**Thyroid in Pregnancy**

Drahomira Springer, Zdenka Limanova and Tomas Zima *First Faculty of Medicine of the Charles University Prague Czech Republic* 

## **1. Introduction**

Many changes in the functioning of the thyroid gland occur during pregnancy and some diseases of the thyroid gland can affect both the pregnant woman and the fetus. (Casey et all., 2006; Lazarus & Premawardhana, 2005; Poppe et all., 2007). Hypothyroidism is the most serious disorder of those occurring during pregnancy, and it might go unnoticed as some 'nonspecific' problem. Pregnant women with subclinical hypothyroidism seem to escape early clinical detection (Lazarus, 2002). While the hyperfunction during pregnancy usually manifests itself by clinical symptoms or a relapse of a previously cured disease (mostly Graves - Basedow) (Abalovich et all., 2007), lowered functioning is much more dangerous because of its non-specific symptoms. During the 1st trimester, the fetus is completely dependent upon thyroxin produced by the mother (Smallridge & Landerson, 2001). Even a small unnoticed malfunction of the thyroid gland, which doesn't have to endanger the course of the pregnancy, can affect the psychomotor developement of the child (Morreale de Escobar et all., 2004; Mitchell & Klein, 2004)). Some women with subclinical hypothyroidism are absolutely asymptomatic and there is no reliance on the clinical image, while diagnostic of thyroid dysfunction (Klein et all., 2001).

Malfunction of the thyroid gland during pregnancy is long-term, and still not a sufficiently solved problem (Lazarus, 2002). On many pages of scientific literature and specialist literature there are still new arguments to systematically screen pregnant women for thyroid dysfunction and asymptomatic chronic thyroiditis in order to give such women the appropriate treatment (Surks et all., 2004). Results of surface population screenings are slightly varied, depending upon on level of medical care and approach to prevention, geographical conditions, supplementing with iodine, and other circumstances (including used diagnostic criteria) (Vaidya et all., 2007). Evaluating thyroidal function during pregnancy is difficult, considering the other differing influences of pregnancy.

Guidelines for management of thyroid dysfunction during pregnancy and postpartum (Abalowich et al. 2007) recommend not universal but only case finding screening. The first aim of the study was to assess the value of this recommendation. The other aim was to introduce an estimation of thyroid dysfunction during pregnancy, selection of suitable biochemical markers and determination of reference intervals for these markers in pregnancy.

#### **2. Investigation of thyroidal dysfunction in pregnancy**

In cooperation with General insurance company in Czech Republic was in 2009 started a pilot project for universal screening of thyroid dysfunction among women in the first

Thyroid in Pregnancy 39

mortality (Poppe et all., 2007). Poorly controlled thyrotoxicosis is associated with thyroid storm especially at labor and delivery. Beta blockers and propylthiouracil (PTU) can be safely used in pregnancy and in nursing mothers. PTU crosses the placenta but does not usually cause fetal hypothyroidism and goiter unless used in high doses. Treatment goals favor mild hyperthyroidism over hypothyroidism. Like other immune mediated diseases in pregnancy, Grave's disease tends to improve in the third trimester. Exacerbations may occur in the first trimester and postpartum. Neonatal and fetal thyrotoxicosis may occur because

Postpartum thyroiditis is a destructive autoimmune thyroiditis that begins with a period of hyperthyroidism followed by a period of hypothyroidism (Negro et all., 2007). The gland is often enlarged. There is usually complete recovery but a chance of recurrence in subsequent pregnancies exists. 80-85% of patients will have positive antithyroid antibodies. A radioactive iodine uptake scan can differentiate postpartum thyroiditis from an exacerbation

TPO Ab antibodies are markers of autoimmune process in the thyroid gland, their determination is diagnostically and prognostically important. Presence of TPO Ab during pregnancy also alerts to the danger of development of postpartum tyreoiditidis (Nicholson at all., 2006; Dosiou et all., 2008); about 50% of TPO Ab positive women have some thyroid dysfunction after delivery (Premawardhana et all., 2004; Nicholson at all., 2006), so it is necessary to follow-up these women. Postpartum thyroiditis is in an important

Hyperemesis is associated with abnormal thyroid function tests in a significant number of cases. Hyperthyroidism may be the cause of hyperemesis or hyperemesis may be the cause

The iodine requirement during pregnancy is sharply elevated because of an increase in maternal thyroxine production to maintain maternal euthyroidism and to transfer thyroid hormone to the fetus, iodine needs to be transferred to the fetus for fetal thyroid hormone production in later gestation and a probable increase in renal iodine clearance. The recommended dietary allowance for nonpregnant, nonlactating women aged 14 year is 150 µg/d, for pregnant women is it 220 µg/d (Zimmermann & Delange, 2004),. In Czech Republic has been iodized salt in regular use since the 1950s, a good level of iodine supplementation can be expected also on Zamrazil study (Zamrazil, 2004). Women in this

The study group consists of 3 577 asymptomatic pregnant women (in their 9th – 11th week of pregnancy, 99% Caucasian) who were undergoing their first trimester prenatal screening. In the pilot project were used laboratories, which were able to investigate serum for the first trimester screening (investigation of PAPP-A and free β hCG) and simultaneously in the same sample determine TSH (thyroid stimulating hormone), TPO Ab (antibodies to thyroid

of transplacental passage of thyroid stimulating antibodies.

consideration in women with postpartum depression.

of the hyperthyroidism (Goodwin et all., 1992).

**2.1.2 Iodine supplementation in pregnancy** 

study were in addition supplemented by 100-150 ug of iodide daily.

**2.1.1.3 Postpartum thyroiditis** 

of Graves- Basedow disease.

**2.1.1.4 Hyperemesis gravidarum** 

**2.1.3 Timing of the blood taking** 

peroxidase) and FT4 (free thyroxine).

trimester of pregnancy. A pilot project was performed during 2009-2010 in 13 regions, (only 4 regions in 2010) of the Czech Republic. The data from 3577 pregnant women with sufficient iodine intake were available. The blood for TSH (thyroid stimulating hormone), TPO Ab (antibodies to thyroid peroxidase) and FT4 (free thyroxine) estimation was collected in 9-11 week of pregnancy. All participating pregnant women gave informed written consent with this subsequent investigation.
