Unravelling the Origins of Polycystic Ovary Syndrome: Analyzing Clinical Biomarker Profiles in Adolescent and Middle-Aged Women
Abstract:
Polycystic Ovary Syndrome
(PCOS) is a complex and multifactorial condition, involving a combination of
genetic, hormonal, and environmental factors, and its etiology is unknown. PCOS
poses a diagnostic challenge in adolescents, and assessing the status of
biomarkers in adolescents and middle-aged women will elucidate the aetiology of
PCOS. To evaluate the clinical biomarkers - SHBG, testosterone, AMH, insulin,
and leptin - in both adolescence and middle-aged groups. This cross-sectional
study was conducted at Sree Balaji Medical College and Hospital and involved a
total of 200 subjects. The participants were divided into two groups, each
having two subgroups. Adolescent females with regular periods made up Group
1(a), whereas those with irregular cycles and ages ranging from 18 to 19 made
up Group 1(b). Middle-aged women with PCOS made up Group 2(a), whereas control
subjects between the ages of 30 and 38 made up Group 2(b). The data were
presented in the form of mean ± SD. To assess the variance in the data among
multiple groups, a one-way analysis of variance (ANOVA) was employed to
identify the least significant difference during group-wise comparisons.
Statistical Package for the Social Sciences (SPSS) was used for all statistical
analyses, with a significance threshold of P<0.05. The values of SHBG and
AMH were significantly different between the four groups, and the value of
insulin was significant between controls and oligomenorrhea in the adolescent
group. This study reveals the sequential expression of physiological and
clinical biochemical variations, suggesting that compensatory hyperinsulinemia
may play a role in initiating PCOS pathogenesis.
References:
[1].
Azziz,
R., Carmina, E., Chen, Z., Dunaif, A., Laven, J.S., Legro, R.S., Lizneva, D.,
Natterson-Horowtiz,B.,Teede,H.J.,Yildiz,B.O.,2016, Polycysticovary syndrome. Nature
reviews Disease primers, 2(1), 1-18.
[2]. Bharali, M.D., Radhika
R., Jayshree G., Kusum S., and Vinoth R., 2022,Prevalence of Polycystic
Ovarian Syndrome in India: A Systematic Review and Meta-Analysis. Cureus,
14(12): e32351.
[3]. Pena, A.S.,
Witchel, S.F., Hoeger, K.M.,
Oberfield, S.E., Vogiatzi, M.G, Misso, M., Garad, R.,
Dabadghao Preeti., and Teede H., 2020, Adolescent polycystic
ovary syndrome according to the international evidence- based guideline.
BMC Med, 18, 72.
[4].
Sirmans, S.M and Pate, K.A., 2014, Epidemiology,
diagnosis, and management of polycystic ovary syndrome. Clin Epidemiol, 6, 1–13.
[5]. Bulsara J., Patel P., Soni
A., Acharya A., 2021, A review: brief
insight into polycystic ovarian
syndrome. Endocr Metab Sci,
3,100085.
[6].
Capozzi, G., Scambia, S., Lello., 2020, Polycystic ovary syndrome (PCOS) and
adolescence: How can we manage it? European
Journal of Obstetrics & Gynecology and Reproductive Biology, 250,
235-240.
[7].
Patel,
S.,
2018, Polycystic ovary
syndrome (PCOS), an inflammatory, systemic, lifestyle endocrinopathy.The Journal of Steroid
Biochemistry and Molecular Biology,182, 27-36.
[8].
Pappalardo, M.A., Russo G.T., Pedone, A.,
Pizzo, A., Borrielli, I., Stabile, G., Artenisio, A.C., Amato, Ucinotta, D. et al., 2010,Very high frequency of
the polymorphism for the insulin receptor substrate 1 (IRS-1) at codon 972 (
glycine 972 Arginine) in southern Italian women with polycystic syndrome.
Horm.Metab.Res, 42, 575-584.
[9].
Kandarakis, D.E. and Dunaif, A., 2012,
Insulin resistance and the polycystic ovary syndrome revisited: an update on
mechanisms and implications. Endocrine reviews,33 (6),981-1030.
[10].
RaymondLi, H.W.,
Yeung,
W.S.B., Chung
Ho, P., Hung,
E.Y. N., 2011, Evaluation of serum antimullerian hormone and inhibin B
concentrations in the differential diagnosis of secondary
oligoamenorrhea.Fertil Steril, 96, 774-779.
