Resumen
El síndrome de ovario poliquístico (SOP) parece surgir como un rasgo complejo que resulta de la interacción de diversos factores genéticos y ambientales. Una de las principales hipótesis es que el SOP resulta del hiperandrogenismo ovárico funcional (HOF) debido a la desregulación de la secreción de andrógenos. Hay una contribución de los andrógenos suprarrenales como la DHEA, que se metabolizan en el ovario a androstenediona y testosterona. Los factores hereditarios incluyen PCOM, hiperandrogenemia, resistencia a la insulina y defectos secretores de la insulina. Los factores ambientales incluyen la exposición prenatal a andrógenos y el crecimiento fetal deficiente, mientras que la obesidad adquirida es un factor posnatal importante. Un síndrome metabólico de resistencia a la insulina relacionada con la obesidad y/o intrínseca ocurre en aproximadamente la mitad de las pacientes con SOP, y el hiperinsulinismo compensatorio tiene efectos selectivos de tejido, que incluyen agravación del hiperandrogenismo. La variedad de vías involucradas y la falta de un hilo común atestiguan la naturaleza multifactorial y la heterogeneidad del síndrome. Conocer la base fundamental del trastorno es necesario para corregir de manera óptima los niveles de andrógenos, la ovulación y la homeostasis metabólica, y también para resolver los problemas de ginecología y obstetricia.
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