Download as pdf or txt
Download as pdf or txt
You are on page 1of 4

The New Journal of Medicine 2011;28: 23-26

Original article

Does Maternal High TSH Level Cause Breech


Presentation at Term?
Deniz HIZLI 1, Saynur Sarc YILMAZ 2, Emel RN 1, Nilgn ztrk TURHAN 1
1

Fatih University Faculty of Medicine, Department of Obstetrics and Gynecology, ANKARA


Zekai Tahir Burak Womens Health Research and Education Hospital, Department of Obstetric and
Gynecology, ANKARA

ZET
Yksek maternal TSH dzeyleri makat gelie neden
olur mu?
Makat prezentasyon en sk grlen anormal prezentasyon
eklidir ve maternal ve neonatal morbidite ve mortalite
ile ilikilidir. Son zamanlarda bozuk maternal tiroid
fonksiyon testinin makat prezentasyona yol at iddia
edilmitir. Bu almada yksek tiroid stimule edici hormonun (TSH) termde makat gelie yol ap amad
incelenmitir.
Fatih niversitesi Tp Fakltesi Kadn Hastalklar ve
Doum Blmnde, >37 gebelik haftasnda doum yapm olan ve TSH deerlerine baklm olan toplam 60
hasta almaya dahil edildi. Altm hastann 30u makat
(grup A), 30u ba (grup B) prezentasyonunda idi. TSH
seviyeleri ile makat geli arasnda iliki olup olmad
SPSS 16.0 program ile deerlendirildi.
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 deildi (p=0,1). Sonrasnda
hastalar TSH seviyelerine gre 2 gruba ayrld (2,5 mU/l
veya 2,5 mU/l) ancak gruplar arasnda prezentasyon
ynnden istatistiksel olarak fark saptanmad.
Bu almada TSH seviyeleri ile makat prezentasyon
arasnda herhangi bir iliki saptanmamtr.
Anahtar Kelimeler: Makat prezentasyon, TSH, hipotiroidizm

INTRODUCTION

Breech presentation is the most common abnormal


fetal presentation and generally associated with
maternal and neonatal morbidity and mortality.
The incidence decreases 16% at 32 weeks to 35% at term1. Risk factors such as prematurity,
intrauterin growth retardation, pelvic abnormalities, uterus anomalies, placenta previa, polyhydroamnios, multiparity, umblical cord anomalies
and congenital fetal abnormalities are responsible
for only 15% of breech presentation2-8.

Correspondence:
Deniz HIZLI M.D.
Fatih University Faculty of Medicine
Department of Obstetrics and Gynecology, Ankara
e-mail: denizhizli@yahoo.com
Arrival date
: 03.11.2010
Acceptance date : 23.12.2010

ABSTRACT
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.
Key Words: Breech presentation, TSH, hypothyroidism

The physiopathology of breech presentation stil


remains unclear. Recently, maternal hypothyroidism
was described as a risk factor for breech presentation. It is obvious that transplacental passage of
maternal T4 for fetal brain development in the
early first trimester is important and adverse
effects such as pregnancy-induced hypertension,
abruption, postpartum hemorrhage,_an increase
in the frequency of low-birth-weight infants and
increased risk of impaired neurodevelopment growth
are previously described9. Above all, there is
increasing attention to evaluate the impact of
thyroid function tests on fetal presentation in
recent times10-12. From this point of view, the aim
of this study was to evaluate the effect of TSH on
breech presentation.

23

D.Hzl et al.

MATERIAL AND METHODS

Between August 2009 to September 2010, 30


women who had delivery with breech presentation
after 37 gestational weeks and whose thyroid
hormon levels were available in the first trimester
were included in the study and defined as group
A. Similarly, 30 consecutive women who had
delivery with cephalic presentation after 37 weeks
and whose thyroid hormon levels were available
were defined as group B. Women on thyroid
medication, those with known clinical hyperthyroidism
or hypothyroidism at screening, those who became
pregnant after hormonal stimulation, those with
multiple pregnancy and known Type 1 diabetes,
babies born with congenital anomalies were
excluded. Breech presentation before 37 weeks
were not regarded as abnormal fetal presentation
so births before 37 weeks were also excluded.
Totally 60 patients were enrolled in this study (30
patients in group A, 30 in group B).
Term was assessed from the date of the last
menstruel period and from an ultrasound scan in
the first trimester. Gestational age was expressed
in weeks and days. Fetal position was cathegorized as cephalic or breech (complete, incomplete
or frank).
TSH (reference range for women aged between
20 and 40 years: 01520 mIU/l) was measured
using a solid-phase, two-site chemiluminescent
enzyme immunometric assay (IMMULITE third
generation TSH, Diagnostic Corporation, Los
Angeles, CA, USA). The interassay coefficients of
variation were 98, 69 and 46%, at concentrations of 002, 015 and 11mIU/l, respectively. The
fT4 concentration (reference range for women
aged between 20 and 40 years: 87196 pmol/ l)
was also measured by means of a solid-phase
immunometric assay (IMMULITE Free T4). The
interassay coefficients of variation for this
technique were 20, 53 and 52% at concentrations of 31, 198 and 55 pmol/l, respectively.
Statistical analysis was performed using the
Statistical Package of Social Science and Problems
Solutions Version 16.0 (SPSS). Kolmogorov
Smirnov tests revealed abnormal distribution of
FT4 and FT3 in the sample at all assessments.
Therefore, FT4 and FT3 were compared in the
breech vs. cephalic presentation groups using
MannWhitney
U-tests.
Differences
in
the
prevalence of breech presentation were also
examined using chi-square tests to compare
groups based on TSH cutoffs and/or gestation.

