Estudio farmacogenómico mediante microarrays en monocitos de pacientes con hiperlipemia familiar combinada tratados con atorvastatina

Monocyte gene expression profiling can provide insight into the pathogenesis of FCH. The results suggest that alterations in the expression of some genes (MNDA, CD36, TFPI2, LRIG1 and DR3) may be related to a proinflammatory environment in FCH monocytes, which is partially reversed by atorvastatin. However, metabolic dysfunction in adipose tissue may account for lower adiponectin and higher FFA and triglyceride plasma levels in FCH, which are not corrected by treatment. These abnormalities could also trigger changes in gene expression that atorvastatin cannot modify.