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Vol. 53. Núm. S1.
Resistencia a la insulina y síndrome del ovario poliquístico (SOP)
Páginas 7-14 (septiembre 2006)
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Vol. 53. Núm. S1.
Resistencia a la insulina y síndrome del ovario poliquístico (SOP)
Páginas 7-14 (septiembre 2006)
Resistencia a la insulina y síndrome del ovario poliquístico (SOP)
Acceso a texto completo
Etiología del síndrome del ovario poliquístico
Etiology of polycystic ovary syndrome
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18090
H.F. Escobar-Morreale
Autor para correspondencia
hescobarm.hrc@salud.madrid.org

Correspondencia: Dr. H.F. Escobar-Morreale. Servicio de Endocrinología. Hospital Ramón y Cajal.Ctra. Colmenar, km 9,1. 28034 Madrid. España.
Servicio de Endocrinología. Departamento de Medicina. Hospital Ramón y Cajal. Madrid. Universidad de Alcalá. Madrid. España
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Bibliografía
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El síndrome de ovario poliquístico (SOP) es un trastorno endocrinometabólico de etiología compleja. En su fenotipo coinciden pacientes con mecanismos etiopatogénicos diferentes.

El defecto primario del SOP parece residir en una capacidad aumentada de secretar andrógenos en el ovario y, posiblemente, la glándula suprarrenal, de etiología aún desconocida. Sobre éste actúan diversos factores desencadenantes, entre los que destacan el hiperinsulinismo endógeno derivado de la resistencia insulínica y la obesidad. Dependiendo de la gravedad del defecto esteroidogénico, los factores desencadenantes tendrán un peso mayor o menor en la aparición del síndrome, como se ejemplifica en las diferencias fenotípicas marcadas entre pacientes delgadas y obesas con SOP.

La etiología del SOP es multifactorial y compleja, y en su aparición y desarrollo influyen factores genéticos y ambientales, cuya interrelación es aún objeto de estudio. El escenario más probable es una herencia poligénica sujeta a una influencia ambiental marcada, derivada de factores como la dieta, el sedentarismo y el estilo de vida, sujetos a una marcada variabilidad étnica y geográfica.

Palabras clave:
Síndrome de ovario poliquístico
Resistencia insulínica
Obesidad
Etiología
Fisiopatología

The polycystic ovary syndrome (PCOS) is a complex endocrine-metabolic disorder, in which patients with different etiopathogenic mechanisms show the same phenotype.

The primary defect in PCOS consists of an exaggerated synthesis and secretion of androgens by the ovary and, possibly, by the adrenal gland. The etiology remains unknown.

This primary defect is triggered by several factors, of which the endogenous hyperinsulinism secondary to insulin resistance and obesity is the best known.

Depending on the severity of the steroidogenic defect, the triggering factors play a greater or lesser role in the development of the disorder, as exemplified by the marked phenotypic differences among lean and obese PCOS patients.

The etiology of PCOS is complex and multifactorial and involves interaction among genetic and environmental factors. This interaction is currently under study. The most probable scenario involves a complex inheritance combined with a strong environmental influence. The latter derives from factors such as diet, exercise, and lifestyle, which are heavily dependent on ethnic and geographic variability.

Key words:
Polycystic ovary syndrome
Insulin resistance
Obesity
Etiology
Physiopathology
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