POLİKİSTİK OVER SENDROMLU HASTALARDA SERUM SKLEROSTİN VE DİCKKOPF-1 SEVİYELERİ

Year 2022, Volume: 23 Issue: 3, 252 - 256, 18.07.2022

Ogün Bilen Yıldız Bilen Mustafa Eroğlu Hakan Türkön Yasemin Akdeniz Mehmet Asik

https://doi.org/10.18229/kocatepetip.833378

Cited By: 1

Abstract

AMAÇ: Polikistik over sendromu (PKOS), premenopozal kadınlarda en sık görülen endokrin patolojidir ve çeşitli sistemleri etkileyen karmaşık bir sendromdur. PKOS'un kemik metabolizması üzerindeki etkileri hakkında çok sayıda çalışma yapılmıştır, ancak PKOS’da osteoporoz riski konusundaki veriler çelişkilidir. Wingless-type mouse mammary tumor virus integration site (Wnt) yolu, kemik metabolizmasının düzenlenmesinde önemli rol oynar. Bu yolun inhibitörleri olarak Sklerostin (Scl) ve Dickkopf-1 (DKK1) son zamanlarda osteoporozun terapötik tedavisiiçin hedefler haline gelmiştir. Bu çalışma, PKOS'lu kadınlarda Scl ve DKK1 düzeylerini belirlemeyi amaçlamıştır.
GEREÇ VE YÖNTEM: Bu çalışmada PKOS tanısı konulmuş 36 kadın ve 35 sağlıklı gönüllü retrospektif olarak incelendi. Her iki grup, demografik, antropometrik, biyokimyasal parametrelerin yanı sıra Scl ve DKK1 seviyeleri açısından karşılaştırıldı.
BULGULAR: Scl seviyesi, PKOS grubunda 42,68 ± 13,28 pg / mL ve kontrol grubunda 45,69 ± 11,79 pg / mL idi ve istatistiksel olarak benzerdi. DKK1 seviyesi, PKOS grubunda 1444,73 ± 611,30 pg / mL ve kontrol grubunda 1204,26 ± 660,88 pg / mL idi ve istatistiksel olarak benzerdi. PKOS grubunun vücut kitle indeksi (VKİ) ve bel/kalça oranı (BKO) değerleri, istatistiksel olarak anlamlı olmamasına rağmen, kontrol grubuna göre daha yüksekti.
SONUÇ: Bu çalışma, PKOS'lu kadınlarla sağlıklı bireyler arasında, Scl ve DKK1 düzeyleri bakımından anlamlı bir fark olmadığını göstermiştir. Amenore PKOS olgularında kemik kaybına neden olsa da, hiperandrojenemi ve hiperöstrojeneminin kemik yoğunluğu üzerindeki olumlu etkileri dengeleyici bir unsur olarak kabul edilebilir.

Keywords

Polikistik over sendromu, Osteoporoz, Sclerostin, Dickkopf-1.

SERUM SCLEROSTIN AND DICKKOPF-1 LEVELS IN PATIENTS WITH POLYCYSTIC OVARY SYNDROME

Abstract

OBJECTIVE: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in premenopausal women, and it is a complex syndrome affecting various systems. Numerous studies have been carried out, on the effects of PCOS on bone metabolism, but currently, there is no clear information about the risk of osteoporosis in PCOS. The wingless-type mouse mammary tumor virus integration site (Wnt) pathway plays an important role in the regulation of bone metabolism. As inhibitors of this pathway, Sclerostin (Scl) and Dickkopf-1 (DKK1) have recently become therapeutic targets for osteoporosis treatment. This study aims to determine Scl and DKK1 levels in women with PCOS.
MATERIAL AND METHODS: In this study, 36 women diagnosed with PCOS and 35 healthy volunteers were examined retrospectively. Both groups were compared in terms of demographic, anthropometric, and biochemical parameters as well as Scl and DKK1 levels.
RESULTS: The level of Scl was 42,68 ± 13,28 pg/mL in the PCOS group and 45,69 ± 11,79 pg/mL in the control group, indicating no statistically significant difference. The level of DKK1 was 1444,73 ± 611,30 pg/mL in the PCOS group, and 1204,26 ± 660,88 pg/mL in the control group, indicating no statistically significant difference. The body mass index (BMI) and waist to hip ratio (WHR) values of the PCOS group were higher than the control group, although these differences did not reach statistical significance.
CONCLUSIONS: This study shows that there were no significant differences between women with PCOS and healthy individuals in terms of Scl and DKK1 levels. Although amenorrhea causes bone loss in PCOS patients, the positive effects of hyperandrogenemia and hyperestrogenemia on bone density can be regarded as a balancing effect.

