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Manuel R. García-Sáenz 1
, Claudia Ramírez-Rentería 2
, Nitzia G.López-Juárez 3
, Aldo Ferreira-Hermosillo 2 
1 Servicio de Endocrinología, Hospital de Especialidades Dr. Bernardo Sepúlveda, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Mexico City, Mexico; 2 Unidad de Investigación Médica en Enfermedades Endocrinas, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Mexico City, Mexico; 3 Servicio de Endocrinología, Hospital de Cardiología. Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social (IMSS), Mexico City, Mexico
Manuel R. García-Sáenz, Claudia Ramírez-Rentería, Nitzia G.López-Juárez, Aldo Ferreira-Hermosillo
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*Correspondence: Aldo Ferreira-Hermosillo, Email not available
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age, characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. Its coexistence with type 1 diabetes (T1D) represents a distinctive model of endocrine, immune, and metabolic interaction. Unlike classical PMOS, typically associated with insulin resistance and endogenous hyperinsulinemia, T1D may promote a distinct phenotype in which therapeutic exogenous hyperinsulinemia, systemic inflammation, and central adiposity converge to disrupt ovarian function. In Mexico, PCOS prevalence among women with T1D has been reported at up to 39%, within the upper range of international estimates and comparable to Latin American cohorts using Rotterdam criteria. This association may be influenced by body composition and the inflammatory milieu, given the high prevalence of obesity and metabolic syndrome. Recent Mexican studies show that circulating IL-6 correlate with body mass index and metabolic syndrome, but not PCOS, suggesting predominantly systemic adipose-derived rather than ovarian inflammation in women with T1D.
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