**2.3 Thyroid hormone receptor antibodies**

These antibodies bind to thyroid cell membrane at/near TSH receptor and mimics the action of TSH as "occupied" receptor. This leads to excess thyroxin synthesis by the gland which escapes feedback control mechanisms. It is demonstrated frequently in Grave's disease-also known as long acting thyroid stimulator (LATS) antibodies.

Excess of synthesis of thyroid hormones is known as hyperthyroidism and deficiency leads to hypothyroidism. Both the conditions are associated with deleterious effects to various metabolic processes of the body [1].

## **3. Thyroid hormones and pregnancy**

Thyroid hormones T4 and T3 affect almost every metabolic processes of the body. Pregnancy is considered to be a physiologically altered state of metabolism as the body tries to cater to the needs of the growing fetus. There is an increased need

of thyroid hormones in pregnancy as the developing fetus is completely dependent on maternal thyroid hormones till 12 weeks of gestation. Hence, the gland becomes over stimulated and hyperactive to secrete more T4 and T3 to meet the increased demand and this is brought about through hypothalamus-pituitary-thyroid axis regulatory mechanisms. Thyroxin and TBG (thyroid binding globulins) levels rise in pregnancy along with a simultaneous decrease in TSH (thyroid stimulating hormone) level [13]. A placental deiodinase enzyme also results in more thyroid hormone synthesis in pregnancy [14–16]. hCG is known to have a TSH simulating effect and hence attributes to raise the thyroid hormone synthesis to meet the increased demand via its thyrotrophic effect [17]. Absolute fetal dependency on mother's thyroid hormones can result in adverse obstetric and fetal outcome if the increased demand for T4 and T3 is not met adequately in the first 12 weeks of gestation [18]. There has also been documented evidences that proper placental development is also dependent on thyroid hormones and lack of it can result in improper placenta formation [19] with adverse obstetric outcomes like abruptio placentae, preeclampsia, miscarriages, preterm delivery, low birth weight (LBW), IUGR (intrauterine growth retardation) and small for gestational age babies (SGA) [20–22]. Impaired intellectual development of off springs of hyper/hypothyroid mothers has also been documented [23].
