Increased uric acid levels and clinical relationship in Polycystic Ovary Syndrome

Year 2016, , 34 - 38, 29.10.2016

Havva Keskin Özge Timur , Yasemin Kaya Mustafa Utlu Faruk Yıldız Esra Ademoğlu Melek Kadı Mehmet Emin Budak Hakan Gözcü Hakan Sevimli Şenay Arıkan Ayşe Çarlıoğlu Zeynep Kamalak

https://doi.org/10.18663/tjcl.79713

Abstract

Aim: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder that affects women of reproductive age. Clinical and biochemical characteristics are similar to metabolic syndrome. Insulin resistance in patients with metabolic syndrome is associated with serum uric acid levels. In our study, we aimed to investigate the relationship between serum uric acid levels and clinical and laboratory in PCOS patients.

Material and Method: 172 PCOS patients and, 34 years old, body mass index (BMI) matching control group of a total 206 cases attended to endocrinology outpatient clinic were included in the study. At early follicular phase, blood samples were taken after a 12-hour fasting period. Basal serum hormone levels were measured by immunoassay.

Results: Uric acid levels was significantly higher in PCOS than control group (4.25 ± 1.07 PCOS, 3.7 ± 0.79 control, P = 0,048). Uric acid levels were positively correlated with BMI, total cholesterol, insulin, cycle time, Feriman Gallwey score and negatively correlated with HDL cholesterol levels. Uric acid levels were 2 times higher than in PCOS group independent to age and BMI with multivariate logistic regression.

Conclusion: Uric acid levels in study group was significantly higher independent to age and BMI. Cardiovascular risk factors; LDL, insulin, triglycerides, BMI was positively correlated with uric acid in PCOS group. Clinical indicators; Feriman Gallwey score and cycle time was also positively correlated. Elevated uric acid levels in PCOS patients may be an independent risk factor for cardiovascular disease, may show negative results in the clinic.

Key words: cardiovascular disease, polycystic ovary syndrome, uric acid,

Polikistik Over Sendromlu hastalarda artmış ürik asit düzeyleri ve klinik ile ilişkisi

Abstract

Amaç: Polikistikover sendromu (PKOS) üreme çağındaki kadınları etkileyen en sık endokrin bozukluktur. Klinik ve biyokimyasal özellikleri metabolik sendrom ile benzerlik göstermektedir. Metabolik sendromlu hastalarda insülin direnci, serum ürik asit düzeyi ile ilişkilidir. Çalışmamızda PKOS hastalarında serum ürik asit düzeylerinin laboratuar ve klinik ile ilişkisini incelemeyi amaçladık.

Gereç ve Yöntemler: Hastanemiz Endokrin Kliniğinde takip edilen 172 PKOS hastası, 34 yaş ve vücut kitle indeksi (VKİ) uyumlu kontrol grubu toplam 206 olgu katılmıştır. Erken folliküler fazda, 12 saat açlık sonrası kan örnekleri alınmıştır. Bazal serum hormon düzeyleri immunoassay ile değerlendirildi.

Bulgular: Ürik asid düzeylerinin PKOS grubunda kontrol grubuna göre istatistiksel olarak anlamlı bir şekilde daha yüksek saptanmıştır (4,25 ± 1,07 PKOS, 3,7 ± 0,79 kontrol, P = 0,048). Ürik asit ile VKİ, total kolesterol, insülin, siklus süresi, Ferriman Gallwey skoru arasında pozitif anlamlı korelasyon, HDL kolesterol ile anlamlı negatif korelasyon bulunmuştur. Çok değişkenli logistik regresyon yapıldığında ürik asit düzeylerinin PKOS grubunda yaş ve VKİ’den bağımsız olarak iki kat daha yüksek olduğu saptanmıştır.

Sonuçlar: Çalışmamızda PKOS grubunda ürik asit düzeyleri anlamlı bir şekilde yüksek bulunmuş ve bu yüksekliğin yaş ve VKİ’den bağımsız olduğu görülmüştür. Ürik asit ile kardiyovasküler risk faktörü olan kolesterol, Trigliserit, VKİ, insülin arasında pozitif korelasyon görülmüştür. Klinik gösterge olan Ferriman Gallwey, siklus süresi açısından da pozitif korelasyon saptanmıştır. Artmış ürik asit düzeyleri PKOS hastalarında kardiyovasküler hastalık oluşumu için bağımsız bir risk faktörü olabilir, klinikte olumsuz sonuçları gösterebilir.

