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 Table of Contents  
ORIGINAL ARTICLE
Year : 2013  |  Volume : 1  |  Issue : 1  |  Page : 30-34

Hormonal, metabolic and clinical profile of Saudi women with polycystic ovary syndrome


1 Department of Obstetrics and Gynecology, King Fahd Hospital of the University, University of Dammam, Saudi Arabia
2 Department of Obstetrics and Gynecology, Mutah University Medical School, Al-Karak, Jordan

Date of Web Publication3-Jun-2013

Correspondence Address:
Abdulaziz A Al-Mulhim
Professor of Obstetrics and Gynecology, King Fahd Hospital of the University, University of Dammam
Saudi Arabia
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DOI: 10.4103/1658-631X.112920

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  Abstract 

Objective: To establish the hormonal, metabolic and clinical profile for Saudi women with polycystic ovary syndrome (PCOS).
Design: This is a prospective, cross-sectional study conducted at the University Hospital. All women were seen at the gynecology clinic. One hundred women aged between 18 and 45 years were included in the study; 50 women with polycystic ovary disease (PCOS) comprised the study group and 50 women without PCOS comprised the control group. The hormonal, metabolic and clinical profiles were assessed for both groups.
Results: There are significantly higher levels of luteinizing hormone, prolactin, free testosterone dehydroepianosterone sulfate, 17α-hydroxy progesterone and fasting insulin in the study group. There were no differences in the levels of total testosterone, estradiol and cortisone levels between both groups. The levels of follicular stimulating hormone and sex hormone binding globulin were significantly lower in the study group. There were no differences in the blood sugar level, cholesterol, triglycerides and low- and high-density lipoproteins. The womens' ages, body mass index, blood pressure, uterine dimensions and endometrial thickness were similar in both groups. The size of both ovaries was significantly greater in the study group. There were more follicles in the ovaries of the study group.
Conclusion: Hormonal profile of Saudi women with PCOS was similar with what is already published in the medical literature. But, despite the fact that Saudi women with and without PCOS are overweight, they do not suffer from raised blood pressure and metabolic syndrome; this may be due to the fact that women included in this study were relatively young and the sample size might be too small to draw effective conclusions.

Keywords: Hormone profile, metabolic profile, poly cystic ovary syndrome


How to cite this article:
Al-Mulhim AA, Abul-Heija AA, Al-Talib AA, Al-Turki HA, Gasim TG. Hormonal, metabolic and clinical profile of Saudi women with polycystic ovary syndrome. Saudi J Med Med Sci 2013;1:30-4

How to cite this URL:
Al-Mulhim AA, Abul-Heija AA, Al-Talib AA, Al-Turki HA, Gasim TG. Hormonal, metabolic and clinical profile of Saudi women with polycystic ovary syndrome. Saudi J Med Med Sci [serial online] 2013 [cited 2017 Jul 20];1:30-4. Available from: http://www.sjmms.net/text.asp?2013/1/1/30/112920


  Introduction Top


According to the available literature, the criteria fulfilling sufficient specificity and sensitivity to define the polycystic ovary are the presence of 12 or more follicles measuring 2-9 mm in diameter and/or increased ovarian volume (>10 cm 3 ). The presence of a single polycystic ovary is sufficient to provide the diagnosis. [1] Polycystic ovary syndrome (PCOS) is a common endocrine disorder in females that affects 5-10% of women of the reproductive age group. [2] PCOS is a complex abnormality of unknown etiology, but it may have a genetic etiology. [3],[4],[5]

It is a major cause of female subfertility. [6],[7],[8] The principal features are ovulation failure, resulting in amenorrhea or oligomennorhea. Excessive amounts of androgenic hormones result in acne and hirsutism, alopecia, breast atrophy and acanthosis negricans. Usually, PCOS is associated with insulin resistance, which may be associated with pathogenesis of the disease. Other associations are obesity, type 2 diabetes and hyperchlostremea, [9] and it may also have an increased incidence of cardiovascular disease. [10],[11] Majority of the women had biochemical and metabolic disturbances such as biochemical hyperandrogenism, [12] insulin resistance and impaired glucose tolerance. [13]

In this study, we are aiming to establish the hormonal, metabolic and clinical profile for Saudi women with PCOS.