RESULTS

A total of 60 patients were evaluated, 30 of 60


patients had delivery with breech presentation
24
24

The New Journal of Medicine 2011;28: 23-26

(Group A) and 30 had cephalic presentation


(Group B). The mean age of patients was 26.5 and
28.6 years in group A and group B, respectively.
Mean birthweight was 3340 g in patients with
breech presentation and 3400 g in cephalic
presentation. Of 60 patients 13 had female
offspring in group A and 10 had female offspring
in group B. Gestational age at birth was 38 weeks
and 5 days and 38 weeks and 3 days in group A
and group B, respectively. The groups were not
different with regard to maternal age, parity,
gestational age at birth, birthweight and fetal
gender. All patients in group A had cesarean
section delivery and 10 patients in group B had
cesarean section, 20 patients had vaginal delivery.
Postpartum period was uneventful in all patients.
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. However, FT4
levels were available in 25 patients and FT3 in 23
patients, therefore FT4 and FT3 were not
evaluated statistically.
Furthermore, patients were divided into 2
groups according to TSH levels and compared
according to presentation and other demographic
factors. TSH level <2.5 mIU/l was defined as
group 1 and TSH level 2.5 mIU/l was defined as
group 2. Sixteen patients (26.6%) were in group
2, 10 with breech presentation and 6 with cephalic
presentation.
However
groups
were
not
statistically different with regard to presentation,
maternal age, birthweight, gestational age at birth
and fetal gender.

DISCUSSION

Thyroid disease is the second most common


endocrine disorder (after diabetes) affecting
women of reproductive age. The subject of thyroid
disease in pregnancy is receiving increasing
attention from many scientific disciplines due to
adverse effects on pregnancy. Hypothyroidism is
reported to occur in 2.5% of pregnancies13 and
generally is associated with an elevated serum
TSH and a low free T4. Symptoms of hypothyroidism can often be masked by the hypermetabolic
state of pregnancy. Additionally, pregnancy may
alter the thyroid function tests like a fall in serum
TSH and increase in free thyroxine is observed
during the early weeks of pregnancy, that may
confuse the diagnosis of hypothyroidism14.
Subclinical hypothyroidism characterized by an
elevated serum TSH concentration but a normal
serum free thyroxine level is reported to have a
prevalence of 2%5% in pregnant women14.
Transplacental passage of maternal T4 is very
important for fetal brain development especially in

The New Journal of Medicine 2011;28:


D.Hzl23-26
et al.

