FUNCTIONAL FEATURES OF THE RELATIONSHIP BETWEEN LEVELS OF VITAMIN D, MARKERS OF CHRONIC INFLAMMATION, HOMOCYSTEINE AND HORMONAL-METABOLIC PARAMETERS IN WOMEN WITH POLYCYSTICOVARY SYNDROME
DOI:
https://doi.org/10.21856/j-PEP.2021.1.01Keywords:
polycystic ovary syndrome, vitamin D, C-reactive protein, interleukin-6, homocysteine, dyslipidemia, insulin resistanceAbstract
Objective: to study the levels of vitamin D, C-reactive protein (CRP), interleukin-6 (IL-6), homocysteine (HC) and to evaluate their correlation with hormonal-metabolic parameters, the violation of which is inherent in polycystic ovary syndrome (PCOS).
Materials and methods. 60 patients with PCOS (24.2 ± 0.2 years) and 30 healthy women of the appro- priate age were examined. Depending on the level of vitamin D, the examined were divided into subgroups: 44 women with PCOS and vitamin D ≤ 30 ng/ml (average 12.9 ± 0.2 ng/ml); 16 patients with an average level of vitamin D ≥ 30 ng/ml (31.4 ± 0.3 ng/ml); 12 healthy women with vitamin D ≤ 30 ng/ml (24.2 ± 0.3 ng/ml); 18 healthy subjects with vitamin D ≥ 30 ng/ml (35.6 ± 0.3 ng/ml). The blood lipid spectrum, indicators of carbo- hydrate metabolism, total testosterone (T), estradiol (E2), sex hormone binding globulin, CRP, IL-6, HC were determined.
Results. Vitamin D deficiency in PCOS is characterized by a higher degree of severity. There is a nega- tive correlation between levels of vitamin D and abdominal adipose tissue distribution (r = – 0,501, P < 0,001), dyslipidemia (P < 0,001), insulin resistance (r = – 0,351, P < 0,01), hypeandrogenemia (r = – 0,603, P < 0,001). It was found that in patients with PCOS levels of CRP and IL-6 were significantly (P < 0,05) higher than the women in the control group and were associated with vitamin D deficiency (CRP r = – 0,375, Р < 0,01; IL-6 r = – 0,281, Р < 0,05), insulin resistance (CRP r = 0,351, Р < 0,01; IL-6 r = 0,270; Р < 0,05), dyslipidemia (P < 0,05) hyperandrogenemia (CRP r = 0,441, Р < 0,001; IL-6 r = 0,437, Р < 0,001). It was shown that hyperho- mocysteinemia in PCOS is caused by impaired androgen-estrogen balance (T/E2 r = 0,279, P < 0,05), systemic chronic inflammation (CRP r = 0,283, P < 0,05; IL-6 r = 0,261, P < 0,05) and deficiency of vitamin D (r = – 0,319; P < 0,02).
Conclusion. PCOS is accompanied by an increase in levels of CRP and IL-6, which indicates the existence of a link between this pathological process and low-grade systemic inflammation. Vitamin D deficiency contribu- tes to a further increase in markers of chronic inflammation and HC.
References
Mohort T, Velesevich EI, Jurenja EV, et al. Medicinskie Novosti 2014; 12: 16-21.
Couto Alves A, Valcarcel B, Mäkinen VP, et al. Int J Obes (Lond) 2017; 41(9): 1331-1340. https://doi.org/10.1038/ijo.2017.126.
Escobar-Morreale HF, Luque-Ramírez M, González F. Fertil Steril 2011; 95(3): 1048-1058. https://doi.org/10.1016/j.fertnstert.2010.11.036.
Phelan N, O'Connor A, Kyaw Tun T, et al. Clin Endocrinol (Oxf) 2013; 78(1): 107-113. https://doi.org/10.1111/j.1365-2265.2012.04454.x.
Garbossa SG, Folli F. Rev Endocr Metab Disord 2017; 18(2): 243-258. https://doi.org/10.1007/s11154-017-9423-2.
Tatarchuk TF, Dejnjuk KD, Zan'ko OV, et al. Reproduktyvna Endokrynologija 2018; 3(41): 84-94.
Hang Wun Raymond Li, Brereton RE, Anderson A, et al. Metabolism 2011; 60(10): 1475-1481. https://doi.org/10.1016/j.metabol.2011.03.002.
Kabadi SM, Liu L, Auchincloss AH, Zakeri IF. Dis Markers 2013; 35(3): 187-193. https://doi.org/10.1155/2013/497256
Jun Sun, Juan Kong, Yingli DuanAm J, et al. Physiol Endocrinol Metab 2006; 291(2): E315-22. https://doi.org/10.1152/ajpendo.00590.2005.
Tumu VR, Govatati S, Guruvaiah P, et al. J Assist Reprod Genet 2013; 30(12): 1541-1546. https://doi.org/10.1007/s10815-013-0111-1.
Nehir Aytan A, Bastu E, Demiral I, et al. Gynecol Endocrinol 2016; 32(9): 709-713.
Kucuk M, Altinkaya SO, Nergiz S, et al. Gynecol Endocrinol 2014; 30(6): 423-427. https://doi.org/10.3109/09513590.2014.895981.
Moran LJ, Noakes M, Clifton PM, et al. J Clin Endocrinol Metab 2007; 92(8): 2944-2951. https://doi.org/10.1210/jc.2006-2336.
Ün B, Dolapçıoğlu KS, Güler Okyay A, et al. Eur J Obstet Gynecol Reprod Biol 2016; 204: 16-20. https://doi.org/10.1016/j.ejogrb.2016.06.022.
Maleedhu P, Vijayabhaskar M, Sharma S, et al. J Clin Diagn Res 2014; 8(2): 31-33. https://doi.org/10.7860/JCDR/2014/7070.3999.
Amer M, Qayyum R. J Clin Endocrinol Metab 2014; 99(2): 633-638. https://doi.org/10.1210/jc.2013-3262.
Kriebitzsch C, Verlinden L, Eelen G. J Bone Miner Res 2011; 26(12): 2991-3000. https://doi.org/10.1002/jbmr.493.
Orio F, Palomba S, Cascella T, et al. J Clin Endocrinol Metab 2005; 90(1): 2-5. https://doi.org/10.1210/jc.2004-0628.
Rudnicka E, Kunicki M, Suchta K, et al. Biomed Res Int 2020; 2020: 4092470. https://doi.org/10.1155/2020/4092470.
Yang F, Sun M, Sun C, et al. Sci Rep 2020; 10(1): 5883. https://doi.org/10.1038/s41598-020-62754-w