  Materials and Methods Top


This is a prospective, cross-sectional study conducted at the King Fahd Hospital of the University from the period January 2009 to December 2010. All women were seen at the gynecology clinic and history was obtained from cases and controls prior to the study for intake of any hormonal drugs, including oral contraceptives as well as medication for lowering blood pressure, blood lipids and glucose. One hundred women were included in the study and all were Saudi married women aged between 18 and 45 years. Women with PCOS (n = 50) comprised the study group and women without PCOS comprised the control group (n = 50). Women with PCOS were selected according to the Rotterdam ESHRE criteria. [11] Women in the control group were with other gynecological diseases, not on any hormonal medication, no known infertility and endocrinologic or dermatologic problems, and were apparently normal healthy women. Each woman in the study had her body mass index and sitting and lying down blood pressure checked electronically once. Vaginal ultrasound scan was performed at mid-cycle to assess the uterine dimensions, ovarian size and endometrial thickness. Blood samples were obtained between Day 2 and Day 5 of the cycle to assess the level of the following hormones: Follicular stimulating hormone (FSH), luteinizing hormone (LH), esradiole (E2), prolactin, dehydroepianosterone sulfate (DHEA-SO 4 ), cortisol (C), androsteindione (A), total and free testosterone (T), 17 α OH-progesterone (OH-P), sex hormone binding globulin (SHBG) and fasting insulin. The metabolic profile was assessed for all women in the study; therefore, the blood levels of fasting and 2 hours posts 75 g of glucose loading blood glucose, cholesterol, triglycerides and high- and low-density lipoproteins were estimated. Cases and controls were matched by age and body mass index. This study was approved by the ethical committee of the university. All women in both groups were counseled about the study and signed an informed consent.

Statistical analysis

Statistical analysis was performed using the Mann Whitney test, and the difference between values was considered significant when P ≤ 0.05.


  Results Top


[Table 1] shows significantly higher levels of LH (P = 0.0026), prolactin (P < 0.0001), free testosterone (P < 0.0001), DHEA-S (P = 0.0006), 17-hydroxy progesterone (P = 0.0021) and fasting insulin (P = 0.0025) in the study group compared with the control group. There were no differences in the levels of total testosterone, estradiol and cortisone levels in both groups. The levels of FSH and sex hormone binding globulin were significantly lower in the study group compared with the control group (P < 0.0001 and P = 0.0015, respectively).
Table 1: Comparison of hormonal profile between the study and control groups

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[Table 2] shows the metabolic profile of the two groups. There were no significant differences in the blood sugar level, either fasting or after 75 g of glucose loading, cholesterol, triglycerides and low- and high-density lipoproteins.
Table 2: Metabolic profile of the study and control groups

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[Table 3] shows that the ages of the women, body mass index, sitting and lying down blood pressure (systolic and diastolic), uterine length, uterine width and endometrial thickness were similar in both groups. The size of both ovaries, right and left, were significantly greater in the study group compared with the control group (P < 0.0001 and P = 0.0054, respectively).
Table 3: Clinical profile of the study and control groups

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There were significantly more small cysts (2-8 mm) in the ovaries in the study group compared with the control group (P < 0.0001).


  Discussion Top


In this study, we found that Saudi women with PCOS had higher free testosterone but lower FSH and SHBG than controls, and our results were similar with what was reported by others. [14],[15] LH, prolactin, androstenedione and DHEA-S were significantly higher in the study group, while total testosterone and estradiol were similar in PCOS and controls. [14] As expected, insulin was significantly higher in the study group compared with the control group. Women with PCOS usually have insulin resistance, which leads to hyperinsulinemia. The ovaries of women seem to be particularly sensitive to high blood levels of insulin and respond by overproducing androgens like testosterone. [16],[17] Results of this study showed that when women in the PCOS group where compared with those in the control group, the ovarian volumes and the number of follicles were significantly higher in the PCOS group. And, this result is in agreement with what is published in the literature. [18]

Women with PCOS are generally overweight or obese. [19] It is difficult to draw conclusions about overweight status and PCOS in this study as the majority of the study population, both cases and controls, were overweight.