Anahtar Kelimeler: Kardiyovasküler, polikistik over sendromu, ürik asit

Keywords

Kardiyovasküler, polikistik over sendromu, ürik asit

References

• 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 Metab 2004; 89: 2745-9.
• Zawadski JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome towards a rational approach. In: Dunaif A, Givens JR, Haseltine FP, Merriam GR, eds. Polycystic ovary syndrome. Boston: Blackwell Scientific Publications; 1992. p.377-84.
• Franks S. Polycystic ovary syndrome. N Engl J Med 1995; 333: 853-61.
• Ehrmann DA, Rosenfield RL, Barnes RB, Brigell DF, Sheikh Z. Detection of functional ovarian hyperandrogenism in women with androgen excess. N Engl J Med 1992; 327: 157-62.
• Polson DW, Adams J, Wadsworth J, Franks S. Polycystic ovaries, a common finding in normal women. Lancet 1988; 1: 870-2.
• Kousta E, Efstathiadou Z, Lawrence NJ, et al. The impact of ethnicity on glucose regulation and the metabolic syndrome following gestational diabetes. Diabetologia 2006; 49: 36-40.
• Cristine E, Berry MH, Joshua MH. Xanthine oxido reductase and cardiovascular disease, molecular mechanism and pathophysiological implication. J Physiol 2004; 555: 589-606.
• Manzato E. Uric acid. An old actor for a new role. Intern Emerg Med 2007; 2: 1-2.
• Conway GS, Agrawal R, Betteridge DJ, Jacobs HS. Risk factors for coronary artery disease in lean and obese women with the polycystic ovary syndrome. Clin Endocrinol (Oxf) 1992; 37: 119-25.
• Dahlgren E, Johansson S, Lindstedt, et al. Women with polycystic ovary syndrome wedge resected in 1956 to 1965: a long-term follow-up focusing on natural history and circulating hormones. Fertil Steril 1992; 57: 505-13.
• Wild RA. Hyperandrogenism, implications for cardiovascular disease In: Redmond GP, ed.1995, Androgenic Disorders. New York:Raven Press; p.261-78.
• Vuorinen-Markkola H, Ykı-Jarvinen H. Hyperuricemia and insulin resistance. J Clin Endocrinol Metab 1995; 78: 25-9.
• Luque-Ramírez M, Alvarez-Blasco F, UriolRivera MG, Escobar-Morreale HF. Serum uric acid concentration as non-classic cardiovascular risk factor in women with polycystic ovary syndrome: effect of treatment with ethinyl estradiol plus cyproteroneacetate versus metformin. Hum Reprod 2008; 23: 1594-601.
• Anttila L, Rouru J, Penttilä T, Irjala K. Normal serum uric acid concentrations in women with polycystic ovary syndrome. Hum Reprod 1996; 11: 2405-7.
• Macut D, Bacevic M, Bozic-Antic I, et al. Predictors of subclinical cardiovascular disease in women with polycystic ovary syndrome: inter relationship of dyslipidemia and arterial blood pressure. Int J Endocrinol 2015. doi: 10.1155/2015/812610.
• Gill SK. Cardiovascular risk factors and disease in women. Med Clin North Am 2015; 99: 535-52.
• Johnson RJ, Lanaspa MA, Gaucher EA. Uric acid, a danger signal from the RNA world that may have a role in rhe epidemic of obesity, metabolic syndrome and cardiorenal disease: evolutionary considerations. Semin Nephrol 2011;31 : 394-9.
• Schulz E, Gori T, Münzel T. Oxidative stres and endothelial dysfunction in hypertension. Hypertens Res 2011; 34: 665-73.
• Bergamini C, Cicoira M, Rossi A, Vassanelli C. Oxidative stres and hyperuricemia, pathophysiology, clinical relevance, and the rapeutic implications in chronic heart failure. Eur J Heart Fail 2009; 11: 444-52.
• Feig DI, Kang DH, Johnson RJ. Uric acid and cardiovascular risk. N Engl J Med 2008; 359: 1811-21.
• Khosla UM, Zharikov S, Finch JL, et al. Hyperuricemia induces endothelial dysfunction. Kidney Int 2005; 67: 1739-42.
• Gersch C, Palii SP, Kim KM, Angerhofer A, Johnson RJ, Henderson GN. Inactivation of nitric oxide byuric acid. Nucleos Nucleot Nucl 2008; 27: 967-78.
• Zharikov S, Krotova K, Hu H, et al. Uric acid decreases NO production and increases arginase activity in cultured pulmonary artery endothelial cells. Am J Physiol Cell Physiol 2008; 295: 1183-90.
• Yildiz BS, Sahin A, Aladag NB, Yildiz M. Association of endogenous melatonin with uric acid and traditional cardiovascular risk factors in healty young male. Adv Clin Exp Med 2015; 24: 233-7.
• Orio F, Vuolo L, Palomba S, Lombardi G, Colao A. Metabolic and cardiovascular consequences of polycystic ovary syndrome. Minerva Ginecol 2008; 60: 39-51.
• Ravn P. New paradigms in PCOS, impaired glucose tolerance and cardiovascular risk. Clinical approach. Minerva Ginecol 2015; 67: 217-23.
• Wild RA, Grubb B, Hartz A, Van Nort JJ, Bachman W, Bartholomew M. Clinical signs of androgen excess as risk factors for coronary artery disease. Fertil Steril 1990; 54: 255-9.