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Assessment of Serum Adiponectin Level and Insulin Resistance in Premenopausal Females with Hirsutism


Hesham Ahmed Nada
Fadia Mostafa Attia
Radwa El-Sayed Mahmoud Marie
Asmaa Hamed Soliman

Abstract

Background: The existence of profuse terminal hair in androgen-dependent areas of a women constitutes hirsutism. The association  between insulin resistance & hirsutism, especially when accompanied by ovarian or adrenal hyperandrogenism, has been extensively  documented. Nevertheless, the adiponectin role, as an indicator of metabolic consequences, in cases with hirsutism has not been  conclusive.


Aim: This study aimed to assess serum adiponectin level & insulin resistance in females with idiopathic hirsutism, as well as hirsutism  with polycystic ovary syndrome (PCOS), compared to controls.


Patients and methods: This case control investigation included twenty- five cases with hirsutism, & 25 age matched non-hirsute control females. Height, body weight, BMI, modified ferrimangallawy (mFG)  scale, serum fasting glucose, & insulin were measured. Homeostasis model assessment of insulin resistance (HOMA-IR) & serum  adiponectin were evaluated by enzyme-linked immune-sorbent assay. Serum total testosterone has been measured for females with menstrual irregularities.


Results: Females with hirsutism either with or without PCOS had significantly lower serum adiponectin level  compared to controls (p<0.001). Serum fasting glucose, HOMA-IR & serum fasting insulin, were significantly greater in cases with  hirsutism, especially with polycystic ovary syndrome, than controls (p<0.001in all comparisons). HOMA-IR was significantly greater in  females with lateral hirsutism, progressive course, high testosterone, acne, menstrual irregularities, with a significant positive association  with body mass index and mFG scale (p<0.001in all comparisons).


Conclusion: Hirsutism, whether idiopathic or associated  with PCOS, is correlated to insulin resistance & low adiponectin level, implying that this metabolic abnormality potentially contributes to  the pathogenesis of the illness. 


Journal Identifiers


eISSN: 2090-7125
print ISSN: 1687-2002