the Shapiro-Wilks, K-S Lilliefors, and sign tests. Percentages were analyzed with the chi-square test. RESULTS. Seventy-eight patients were started on rosuvastatin for dyslipidemia, 60 as single therapy. After 16 weeks of treatment, a significant median decrease was seen in both LDL-cholesterol and non-HDL cholesterol (31.3% reduction in LDL and 29.9% in non-HDL). The therapeutic goal for non-HDL was achieved in 65.8% of patients. The decrease in triglyceride levels was also significant (34.1%); 35% of subjects achieved the therapeutic goal. The drug was withdrawn in 2 patients because of myositis, and in 1 because of gastrointestinal intolerance. There were no differences in efficacy or toxicity between patients receiving protease inhibitors, non-nucleoside reverse transcriptase inhibitors, or fibrates. CONCLUSION. Rosuvastatin was safe and effective for treating dyslipidemia in HAART-treated HIV-infected patients. Results were similar to those observed in the HIV-uninfected population (AU)