We studied uterine dimensions and endometrial thickness, and found that neither uterine length nor width in women with PCOS differ from other PCOS women, and this is in agreement with that reported from the other authors. [20] In our study, mid-cycle endometrial thickness was similar in women with and without PCOS, and this is in contrast with what was found by the other authors. [21]

Although PCOS women have a higher incidence of type 2 diabetes, none of the women included in this study were found to be diabetic, and even blood glucose levels, either fasting or after loading with 75 g of glucose, were within normal limits. Also, no differences in blood sugar level were noticed between the groups.

Our study failed to show any association of hypertension, whether it is systolic or diastolic, during sitting or lying down between the two groups of women; this was contrary with what was reported. [21],[22] Both investigators Zachurzok-Buczynska et al. and Azevedo et al. showed an elevation of blood pressure in women with PCOS.

Contrary to the expectations and to what was observed by other authors, [23] all women included in this study showed normal cholesterol, triglycerides and high- and low-density lipoproteins, and the differences in their metabolic profile were not statistically significant.

The hormonal profile of Saudi women with PCOS was similar with what is already published in the medical literature. [24] But, despite this, Saudi women with and without PCOS are overweight and they do not suffer from raised blood pressure and metabolic syndrome; this may be due to the fact that women included in this study were relatively young and the sample size might be too small to draw conclusions.

A larger sample size and data from different provinces are recommended.


  Acknowledgment Top


The authors would like to thank the Deanship of Scientific Research at the University of Dammam for the technical and financial support. They would also like to thank Professor M.H. Al Sibai for his valuable contribution and supervision and Moufida Darmoul for her valuable secretarial support.

 
  References Top

1.Balen AH, Laven JS, Tan SL, Dewailly D. The ultrasound assessment of the polycystic ovary: International consensus definitions. Hum Reprod Update 2003;9:505-14.  Back to cited text no. 1
    
2.Codner E, Iñíguez G, Villarroel C, Lopez P, Soto N, Sir-Petermann T, et al. Hormonal profile in women with polycystic ovarian syndrome with or without type 1 diabetes mellitus. J Clin Endocrinol Metab 2007;92:4742-6.  Back to cited text no. 2
    
3.Fauser BC, Diedrich K, Bouchard P, Dominguez F, Matzuk M, Franks S, et al. Contemporary genetic technologies and female reproduction. Hum Reprod Update 2001;17:829-47.  Back to cited text no. 3
    
4.Legro RS, Strauss JF. Molecular progress in infertility: Polycystic ovary syndrome. Fertil Steril 2002;78:569-76.  Back to cited text no. 4
    
5.Diamanti-Kandarakis E, Kandarakis H, Legro RS. The role of genes and environment in the etiology of PCO". Endocrine 2006;30:19-26.  Back to cited text no. 5
    
6.Goldenberg N, Glueck C. Medical therapy in women with polycystic ovary syndrome before and during pregnancy and lactation. Minerva Ginecol 2008;60:63-75.  Back to cited text no. 6
    
7.Boomsma CM, Fauser BC, Macklon NS. Pregnancy complications in women with polycystic ovary syndrome. Semin Reprod Med 2008;26:72-84.  Back to cited text no. 7
    
8.Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO. The Prevalence and Features of the Polycystic Ovary Syndrome in an Unselected Population. J Clin Endocrinol Metabol 2004;89:2745-9.  Back to cited text no. 8
    
9.Hudecova M, Jan H, Christian B, Poromaa Inger S. Long-term Reproductive and Metabolic Consequences of PCOS. Curr Diabetes Rev 2012;8:444-51.  Back to cited text no. 9
    
