Re: Clinical and biochemical presentations of polycystic ovary syndrome among obese and nonobese women

29 12 2009

To the Editor:

I read the article by Liou et al. (1) with interest. The aim of the study was to investigate the impact of obesity on the clinical and biochemical presentations of polycystic ovary syndrome (PCOS). Obesity with PCOS was associated with hyperandrogenism and prolonged menstrual intervals. However, this group had a significantly lower frequency of acne in the study.

Insulin resistance is highly prevalent in PCOS and also closely associated with obesity, clinical or biochemical features of the syndrome such as hyperandrogenism and oligo- or amenorrhea (2,3). It is also one of the important biochemical parameters of PCOS. However, insulin resistance was not mentioned in the text. It would be better if the percentage of the insulin resistance in the overall group was defined and adjusted statistically to exclude the possible effect of insulin on biochemical and clinical hyperandrogenism and menstrual abnormalities. It is better to demonstrate the impact of obesity solely, but not the hidden effect of insulin resistance on these clinical and biochemical parameters of PCOS.

The PCOS group composed of 39% (115/295) obese and 61% (180/295) non-obese women. The control group consisted of 38/169 obese and 131/169 non-obese women. The results of the study might be different if the number or the percentage of all of these groups were identical. Besides fasting insulin and glucose levels, free testosterone (T), sex hormone binding globulin, DHEAS, 17-hydroxyprogesterone, cortisol and lipid parameters should also be added that would show the characteristics of the study group.

The correlations between body mass index (BMI) and total T, modified Ferriman-Gallwey (m F-G) score, average menstruation interval, LH, and LH/FSH ratio in women with PCOS and non-PCOS were evaluated with Pearson correlation analysis. Although odds ratios of some clinical manifestations in obese versus non-obese women with PCOS were shown in Figure 1, the relationship between BMI and these parameters was not defined in obese and non-obese women with non-PCOS. It would be better to perform correlation analysis between BMI and the presence of polycystic ovary morphology, oligo or amenorrhea, hyperandrogenism, acne and hirsutism in both PCOS and non PCOS group to show the relationship between these clinical parameters and BMI and the impact of obesity on PCOS-associated morbidities that reflect the purpose of the study.

The percentage of hirsutism and m F-G score were not significant in obese and non-obese women with PCOS, but both of them were higher in obese non-PCOS compared with non-obese non-PCOS in Table 1. There was a positive correlation between ovarian volume and BMI in total group, but not in PCOS or non-PCOS group in Table 2. What were the possible explanations? I think these should be discussed in the text.

Fatma Ferda Verit, M.D.
Department of Obstetrics and Gynecology
Harran University, Faculty of Medicine
Sanliurfa, Turkey

References:
1. Liou TH, Yang JH, Hsieh CH, Lee CY, Hsu CS, Hsu MI. Clinical and biochemical presentations of polycystic ovary syndrome among obese and nonobese women. Fertil Steril 2009;92:1960-5.

2. Ohgi S, Nakagawa K, Kojima R, Ito M, Horikawa T, Saito H. Insulin resistance in oligomenorrheic infertile women with non-polycystic ovary syndrome. Fertil Steril 2008;90:373-7.

3. Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, Janssen OE, Legro RS, Norman RJ, Taylor AE, Witchel SF; Task Force on the Phenotype of the Polycystic Ovary Syndrome of The Androgen Excess and PCOS Society. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 2009;91:456-88.

Published online in Fertility and Sterility doi:10.1016/j.fertnstert.2009.12.078

The Authors Respond:

We do appreciate Dr. Verit for the careful reading of and suggestions for our paper. This study’s aim is to evaluate the impact of obesity on the diagnostic criteria of polycystic ovary syndrome (PCOS) (1). We restricted this study to discussing the relationship between obesity and the parameters of chronic anovulation, androgen excess, and polycystic ovary morphology (PCOM). The status of insulin resistance in the studied population will not alter the results. Furthermore, the major purpose of this study was to compare obese PCOS subjects vs. non-obese PCOS subjects.

The distribution of obese and non-obese women in the control group will also not change the main results. Obesity was defined as body mass index (BMI) >25 in this study. Our results showed BMI had a strong positive correlation with serum total testosterone level (p<0.001) and an average menstrual interval (p<0.001) in all studied populations (Table-2). Similarly, obese women with PCOS had a higher prevalence of oligomenorrhea (OR=2.2) and biochemical hyperandrogenism (OR=2.6) than non-obese women (Figure-1). PCOM was defined by the number of follicles and/or ovarian volume. Average ovarian volume had a borderline correlation with BMI in the total studied population (N=464, p=0.041) but not in the PCOS subgroup (N=295, p=0.158) or the non-PCOS subgroup (N=169, p=0.197). Therefore, Figure-1 and Table-2 show similar results.

Hirsutism and acne are represented as clinical hyperandrogenism. It is well known that obese women suffer from significantly higher free testosterone due to higher total testosterone and lower sex hormone binding globulin (SHGB), therefore, we usually assume obese women must have a higher prevalence of hirsutism and/or acne than non-obese subjects. Our clinical results could not support the above assumption; on the contrary, there was a lower prevalence of acne among obese women. Actually, the presentation of clinical hyperandrogenism is impacted by several factors: genetics, free androgen index, and inflammation. We suggested that subcutaneous adipose tissue might play some role. Sebaceous glands and hair follicles may have different degrees of sensitivity to androgenic stimulation, meaning that these two presentations do not necessarily appear concomitantly (2). Further studies are needed to clarify all these questions.

We do know there are several other important markers that one could include such as fasting insulin and glucose levels, free testosterone, SHBG, DHEAS, 17-hydroxyprogesterone, cortisol, and lipid parameters. However, the purpose of this study was restricted to evaluate the relationship between diagnostic parameters and obesity. It would be extremely challenging to discuss all PCOS-related parameters in a single article. Actually, our unpublished data showed obesity also plays a predominant role in the development of insulin resistance.

Ming-I Hsu, M.D.
Department of Obstetrics and Gynecology
Taipei Medical University-Wan Fang Medical Center
Taipei, Taiwan

References
1. Liou TH, Yang JH, Hsieh CH, Lee CY, Hsu CS, Hsu MI. Clinical and biochemical presentations of polycystic ovary syndrome among obese and nonobese women. Fertil Steril. 2009;92:1960-5.

2. Toscano V, Balducci R, Bianchi P, Guglielmi R, Mangiantini A, Rossi FG, Colonna, LM, Sciarra F. Two different pathogenetic mechanisms may play a role in acne and in hirsutism. Clin Endocrinol (Oxf). 1993;39:551-6.

Published online in Fertility and Sterility doi:10.1016/j.fertnstert.2009.12.077

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