[11].
Aghadavod, E., Zarghami, N., Farzadi, L.,
2015,Evaluation of relationship between serum levels of anti-mullerian hormone,
androgen, and insulin resistant with retrieval Oocytes in overweight patients
with polycystic ovary syndrome. Adv Biomed Res, 4, 76.
[12].
Farquhar,
C., 2007, Introduction and history of polycystic ovary syndrome. In: Kovacs
G,Norman R, editors. Polycystic
Ovary Syndrome. 2nd ed. Cambridge, UK: Cambridge University
Press, 4–24.
[13].
Bull, J.R.,
Rowland, S.P., Scherwitzl, E.B., Scherwitzl, R., Danielsson, K.G., Harper, J.,
2019, Real-world menstrual cycle characteristics of more than 600,000 menstrual
cycles. NPJ Digit Med, 2(1),83.
[14].
Rotterdam ESHRE/ASRM – 2004, Sponsored
PCOS Consensus Workshop group. Revised 2003 consensus on diagnostic criteria
and long term health risk related to poly cystic ovaries syndrome (PCOS). Hum
Reprod, 19(1), 41 – 7.
[15].
Robert L. Rosenfield and David A. Ehrmann., 2016,The
Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as
Functional Ovarian Hyperandrogenism Revisited.Endocr Rev, 37(5),467–520.
[16].
Zephne, M., Van der spuy., Silke,
J.D.,2004, The pathogenesis of infertility and early pregnancy loss in
polycystic syndrome. Best Pract Res clin Obstetgynaecol,15 ( 5),755-71.
[17].
Rosenfield, R. L., 2015, The Diagnosis of
Polycystic Ovary Syndrome in Adolescents Pediatri,136(6),1154-65.
[18]. Nestler, J.E., 1997, Role
of hyperinsulinemia in the pathogenesis of the polycystic ovary syndrome, and
its clinical implications Semin. Reprod Endocrinol, 15(2),111-22.
[19].
Rosenfield, R.L and Ehrmann, D.A., 2016, The
Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as
Functional Ovarian Hyperandrogenism Revisited. Endocr Rev, 37(5), 467–520.
[20]. Unluhizarci, K., Karaca, Z.,
Kelestimur, F., 2021, Role of insulin and insulin resistance in androgen excess
disorders. World journal of diabetes, 12(5), 616.
[21].
Rouru, J., Anttila, L., Koskinen, P., Penttila, T.A., Irjala, K., Huupponen, R., Koulu, M. 1997, Serum
leptin concentrations in women with polycystic ovary syndrome. J Clin
Endocrinol Metab, 82(6), 1697-700.
[22]. Laughlin, G.A., Morales, A.J., Yen, S.S., 1997,Serum leptin levels in women
with polycystic ovary syndrome: the role of insulin
resistance/hyperinsulinemia. J Clin Endocrinol Metab, 82(6),1692-6.
[23]. Mulders, A.G., Laven, J.S., Eijkemans, M.J., de Jong, F.H.,
Themmen, A.P., Fauser, B.C.,
2004,Changes in anti-Mullerian hormone serum concentrations over time suggest
delayed ovarian ageing in normogonadotrophic anovulatory infertility. Hum
Reprod, 19(9), 2036-42.
[24]. Wang, J. G., Nakhuda, G.S.,
Guarnaccia, M.M., Sauer, M.V., Lobo,
R. A., 2007, Mullerian inhibiting substance and
disrupted folliculogenesis in polycystic ovary syndrome. Am J Obstet Gynecol,
196(1), 77.
[25]. Durlinger, A.L., Kramer, P., Karels, B., de Jong, F.H.,
Uilenbroek, J.T., Grootegoed, J.A, Themmen, A.P., 1999,Control of primordial
follicle recruitment by anti-Mullerian hormone in the mouse
ovary. Endocrinology, 140(12),5789-96.
[26]. Piouka, A., Farmakiotis, D., Katsikis, I., Macut, D., Gerou, S., Panidis, D., 2009,Anti-Mullerian hormone levels reflect severity of PCOS but are negatively influenced by obesity: relationship with increased luteinizing hormone levels. Am physiol EndocrinolMetab, 296(2), E238-43.