ABSTRACT
Introducción: las estatinas son medicamentos hipolipemiantes asociados con miotoxicidad como efecto adverso. Objetivo: determinar la asociación entre el uso de estatinas y la elevación de la creatinafosfoquinasa. Materiales y métodos: se realizó un estudio transversal en pacientes consecutivos que asistieron al Laboratorio Clínico Hematológico (Medellín, Colombia) para la determinación del perfil lipídico. Se incluyeron 661 pacientes, 329 en el grupo de estatinas y 332 en el de no estatinas.A todos se les midieron los niveles séricos de creatina fosfoquinasa y se consideraron como elevados los niveles superiores a 170 mg/dL. Se estableció un nivel de significancia menor de 0,05. Resultados: se registró mayor proporción de pacientes con creatina fosfoquinasa elevada en el grupo con consumo de estatinas (64,9% frente a 47% en el grupo de no estatinas; razón de disparidad: 2,01; intervalo de confianza del 95%: 1,21-3,32; p= 0,0085). No se encontró asociación entre la elevación de la creatina fosfoquinasa y la presencia de dolor (razón de disparidad: 0,78; intervalo de confianza del 95%: 0,40-1,50; p= 0,5615), fatiga (razón de disparidad: 0,85; intervalo de confianza del 95%: 0,45-1,61; p= 0,7385) y debilidad muscular (razón de disparidad: 1,46; intervalo de confianzadel 95%: 0,68-3,12; p= 0,4333); aunque el grupo de estatinas presentó mayor frecuencia de dolor (razón de disparidad: 2,96), fatiga (razón de disparidad: 1,98) y debilidad muscular (razón de disparidad: 4,19). Conclusiones: el consumo de estatinas se relaciona con síntomas musculares y elevación de creatina fosfoquinasa, sin relación entre la elevación de creatina fosfoquinasa y la presencia de síntomas musculares.
Introduction: statins are a class of lipid-lowering medications associated with the adverse effect of myotoxicity. Objetive: To determine the association between statin use and creatine phosphokinase elevation. Materials and methods: A cross-sectional study, involving consecutive patients attending in the clinical laboratory Laboratorio Clinico Hematologico (Medellin, Colombia) for a serum lipid profile test was performance. A total of 661 patients were included, 329 belonged to the statin group and 332 to the non-statin group. All patients were tested for serum creatine phosphokinase and were considered elevated the serum levels higher than 170 mg/dL. The threshold for significance was set as p-value less than 0.05. Results: Creatine phosphokinase levels were more elevated in the statin group (64.9% versus 47% in non-statin group; odds ratio: 2.01; 95% confidence interval: 1.21-3.32, p= 0.0085). No association was found between the degree of creatine phosphokinase elevation and the presence of muscular pain (odds ratio: 0.78; 95% confidence interval: 95%, 0.40-1.50, p= 0.5615), fatigue (odds ratio: 0.85; 95% confidence interval: 0.45-1.61, p= 0.7385) or muscle weakness (odds ratio: 1.46; 95% confidence interval: 0.68-3.12, p= 0.4333). However, the statin group exhibited greater frequency of muscle pain (odds ratio: 2.96), fatigue (odds ratio: 1.98) and muscle weakness (odds ratio: 4.19). Conclusions: statin use is associated with a higher frequency of muscular symptoms and higher creatine phosphokinase levels, with no relationship between creatine phosphokinase elevation and the presence of muscle symptoms.
Subject(s)
Humans , Creatine Kinase , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Hypercholesterolemia , Muscular DiseasesABSTRACT
This review explores the evidence supporting a potential benefit of statins in cancer. In particular, the lipophilic forms (i.e. lovastatin, simvastatin, or similar) would have a therapeutic but not a preventive role. The pleiotropic effects that statins possess mainly explain this phenomenon, influencing the natural history of disease and the response to currently available therapies. By inhibiting the mevalonate pathway, statins would have a systemic effect, similar to that observed in atherosclerosis, reducing the inflammatory stimuli present in the tumor micro-environment and inhibiting the activation of intracellular signaling cascades critical for proliferation, migration/invasion and metastasis of the cancer cell. Despite all this evidence, randomized trials are needed to confirm the benefit of statins on cancer, before promoting their widespread use as a therapeutic or preventive strategy for this condition.
Subject(s)
Animals , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Neoplasms/prevention & control , Antineoplastic Agents/therapeutic use , Atherosclerosis/drug therapy , Atherosclerosis/etiology , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Inflammation/complications , Neoplasms/chemically inducedABSTRACT
All statins inhibit hydroxymethylglutaryl Coenzyme A Reductase but each has a different chemical structure that may have individual advantages. Some pharmaceutical companies have minimized side effects and stated that dose has no relation to incidence. To the contrary, dose is related to side effects with all statins. Myopathy occurs in up to 10.5 percent of patients taking a high dose. There is an attempt to sell statins that have lost patent protection over-the-counter. However, evidence supports medical supervision as offering greatest patient safety. Concerns were raised about ezetimibe after the initial ENHANCE (effcacy) and SEAS (cancer risk) study but these concerns appear to have been answered. Fenofbrate can be used with a statin but gemfbrozil is contraindicated. Coenzyme Q-10 possibly helps to mitigate the risk of myopathy with a statin but evidence is not universally accepted. JUPITER represented a valid outcomes study but made a claim that rosuvastatin has special value in risk management because of decreased high sensitivity C-Reactive Protein. This actually occurs with any statin, a decrease also enhanced by ezetimibe. Statins have benefted the lives of our patients but, as with any treatment, the physician needs to look critically at all the problems and claims made.