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Πέμπτη 21 Σεπτεμβρίου 2017

Prevalence of dermatologic manifestations and metabolic biomarkers in women with polycystic ovary syndrome in north China

Summary

Background

Cutaneous features of hyperandrogenism in polycystic ovary syndrome (PCOS) include acne, hirsutism, seborrhea, androgenic alopecia (AGA), and acanthosis nigricans (AN). However, the relationships have not been well known broadly in terms of clinical hyperandrogenism and biochemical markers.

Objectives

The aim of this study was to investigate biochemical and metabolic parameters in relation to cutaneous characters women in with and without PCOS. Methods: This was a cross-sectional retrospective study including 186 women with PCOS and 113 age-matched without PCOS women. Acne grade, hirsutism, seborrhea, AGA, and AN were recorded. Hormonal and metabolic parameters were measured.

Results

The most common finding was acne, and AN was the least dermatological manifestations between PCOS and non-PCOS groups. The severity location and type of acne did not differ in PCOS women compared to non-PCOS women. Significant differences were found with respect to free androgen index (FAI) (= .036), sex hormone-binding globulin (SHBG) (= .023), and body mass index (BMI) (= .001) between PCOS with acne and PCOS without acne groups. Overall, age (= .005) was significantly decreased, while BMI (= .004) was significantly higher in PCOS with hirsutism. The mean serum total testosterone (TT), dehydroepiandrosterone sulfate, and FAI were significantly elevated, but SHBG was decreased between PCOS with and without hirsutism groups. There were significantly different BMI (= .018) and triglyceride (= .024) except other hormonal parameter of without AGA group.

Conclusion

This study indicated a strong correlation between hirsutism and metabolic abnormalities. Hirsutism is the most common cutaneous finding in PCOS women. Acne and AGA are associated with other manifestations of clinical hyperandrogenism, but not obvious markers of biochemical hyperandrogenemia and metabolic dysfunction.



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