**2.2 Anti-thyroglobulin antibody**

*Goiter - Causes and Treatment*

**pregnancy**

**Table 1.**

**1.1 Anatomical, physiological and biochemical adaption of thyroid gland to** 

which is also associated with a bruit [1]. There is an established increased renal clearance of iodide leading to increased thyroid iodide clearance with associated raised uptake of 131Iodide by the thyroid glands during pregnancy. This results in a relative iodine deficient status in the pregnant mother. There is also an increase in TBG (thyroid hormone binding globulin) for which total thyroxine exhibits a raised value but free thyroxine and free triiodothyronine (fT3) is mostly normal (**Table 1**).

**1.2 Regulation of synthesis of thyroid hormones in pregnancy**

*Normal levels of thyroid hormones and TSH in pregnancy [1].*

results in mild hyperthyroidism status in early pregnancy.

**2. Anti-thyroid antibodies to thyroid antigens**

**2.1 Anti TPO antibody**

A palpable increase in size of the thyroid gland is observed in normal pregnancy

**Parameter Changes during pregnancy Normal values (up to)** TSH Reaches nadir during first trimester; then plateaus 4.0 mIU/L T4 Increases in first trimester; then plateaus 150 ng/mL fT4 Unchanged 30 pg/mL T3 Increases in first trimester; then plateaus 2 ng/mL fT3 Unchanged 4 pg/mL

The synthesis of thyroid hormones is regulated by HPT axis, i.e., hypothalamus-

Polyclonal antibodies directed against some epitopes of thyroperoxidase molecule are present in the blood of some healthy individuals and patients having auto immune thyroid disorders [1–3]. Anti-TPO antibodies from auto immune thyroid patients act as competitive inhibitors of enzymatic activity though those from healthy subjects are not seen to block thyroperoxidase [4, 5]. These antibodies mostly belong to IgG class, more often IgG1and IgG4 subtypes [6]. Prevalence of anti-TPO antibodies are more common than other anti-thyroid antibodies and more symbolic for thyroid hormone imbalance. Excess of oxidative stress markers in blood are seen with anti-TPO antibodies indicating it to be an inducer of oxidative

pituitary-thyroid axis. The TRH released from hypothalamus acts positively on pituitary gland which releases TSH [1]. The TSH in turn stimulates the thyroid gland to synthesize and release T4 and T3. The thyroid gland gives negative feedback signal to hypothalamus and pituitary and thus excess of its synthesis is controlled and regulated. During pregnancy, in addition to the normal regulatory mechanisms, hCG also plays a significant role in regulation of thyroid hormone synthesis. hCG mostly the asialo-hCG fraction secreted from the placenta is known to have weak TSH simulating action and this plays an important role in maintaining the thyroid hormone levels, whose demand is increased in pregnancy due to fetal dependency on mother's thyroid hormones almost exclusively up to 12 weeks of gestation and hCG acts by contributing to thyrotropic action of placenta. This also

**16**

Polyclonal anti thyroglobulin (Tg) antibodies are found in the serum of healthy subjects whereas oligoclonal antibodies are seen in patients having auto immune thyroid disorders. It has been hypothesized that normal blood levels of Tg induce self-tolerance in T cells as low levels of antigens are usually responsible for development of self-tolerance. But this self-tolerance is not seen in case of B cell activity resulting in healthy individuals having very low levels of anti-Tg antibodies which is usually below detection limits. Higher levels of Tg following tissue damage, or due to conformation alteration of the Tg molecule in presence of high iodine levels, or in presence of very high TSH levels, there is alteration in the titers of the anti-Tg antibody. The anti-Tg antibodies are predominantly of IgG4 though minor proportions of IgA and IgM class are also seen. The functional consequence of anti-Tg antibodies is hitherto not known. Circulating antibodies were detected in healthy young subjects and in people >60 years of age to an extent of 10–15%. Presence of anti-Tg antibodies have been documented in auto immune thyroid disorders, Graves' disease and in patients with non-thyroid immune disorders. These antibodies like anti TPO antibodies can cross the placenta barrier but its effects are not very substantially known [1].