the early first trimester. Results of a large


prospective study reported that, during pregnancy,
maternal free thyroxine levels less than the 10th
percentile at 12 weeks' gestation, but not at 32
weeks, are associated with a 6-fold increased risk
for impaired neurodevelopment in infants evaluated at 10 months of age15-16. However, this
observation requires further validation as preterm
birth, also associated with neurodevelopmental
abnormalities, may be a contributing factor.
Children of women whose TSH levels were
elevated during the mid-trimester of pregnancy
had a slight but significant reduction in
intelligence quotient scores between 7 and 9 years
of age when compared with infants of euthyroid
women. Women with TSH values >10 mU/liter
also had significantly more stillborn infants.
Subclinical maternal hypothyroidism may also be
associated with poor pregnancy outcomes such as
placental abruption, preterm birth, and low-birthweight infants17. Iodine deficiency was described
as the most common cause of hypothyroidism in
the worldwide also in Turkey18.
Recently there is increasing attention to
determine whether thyroid function tests have
effect on fetal presentation. As our knowledge,
only 3 studies evaluating the impact of thyroid
function tests on breech presentation are available
in the literature. All 3 studies reported that low
TSH
levels
were
associated
with
breech
presentation10-12.
Relationship between breech presentation at
term and thyroid disorder was first described in
200410. However, limited studies have evaluated
the impact of thyroid hormones on fetal position
since 2004. Firstly, Pop et al.10 claimed that low
FT4 levels at 12 gestational weeks were related to
breech presentation at term but not related at 24
and 32 gestational weeks. Conversely, in a study
performed by Kuppens et al., a total of 1058
women were included in the study and 58 had
breech delivery after >37 weeks were defined as
breech group and 1000 women as cephalic
group11. Thyroid parameters were evaluated at
12, 24 and 36 gestational weeks. TSH levels at 36
weeks were found to be significantly higher in
breech delivery group but not different at 12 and
24 gestational weeks. Additionally, FT4 levels of
breech and cephalic group were not different in
any gestational week. Similarly Kooistra L. et al.
reported that high TSH levels at term were related
to breech presentation12. On the other hand, FT4
immunassays during gestation are found to be less
reliable compared with nonpregnant situations19.
Several possible mechanisms explaining this
relation were described previously. First potential

mechanism was defined as decreased uterine


contractions in hypothyroidism. As it is known,
uterine contractions are important for final
cephalic presentation at term and Medeiros et al.20
found reduced responsiveness to uterine agonists
in hypothyroid rats and similarly Parija et al.21
determined decreased uterine myometrial Ca+2
channel function in hypothyroid rats. Also TSH
receptor is expressed not only in the thyroid, but
also in adipose tissue, brain, orbital tissue,
lymphocytes and bone22. It was speculated that
TSH receptors may be present in uterus. However,
no uterine TSH receptor was detected up to now.
So this mechanism remains paradoxical and
requires further researchs.
Second potential mechanism was described as
less fetal movement may be responsible for
breech presentation10. For example breech
presentation is common in fetuses with congenital
akinesia syndrome. Children of women with
hypothyroxinaemia showed an 8 to 10 point index
delay on the motor scale compared with children
of women normal FT4 levels at one and two years
of age.
And it was claimed that, if low thyroid hormone
levels are associated with motor development
retardation at one and two age, it should also be
intrauterine and cause breech presentation.
Especially in some situations where hypothalamic
function is impaired, so thyroid function, the rate
of breech presentation is 20%23. Similar to first
mechanism, the second mechanism requires to be
confirmed in large randomized controlled trials.
The mechanism of association between maternal
thyroid disorder and breech presentation still
remains to be explained.
The prevalance of breech presentation is 3-4%
at term1. Patients who had breech delivery before
37 weeks were not regarded as abnormal fetal
position and were not included in the present
study because sponton rotation from breech
presentation to cephalic is usually seen before 37
weeks.
Aetiology of breech presentation is not well
decribed, factors such as prematurity, intrauterine
growth retardation, gemelli, pelvic abnormalities,
uterine abnormalities, placenta praevia, polyhydroamnios, multiparity, umblical cord problems and
congenital fetal abnormalities only explain 15% of
breech presentations2-8.
No relation between TSH levels and breech
presentation was determined in the present study.
Patients were divided into 2 groups according to
TSH levels due to reccomendation of cut off value
to set at 2.5 mU/liter in pregnant women24.

25

The New Journal of Medicine 2011;28: 23-26

D.Hzl et al.

However the groups were not different with regard


to presentation.
The limitation of the present and the other
studies is low number of breech delivery, but
these studies at least may set light to further
researchers evaluating impact of hypothyroidism

on presentation. In conclusion, the relation


between TSH level and breech presentation seems
to remain controversial and requires to be
confirmed in further prospective randomized
controlled studies with larger population.

REFERENCES
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: 85152.
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: 2832.
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: 41015.
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: 18.
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: 87580.
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: 34145.
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: 87276.
8. Hardy J. Intergenerational recurrence of breech delivery: maternal
and paternal history of breech increase risk equally. British Medical Journal
2008;336: 84344.
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: 42127.
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: 92530.
11. Kuppens SMI. Maternal thyroid function during gestation is related
to breech presentation at term. Clinical Endocrinology 2010;72: 82024.
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.

26
26

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: 12730.
14. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colarado
thyroid disease prevalence study. Arch Intern Med 2000;160: 52634.
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: 54855.
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: 28288.
17. Casey BM, Dashe JS, Wells E, McIntire DD, Leveno KJ,
Cunningham FG. Subclinical hypothyroidism and pregnancy outcomes.
Obstet Gynecol 2005;105: 23945.
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: 23542.
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:
20713.
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: 65562.
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: 128392.

You might also like