Polycystic Ovarian Syndrome: Clinical Correlation with Biochemical Status

Abstract

Objective: To find out the correlation between various biochemical and clinical features of polycystic ovarian syndrome and to determine the best hormonal marker for the same. Material and Methods: The study included 100 patients of polycystic ovary syndrome (50 married & 50 unmarried) and a control group comprising of 50 women (25 married & 25 unmarried) in the age group of 18 - 30 years. The pregnant females and those having hyperandrogenism due to any other endocrine disorders were excluded. Results: Mean age was 27.66 years in the married study group and 25.46 years in the unmarried study group. About 71% of patients had oligomenorrhea. It significantly correlated with raised LH:FSH ratio and raised total testosterone levels. Body mass index was raised (>25 kg/m2) in 66.7% married and 72.66% unmarried patients in study group and in 22% in control group. 95% of the patients in the study group and 4% in the control group were detected to have polycystic ovaries on ultrasonography. 62% of the patients had raised LH levels; total testosterone was elevated in 57.7%. The LH:FSH ratio was raised in 41% in study group patients more in the unmarried group 56% than in married group 26%. 20% of patients in the control group had an elevated LH:FSH ratio. Total testosterone level was elevated in 60% of our patients. None of the patient in the control group had elevated testosterone levels. About 31% of the patients in study group were hirsute. Conclusion: Hormonal values correlate well with polycystic ovarian syndrome and serum total testosterone served as the best hormonal marker for such patients.

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R. Yousouf, M. Khan, Z. Kounsar, S. Ahangar and W. Lone, "Polycystic Ovarian Syndrome: Clinical Correlation with Biochemical Status," Surgical Science, Vol. 3 No. 5, 2012, pp. 245-248. doi: 10.4236/ss.2012.35048.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] A. H. Zargar, V. K. Gupta, A. I. Wani, S. R. Masoodi, M. I. Bashir, B. A. Laway, M. A. Ganie and M. Salahudin, “Prevalence of Ultrasonically Proved Polycystic Ovaries in North Indian Women with Type 2 Diabetes Mellitus,” Reproductive Biology & Endocrinology, Vol. 3, No. 35, 2005. doi:10.1186/1477-7827-3-35
[2] B. Dipankar, M. S. Kumar, M. Satinath, P. Mamata, “Clinical Correlation with Biochemical Status in Polycystic Ovary Syndrome,” Journal of Obstetrics & Ganecology of India, Vol. 55, No. 1, 2005, pp. 67-71.
[3] P. Dabadgyhae, B. J. Robert, J. Wang, M. J. Davis and R. J. Norman, “Glucose Tolerance Abnormalities in Australian Women with Polycystic Ovary Syndrome,” MJA, Vol. 187, No. 6, 2007, pp. 328-331.
[4] S. Jonard and D. Dewailly, “Follicular Excess in Polycystic Ovaries, Due to Intra Ovarian Hyperandrogenism May Be the Main Culprit for Follicular Arrest,” Human Reproduction Update, Vol. 10, No. 2, 2004, pp. 107-117. doi:10.1093/humupd/dmh010
[5] Rotterdam ESHRE/ASRM Sponsored PCOS Consensus Work Shop Group; Revised 2003 Consensus on Diagnostic Criteria and Long Term Health Risk Related to PCOS, Fertil Steril, Vol. 81, No. 2004, pp. 19-25.
[6] S. Franks, “Diagnosis of Polycystic Ovarian Syndrome in Defense of Rotterdam Criteria,” Journal of Clinical Endocrinology and Metabolism, Vol. 2, No. 3, 2005, pp. 786-789.
[7] A. H. Alankash, “Polycystic Ovarian Syndrome: The Correlation between the LH:FSH and Disease Manifestations,” Middle East Fertility Society Journal, Vol. 12, No. 1, 2007, pp. 35-40.
[8] R. A. Lobo and E. Carmina, “Importance of Diagnosing PCOS,” Annuals of Internal Medicine, Vol. 32, No. 2000, pp. 989-993.
[9] E. A. Nager, PA-C and MMS, “Prompt Treatment Is Necessary to Control and Prevent Further Progression of Pcos Related Insulin Resistance, Dyslipidemia, Type 2 Diabetes, Cardiovascular Disease and Cancer,” Search Archives, Vol. 14, No. 1, 2006, p. 49.
[10] D. A. Ehrmann, “Polycystic Ovary Syndrome,” The New England Journal of Medicine, Vol. 352, No. 2005, pp. 12223-12236. doi:10.1056/NEJMra041536
[11] Polycystic Ovary Syndrome Writing Committee, “AACE Position Statement on Metabolic & CVS Consequences of Polycystic Ovary Syndrome,” Endocrine Practice, Vol. 11, No. 2, 2005, p. 125.
[12] A. A. Nasr, H. Hamzah, Z. A. El Maaty, H. Gaber and O. Azzam, “Transvaginal Appearances of Ovary in Infertile Women with Oligomenorrhae: Association with Clinical & Endocrine Profile,” Middle East Fertility Society Journal, Vol. 9, No. 2, 2004, pp. 140-149.
[13] K. E. Sharquie, A. Al-Bayatti, A. J. Al-Bahar and Q. M. A. Al-Zaidi, “Acanthosis Nigricans as Skin Manifestation of Polycystic Ovary Syndrome in Primary Infertile Females,” Middle East Fertility Society Journal, Vol. 9, No. 2, 2004, pp. 136-139.
[14] F. Nazir, S. Sayeed, M. Malik, H. Aziz and S. A. S. Rana, “Polycystic Ovarian Syndrome—Diagnosis and Management in Fertility Deprivation,” Pakistan Journal of Obstetrics & Gynecology, Vol. 12, No. 1-2, 1999, pp. 59-71.
[15] F. Haq, O. Aftab and J. Rizvi, “Clinical, Biochemical and Ultrasonic Features of Infertile Women with Polycystic Ovarian Syndrome,” J Coll Physicians Surg PAK, Vol. 17, No. 2, 2007, pp. 76-80.
[16] F. Adil, H. Ansar and A. A. Munir, “Polycystic Ovarian Syndrome and Hyperinsulinemia,” Journal of Liaquat University of Medical and Health Sciences, Vol. 4, No. 3, 2005, pp. 89-93.
[17] H. Hassa, H. M. Tanvir and Z. Yildiz, “Comparison of Clinical and Laboratory Characteristic of Cases with Polycystic Ovarian Syndrome Based on Rotterdam Criteria and Women with Only Clinical Signs Are Oligo/Anovolution or Hirsutism,” Archives of Gynecology and Obstetrics, Vol. 274, No. 4, 2006, pp. 227-232. doi:10.1007/s00404-006-0173-8
[18] A. Razak, A. Nadak and A. Tace, “Polycystic Ovarian Syndrome: The Correlation between the LH:FSH and Disease Manifestations,” Middle East Fertility Society Journal, Vol. 12, No. 1, 2007, pp. 35-40.

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