[Treatment of dyslipidemia: how and when to combine lipid lowering drugs]. / Tratamento das dislipidemias: como e quando indicar a combinação de medicamentos hipolipemiantes.

Familial combined hyperlipidemia (FCH) is a frequent familial lipid disorder associated with insulin resistance, low HDL cholesterol, high triglycerides and cholesterol levels with variable phenotypes within the same family. FCH is linked to a high risk for cardiovascular diseases. Treatment goals for lipid abnormalities are changing in recent years. Lowering elevated levels of LDL e Non HDL-cholesterol levels are primary targets of therapy. Lower LDL-C than 70 mg/dL seems to be useful to lower cardiovascular risk in patients with very high risk. Many statins are available, with different potencies and drug interactions. Combination therapy of statins and bile acid sequestrants or ezitimibe may be necessary to further decrease LDL cholesterol levels in order to meet guideline goals. High triglycerides and low HDL cholesterol are also important goals in the treatment of these patients, and frequently statins alone are insufficient to normalize the lipid profile. Combination therapy with fibrates will further lower triglycerides and increase HDL cholesterol levels; this combination is also associated with higher incidence of myopathy and liver toxicity; appropriate evaluation of patients' risk and benefits is necessary. Association of statin/niacin seems be very useful in patients with FCH, especially as niacin is the best drug to increase HDL cholesterol; this association is not linked to a higher frequency of myopathy. Niacin causes flushing, that can in part be managed with use of aspirin and extended release forms (Niaspan); niacin also may increase plasma glucose and uric acid levels. Evaluation of risks and benefits for each patient is needed.

Tratamento das dislipidemias: como e quando indicar a combinação de medicamentos hipolipemiantes / Treatment of dyslipidemia: how and when to combine lipid lowering drugs

Hiperlipidemia combinada familiar (HCF) é a forma mais comum de hiperlipidemia familial e se caracteriza por resistência à insulina, níveis baixos de HDL-C, níveis altos de triglicérides (TGC) e colesterol total associados a vários fenótipos dentro da mesma família. HCF associa-se, também, a um alto risco cardiovascular (RCV), e os níveis-alvo de tratamento das anormalidades lipídicas têm se modificado recentemente. Reduzir os níveis de LDL-C e não HDL-C devem ser os alvos da terapia. Níveis de LDL-C abaixo de 70 mg/dl têm se mostrado benéficos na RCV em pacientes de alto risco. Várias estatinas com diferentes potências e interações medicamentosas estão disponíveis no mercado. A terapia combinada de estatinas com seqüestradores de ácidos biliares ou ezetimiba pode ser necessária para se alcançar os valores-alvo de LDL-C estabelecidos pelas diretrizes. Níveis altos de TGC e baixos de HDL-C devem ser também considerados no tratamento, e freqüentemente somente o uso das estatinas se mostra insuficiente para normalizá-los. A combinação de estatinas com fibratos pode auxiliar para reduzir os níveis de colesterol e aumentar os de HDL-C, mas está associada à maior freqüência de miopatia e toxicidade hepática. Assim, a avaliação cuidadosa dos riscos e benefícios da terapia é recomendável. A associação de estatina e niacina parece ser útil para pacientes com HCF, particularmente por aumentar os níveis de HDL-C, uma vez que tem sido menos relacionada à alta freqüência de miopatia. A niacina pode ser causa de flushings que podem ser reduzidos com o uso de aspirina. O efeito pode também ser minimizado com o uso de formas de liberação lenta (Niaspan). A niacina pode também elevar os níveis de glicemia e ácido úrico. Assim, os riscos e benefícios da associação devem ser avaliados.

Familial combined hyperlipidemia (FCH) is a frequent familial lipid disorder associated with insulin resistance, low HDL cholesterol, high triglycerides and cholesterol levels with variable phenotypes within the same family. FCH is linked to a high risk for cardiovascular diseases. Treatment goals for lipid abnormalities are changing in recent years. Lowering elevated levels of LDL e Non HDL-cholesterol levels are primary targets of therapy. Lower LDL-C than 70 mg/dL seems to be useful to lower cardiovascular risk in patients with very high risk. Many statins are available, with different potencies and drug interactions. Combination therapy of statins and bile acid sequestrants or ezitimibe may be necessary to further decrease LDL cholesterol levels in order to meet guideline goals. High triglycerides and low HDL cholesterol are also important goals in the treatment of these patients, and frequently statins alone are insufficient to normalize the lipid profile. Combination therapy with fibrates will further lower triglycerides and increase HDL cholesterol levels; this combination is also associated with higher incidence of myopathy and liver toxicity; appropriate evaluation of patients' risk and benefits is necessary. Association of statin/niacin seems be very useful in patients with FCH, especially as niacin is the best drug to increase HDL cholesterol; this association is not linked to a higher frequency of myopathy. Niacin causes flushing, that can in part be managed with use of aspirin and extended release forms (Niaspan); niacin also may increase plasma glucose and uric acid levels. Evaluation of risks and benefits for each patient is needed.

Síndrome de Cushing: Estudo comparativo de métodos diagnósticos / Cushing's syndrome: A comparative study of diagnostic methods

Comparamos as respostas dos corticosteróides urinários:17-hidroxicorticosteróides (17-OHCS), 17-cetosteróides (17-KS) e cortisol livre (FC) à supressäo com dexametasona (baixa dose - 2 mg e alta dose - 8mg) em 71 pacientes com síndrome de Cushing (45 com doença de Cushing, 12 com carcinoma adrenal, oito com adenoma adrenocortical e seis com hiperplasia nodular da córtex adrenal). Os pacientes com doença de Cushing e hiperplasia nodular da córtex adrenal näo apresentam supressäo suficiente com 2 mg de dexametasona,porém o fazem com 8 mg. Os tumores adrenais näo demonstram supressäo adequada. A resposta hiperativa dos 17-OHCS, 17-KS e FC ao hormônio adrenocorticotrópico (ACTH) exógeno foi comparada na doença de Cushing. Concluimos que a determinaçäo urinária dos 17-OHCS, 17-KS e FC säo parâmetros diagnósticos úteis, embora a dosagem do FC mostrou ser um índice mais sensível da hiperfunçäo adrenocortical