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MON-037 Vitamin D Levels in Women with Polycystic Ovary Syndrome: Influence of Obesity

Introduction: Polycystic ovary syndrome (PCOS) is the most frequent cause of hyperandrogenism in women of reproductive age. Among its metabolic complications, vitamin D deficiency has been described in relation with insulin resistance’s pathophysiology and other metabolic risk factors. However, it i...

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Detalles Bibliográficos
Autores principales: Maidana, Patricia Nieves Amelia, Fernández, Gladys Isabel, Fritzler, Analy, Ropelato, María Gabriela, Eugenia, Lamas-Majek, Lopez, Mariana, Gonzalez, Diego, Rosales, Mónica, Leiderman, Susana Mabel, Fabre, Bibiana, Mesch, Viviana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7209756/
http://dx.doi.org/10.1210/jendso/bvaa046.944
Descripción
Sumario:Introduction: Polycystic ovary syndrome (PCOS) is the most frequent cause of hyperandrogenism in women of reproductive age. Among its metabolic complications, vitamin D deficiency has been described in relation with insulin resistance’s pathophysiology and other metabolic risk factors. However, it is not clear if this deficiency is inherent to PCOS or it depends on adiposity degree. As well, it is also suggested that vitamin D could regulate leptin levels and high leptin levels should be associated with vitamin D defiency in obesity. Our aim was to evaluate the relationship between vitamin D, leptin and obesity degree in PCOS patients. Subjects and methods: In 84 PCOS women (19 -37 years) and 49 controls (22-45 years), 25 hidroxi-vitamin D (25 OH-D) was measured by direct chemoluminiscence. Body mass index (BMI) was calculated; 20% of PCOS women were overweight and 46% were obese. Waist circumference (WC) was measured as an indicator of abdominal obesity. The lipid accumulation product (LAP) index, a secondary marker of insulin resistance, was calculated (LAP: [waist (cm) - 58] x triglycerides (mmol/l)). In a subgroup of 26 patients, leptin levels were determined by ELISA method. Statistical analysis was performed through SPSS 22. Results: Variables are expressed as mean ± SD or median (range) according to distribution. The following parameters were higher in PCOS women than in controls, BMI: 29.3 (18.6-48.2) vs 22.4 (18.1-37.4) kg/m(2); WC 95 ± 16 vs 82 ± 11 cm and LAP: 47.9 (1.1-198.2) vs 17.5 (6.8-93.4) cm.mmol/L, p<0.0001 in all cases. 25 OH-D was lower in PCOS: 14.5 (10.0-39.0) vs 17.0 (10.0-38.8) ng/ml, p=0.024. Leptin levels in PCOS women were 10.1 ± 5.4, 26.4 ± 7.0 and 33.8 ± 16.9 ng/ml in normal weight, overweight and obese patients, respectively. After a logistic binary regression analysis, differences in 25 OH-D between groups were lost when BMI and WC were considered (p=0.556; RR=0.978; IC95% [0.909-1.063]). 25 OH-D levels were negatively associated with WC (r=-0.286, p=0.006), LAP (r=-0.333, p=0.002) and leptin (r=-0.462, p=0.017). Conclusions: although 25 OH-D levels were lower in PCOS women than in controls and negatively associated with LAP, an insulin resistant marker, the fact than differences between groups was lost after correction by BMI and WC, in addition to the correlation found between 25 OH-D and leptin levels, indicates that obesity degree and abdominal fat distribution should be responsible of decreased vitamin D levels in PCOS.