Determination of Source of Hyperandrogenism and Comparisons of Hormonal and Metabolic Profile in Different Phenotype of PCOS: A Hospital Based StudyRitesh Agrawala1*, Arun Chudhury2, Binoy Mohanty2, Anoj Baliarsinha2 and Suchita Agarwal3
- Corresponding Author:
- Dr Ritesh Kumar Agrawala
Department of Endocrinology
AMRI Hospital, Bhubaneswar, Odisha, India
E-mail: [email protected]
Received Date: October 01, 2015; Accepted Date: June 21, 2017; Published Date: June 28, 2017
Citation: Agrawala R, Chudhury A, Mohanty B, Baliarsinha A, Agarwal S (2017) Determination of Source of Hyperandrogenism and Comparisons of Hormonal and Metabolic Profile in Different Phenotype of PCOS: A Hospital Based Study. J Diabetes Metab 8:747. doi:10.4172/2155-6156.1000747
Copyright: © 2017 Agrawala R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: Metabolic parameters in polycystic ovary syndrome (PCOS) correlate to their phenotypic presentations and sources of hyperandrogenism. Till date no studies have evaluated the source of hyperandrogenism among phenotypic variants of PCOS. Therefore we determined the sources of hyperandrogenism and compared the metabolic parameters in different phenotypes of PCOS.
Material method: Study included 120 PCOS patients and 15 age matched controls. PCOS were diagnosed by revised Rotterdam criteria (2003). Different phenotypic presentations like polycystic ovary (P), ovulatory dysfunction (O) and hyperandrogenism (H) were evaluated and compared for anthropometrical, hormonal and metabolic parameters. They were correlated with the source of androgen excess following post Leuprolide acetate (20 μg/kg) 17-OHP and post synacthen (250 μg) DHEAS measurement.
Result: This study had 2 phenotypic presentations i.e. PHO (80%) and OH (20%) out of 4 phenotypic presentations described by Rotterdam among all PCOS (may be due to referral bias). Among obese PCOS 87.5% had PHO and 12.5% had OH phenotypes, while it was 75% and 25% in normal weight PCOS. PHO phenotypes had adrenal and ovarian source of hyperandrogenism. Fasting insulin and HOMA-IR were higher in non-obese PHO than obese PHO but statistically insignificant. Serum DHEAS (delta steroid) had a negative but serum testosterone (keto steroid) had positive correlation with IR in PCOS.
Conclusion: Both adrenal and ovarian hyperandrogenism was found in PHO as compared to OH phenotype that had only ovarian hyperandrogenism. Normal weight PCOS had less chance of getting ultrasound abnormalities compared to obese PCOS. PHO phenotypes, who had a greater degree of serum DHEAS had a better metabolic profile despite a greater BMI. So our result suggests that distinction between source of hyperandrogenism and evaluation of different phenotype is beneficial in predicting metabolic risk and future management.