Therapeutic monitoring of escitalopram by dexamethasone suppression test.

INTRODUCTION: Depression is associated with a dysfunction of regulation of the hypothalamic-pituitary-adrenal, HPA, which is reflected in the alteration of the dexamethasone suppression test, DST. Escitalopram and other SSRIs decrease the HPA axis response to the DST, beeing the aim of this study validate the DST as a surrogate marker of central serotonergic activity in the treatment with escitalopram and its application to the calculation of the dosage regimens. METHODOLOGY: Prospective observational study on 29 patients, upon whom was performed the DST-test with 0.25 mg of Dexamethasone and subsequent genetic analysis of CYP2C19 by Progenika PHARMAchip test. RESULTS: The range of plasma cortisol levels post-DTS associated with each phenotypic group were: PM phenotype= 0.6 to 1.7 mcg/dl, IM phenotype= 1.2 to 3.5 mcg/dl and EM phenotype = 4.8 to 13.2 mcg/dl, being carried out the dose titration and correspondng, respectively, the following dose regimens: 3-4 mg/day, 5-8 mg/day and 10-31 mg/day. COCLUSIONES: It has been shown that the DST test can be used as a surrogate marker of drug response to escitalopram and as a tool for dose adjustment, providing significant data on different phenotypes of CYP2C19 metabolizers.

Monitorización terapéutica de escitalopram mediante el test de supresión con dexametasona / Therapeutic monitoring of escitalopram by dexamethasone suppression test

Introducción. La depresión está asociada a una disfunción de la regulación del eje hipotálamo-pituitario-adrenal, HPA, que se refleja en la alteración del test de supresión con Dexametasona, DST. Escitalopram y otros ISRS disminuyen la respuesta del eje HPA en el DST, siendo el objetivo del presente trabajo la validación del DST como marcador subrogado de la actividad serotoninergica central en los tratamientos con escitalopram y su aplicación al cálculo de sus regimenes nosológicos. Metodología. Estudio prospectivo observacional sobre 29pacientes, a los que se realizo el DST con 0,25 mg de Dexametasona y posterior análisis genético del CYP2C19 mediante test PHARMA chip de Progenika. Resultados. El rango de valores de cortisol plasmático post-DTS asociados a cada grupo fenotipico fueron: fenotipo PM=0,6-1,7 mcg/dl, fenotipo IM=1,2-3,5 mcg/dl y para el fenotipo EM=4,8-13,2 mcg/dl, realizándose el ajuste nosológico y correspondiéndoles, respectivamente, las siguiente dosis: 3-4 mg/día, 5-8 mg/día y 10-31 mg/día. Conclusiones. Se ha comprobado que el DST test puede utilizarse como marcador subrogado de la respuesta farmacológica al escitalopram y como instrumento para su ajuste nosológico, proporcionando datos significativos sobre distintos fenotipos metabolizadores del CYP2C19 (AU)

Introduction. Depression is associated with a dysfunction of regulation of the hypothalamic-pituitary-adrenal, HPA, which is reflected in the alteration of the dexamethasone suppression test, DST. Escitalopram and other SSRIs decrease the HPA axis response to the DST, beeing the aim of this study validate the DST as a surrogate marker of central serotonergic activity in the treatment with escitalopram and its application to the calculation of the dosage regimens. Methodology. Prospective observational study on 29patients, upon whom was performed the DST-test with0.25 mg of Dexamethasone and subsequent genetic analysis of CYP2C19 by Progenika PHARMA chip test. Results. The range of plasma cortisol levels post-DTS associated with each phenotypic group were: PM phenotype=0.6 to 1.7 mcg/dl, IM phenotype= 1.2 to 3.5 mcg/dl and EM phenotype = 4.8 to 13.2 mcg/dl, being carried out the dosetitration and corresponding, respectively, the following dose regimens: 3-4 mg/day, 5-8 mg/day and 10-31 mg/day. Conclusions. It has been shown that the DST test can be used as a surrogate marker of drug response to escitalopram and as a tool for dose adjustment, providing significant data on different phenotypes of CYP2C19 metabolizers (AU)