Does maternal high TSH level cause breech presentation at term?
Makat prezentasyon en sk görülen anormal prezentasyon şeklidir ve maternal ve neonatal morbidite ve mortalite ile ilişkilidir. Son zamanlarda bozuk maternal tiroid fonksiyon testinin makat prezentasyona yol açtğ iddia edilmiştir. Bu çalşmada yüksek tiroid stimule edici hormonun (TSH) termde makat gelişe yol açp açmadğ incelenmiştir. Fatih Üniversitesi Tp Fakültesi Kadn Hastalklar ve Doğum Bölümünde, >37 gebelik haftasnda doğum yapm ş olan ve TSH değerlerine baklmş olan toplam 60 hasta çalşmaya dahil edildi. Altmş hastann 30’u makat (grup A), 30’u baş (grup B) prezentasyonunda idi. TSH seviyeleri ile makat geliş arasnda ilişki olup olmadğ SPSS 16.0 program ile değerlendirildi. A grubundaki ve B grubundaki hastalarn ortalama TSH seviyeleri srasyla 1,88 mIU/l ve 1,51 mIU/l idi ve gruplar istatistiksel olarak farkl değildi (p=0,1). Sonrasnda hastalar TSH seviyelerine göre 2 gruba ayrld (2,5 mU/l veya ≥2,5 mU/l) ancak gruplar arasnda prezentasyon yönünden istatistiksel olarak fark saptanmad. Bu çalşmada TSH seviyeleri ile makat prezentasyon arasnda herhangi bir ilişki saptanmamştr.
Yüksek maternal TSH düzeyleri makat gelişe neden olur mu?
Breech presentation is the most common abnormal fetal presentation and generally associated with maternal and neonatal morbidity and mortality. Recently, high thyroid stimulating hormone (TSH) levels were claimed to cause breech presentation at term. The aim of this study was to evaluate the effect TSH on breech presentation. A total of 60 patients who had delivery after 37 gestational weeks at Fatih University School of Medicine Department of Obstetrics and Gynecology and whose TSH levels were available were included in the study. 30 of 60 patients had breech presentation and 30 had cephalic presentation at delivery. Statistical analysis between TSH and breech presentation was performed by using the Statistical Package of Social Science and Problems Solutions Version 16.0 (SPSS). TSH levels were 1.88 mIU/l and 1.51 mIU/l in group A and group B, respectively. The groups were not statistically different (p=0.1). Additionally, patients were divided into 2 groups according to TSH levels (<2.5 mU/l or ≥2.5 mU/l), however the groups were also not different with regard to presentation. No relation between TSH levels and breech presentation was determined in the present study.
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- 1. Hickok DE, Gordon DC, Milberg JA, Williams MA, Daling JR. The frequency of breech presentation by gestational age at birth: a large population-based study. American Journal of Obstetrics and Gynecology 1992;166: 851–52.
- 2. Rayl J, Gibson PJ, Hickok DE. A population-based case-control study of risk factors for breech presentation. American Journal of Obstetrics and Gynecology 1996;174: 28–32.
- 3. Albrechtsen S, Rasmussen S, Dalaker K, Irgens LM. The occurrence of breech presentation in Norway 1967-1994. Acta Obstetricia et Gynecologica Scandinavica 1998;77: 410–15.
- 4. Roberts CL, Algert CS, Peat B, Henderson-Smart D. Small fetal size: a risk factor for breech birth at term. International Journal of Gynaecology and Obstetrics 1999;67: 1–8.
- 5. Witkop CT, Zhang J, Sun W, Troendle J. Natural history of fetal position during pregnancy and risk of nonvertex delivery. Obstetrics and Gynecology 2008;111: 875–80.
- 6. Boos R, Hendrik HJ, Schmidt W. Das fetale lageverhalten in der zweiten schwangerschaftshalfte bei geburten aus beckenendlage und schadellage. Geburtshilfe und Frauenheilkunde 1987; 47: 341–45.
- 7. Nordtveit TI, Melve KK, Albrechtsen S, Skjaerven R. Maternal and paternal contribution to intergenerational recurrence of breech delivery: population based cohort study. British Medical Journal 2008;336: 872–76.
- 8. Hardy J. Intergenerational recurrence of breech delivery: maternal and paternal history of breech increase risk equally. British Medical Journal 2008;336: 843–44.
- 9. Glinoer D, Fernandez Soto M, Bourdoux P. Pregnancy in patients with mild thyroid abnormalities: maternal and neonatal repercussions. J Clin Endocrinol Metab 1991;73: 421–27.
- 10. Pop VJ, Brouwers EP, Wijnen H, Oei G, Essed GG, Vader HL. Low concentrations of maternal thyroxin during early gestation: a risk factor of breech presentation? BJOG: an International Journal of Obstetrics and Gynaecology 2004;111: 925–30.
- 11. Kuppens SMI. Maternal thyroid function during gestation is related to breech presentation at term. Clinical Endocrinology 2010;72: 820–24.
- 12. Kooistra L, Kuppens SM, Hasaart TH, Vader HL, Wijnen HA, Oei SG, et al. High thyrotrophin levels at end term increase the risk of breech presentation. Clin Endocrinol 2010;73: 661-5.
- 13. Allan WC, Haddow JE, Palomaki GE, Williams JR, Mitchell ML, Hermos RJ, et al. Maternal thyroid deficiency and pregnancy complications: implications for population screening. J Med Screen 2000;7: 127–30.
- 14. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colarado thyroid disease prevalence study. Arch Intern Med 2000;160: 526–34.
- 15. Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Eng J Med 1999;341: 548–55.
- 16. Pop VJ, Brouwers EP, Vader HL, Vulsma T, van Baar AL, de Vijlder JJ. Maternal hypothroxinaemia during early pregnancy and subsequent child development: a 3 year follow-up study. Clin Endocrinol 2003;59: 282–88.
- 17. Casey BM, Dashe JS, Wells E, McIntire DD, Leveno KJ, Cunningham FG. Subclinical hypothyroidism and pregnancy outcomes. Obstet Gynecol 2005;105: 239–45.
- 18. Kibirige MS, Hutchison S, Owen CJ, Delves HT. Prevalence of maternal dietary iodine insufficiency in the north east of England: implications for the fetus. Arch Dis Child Fetal Neonatal Ed 2004;89: 436– 39.
- 19. Lee RH, Spencer CA, Mestman JH, Miller EA, Petrovic I, Braverman LE, et al. Free T4 immunoassays are flawed during pregnancy. American Journal of Obstetrics and Gynecology 2009;200: 260-66.
- 20. Medeiros YS, Calixto JB. Effect of induced thyroid dysfunction upon uterine responsiveness in strips from pregnant and non pregnant rats. Pharmacology 1989;38: 235–42.
- 21. Parija SC, Raviprakash V, Telang AG, Varshney VP, Mishra SK. Influence of hypothyroid state on Ca (2+) influx and sensitivity of rat uterus to nifedipine and diltiazem. European Journal of Pharmacology 2001;421: 207–13.
- 22. Peeters RP, van der Deure WM, Visser TJ. Genetic variation in thyroid hormone pathway genes; polymorphisms in the, T.S.H receptor and the iodothyronine deiodinases. European Journal of Endocrinology 2006;155: 655–62.
- 23. Butler MG. Prader– Willi syndrome: current understanding of cause and diagnosis. Am J Med Genet 1990;35: 319 –32.
- 24. Casey BM, Leveno KJ. Thyroid disease in pregnancy. Obstet Gynecol 2006;108: 1283–92.