10.Chang AY, Ayers C, Minhajuddin A, Jain T, Nurenberg P, de Lemos JA, et al. Polycystic ovarian syndrome and subclinical atherosclerosis among women of reproductive age in the Dallas heart study. Clin Endocrinol 2011;74:89-96.  Back to cited text no. 10
    
11.de Groot PC, Dekkers OM, Romijn JA, Dieben SW, Helmerhorst FM. PCOS, coronary heart disease, stroke and the influence of obesity: A systematic review and meta-analysis. Hum Reprod Update 2011;17:495-500.  Back to cited text no. 11
    
12.Franks S. Diagnosis of the polycystic ovary syndrome: In defence of the Rotterdam criteria. J Clin Endocrinol Metab2006;91:786-9.  Back to cited text no. 12
    
13.Cleeman JI. Executive Summary of the Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA 2001;285:2486-97.  Back to cited text no. 13
    
14.Rotterdam ESHRE/ASRM-Sponsored PCOS consensus workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2004;19:41-7.  Back to cited text no. 14
    
15.Schmidt J, Brännström M, Landin-Wilhelmsen K, Dahlgren E. Reproductive hormone levels and anthropometry in postmenopausal women with polycystic ovary syndrome (PCOS): A 21-year follow-up study of women diagnosed with PCOS around 50 years ago and their age-matched controls. J Clin Endocrinol Metab 2011;96:2178-85.  Back to cited text no. 15
    
16.Akbarzadeh S, Ghasemi S, Kalantarhormozi M, Nabipour I, Abbasi F, Aminfar A, et al. Relationship among plasma adipokines, insulin and androgens level as well as biochemical glycemic and lipidemic markers with incidence of PCOS in women with normal BMI. Gynecol Endocrinol 2012;28:521-4.  Back to cited text no. 16
    
17.Taponen S, Martikainen H, Järvelin MR. Hormonal profile of women with self-reported symptoms of oligomenorrhea and/or hirsutism: Northern Finland birth cohort 1966 study. J Clin Endocrinol Metab 2003;88:141-7.  Back to cited text no. 17
    
18.Xie M, Li X, Zhou YQ, Zhao NQ, Lin JF. Ovarian ultrasonographic features in reproductive age females with polycystic ovary syndrome and the establishment of ultrasonigraphic criteria. Zhonghua Yi Xue Za Zhi 2012;92:2319-22.  Back to cited text no. 18
    
19.Shah B, Parnell L, Milla S, Kessler M, David R. Endometrial thickness, uterine, and ovarian ultrasonographic features in adolescents with polycystic ovarian syndrome. Pediatr Adolesc Gynecol 2010;23:146-52.  Back to cited text no. 19
    
20.Eryilmaz OG, Sarikaya E, Gulerman C, Akar S, Cicek N. Endometrial thickness measurement throughout a menstrual cycle in non-obese infertile patients with polycystic ovary syndrome. Arch Gynecol Obstet 2012;286:1597-600.  Back to cited text no. 20
    
21.Zachurzok-Buczynska A, Szydlowski L, Gawlik A, Wilk K, Malecka-Tendera E. Blood pressure regulation and resting heart rate abnormalities in adolescent girls with polycystic ovary syndrome. Fertil Steril 2011;96:1519-23.  Back to cited text no. 21
    
22.Azevedo MF, Costa EC, Oliveira AI, Silva IB, Marinho JC, Rodrigues JA, et al. Elevated blood pressure in women with polycystic ovary syndrome: Prevalence and associated risk factors. Rev Bras Ginecol Obstet 2011;33:31-6.  Back to cited text no. 22
    
23.Luo X, Xu L. Association of fat distribution with metabolic syndrome in patients with polycystic ovary syndrome. Nan Fang Yi Ke Da Xue Xue Bao 2012;32:1325-7.  Back to cited text no. 23
    
24.Tamimi W, Siddiqui IA, Tamim H, AlEisa N, Adham M. Effect of body mass index on clinical manifestations in patients with polycystic ovary syndrome. Int J Gynecol Obstet 2009;107:54-7.  Back to cited text no. 24
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]


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[Pubmed] | [DOI]



 

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