Keywords

Polycystic ovary syndrome, Osteoporosis, Sclerostin, Dickkopf-1.

References

• 1. Wendy MW, Rachel AW, Olivia NK, et al.Geographical Prevalence of Polycystic Ovary Syndrome as Determined by Region and Race/Ethnicity. Int J Environ Res Public Health. 2018;15(11): 2589.
• 2. Ritu D, Vinay N, Amita D, et al. The Prevalence of Polycystic Ovary Syndrome: A Brief Systematic Review. J Hum Reprod Sci. 2020; 13(4): 261–71.
• 3. Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS); Human Reproduction. 2012;27(1):14-24.
• 4. David GG, Dolores S. Greenspan's Basic and Clinical Endocrinology, In: Mitchell PR, and Marcelle IC, MD. Female Reproductive Endocrinology and Infertility. 10th Edition, San Francisco: McGraw-Hill Education. 2018; 443-99.
• 5. Di Carlo C, Shoham Z, MacDougall J, et al. Polycystic ovaries as a relative protective factor for bone mineral loss in young women with amenorrhea. Fertil Steril. 1992;57(2):314-9.
• 6. Dagogo-Jack S, Al-Alı N, Qurttom M. Augmentation of Bone Mineral Density in Hirsute Women. Journal of Clinical Endocrinology and Metabolism. 1997;82(9):2821-5.
• 7. Dixon JE, Rodin A, Murby B, et al. Bone mass in hirsute women with androgen excess. Clin Endocrinol (Oxf). 1989;30(3):271-7.
• 8. Adami S, Zamberlan N, Castello R, et al. Effect of hyperandrogenism and menstrual cycle abnormalities on bone mass and bone turnover in young women. Clin Endocrinol (Oxf). 1998;48(2):169-73.
• 9. Aydin K, Cinar N, Yazgan Aksoy D, et al. Body composition in lean women with polycystic ovary syndrome: effect of ethinyl estradiol and drospirenone combination. Contraception. 2013;87(3):358-62.
• 10. Karadağ C, Yoldemir T, Gogas Yavuz D. Determinants of low bone mineral density in premenopausal polycystic ovary syndrome patients. Gynecol Endocrinol. 2017;33(3):234-37.
• 11. Kirchengast S, Huber J. June 2001. Body composition characteristics and body fat distribution in lean women with polycystic ovary syndrome. Human Reproduction. 2001;16(6):1255-60.
• 12. Jacoba AM de B, Cornelis BL, Heleen HH, et al. Growth hormone secretion is impaired but not related to insulin sensitivity in non-obese patients with polycystic ovary syndrome. Hum Reprod. 2004;19(3):504-9.
• 13. David GG, Dolores S. Greenspan's Basic and Clinical Endocrinology, In: Dolores M. S, MD, Anne L. S. and Daniel D. B. Metabolic Bone Disease. 10th Edition, San Francisco: McGraw-Hill Education. 2018: 239-97.
• 14. Stolina M, Dwyer D, Niu Q.T et al. Temporal changes in systemic and local expression of bone turnover markers during sixmonths of sclerostin antibody administration to ovariectomized rats. Bone. 2014;67:305-13.
• 15. HuaZhu Ke, William GR, Xiaodong Li, et al. Sclerostin and Dickkopf-1 as Therapeutic Targets in Bone Diseases. Endocrine Reviews. 2012;33(5):747-83.
• 16. 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(1):41-7.
• 17. Ferriman D, Gallwey JD., 1961. Clinical assessment of body hair growth in women. J Clin Endocrinol Metab. 1961;21:1440-7.
• 18. Matthew TD, Sundeep K. Hormonal and systemic regulation of sclerostin. Bone. 2017;(96):8-17.
• 19. Karin A, Steven A, Camilla D, et al. Sclerostin and its association with physical activity, age, gender, body composition, and bone mineral content in healthy adults. J Clin Endocrinol Metab. 2012;97(1):148-54