**7. Special situation**

## **7.1 Hyperthyroidism in pregnancy**

Hyperthyroidism is not uncommon during pregnancy with prevalence being 0.1–0.4% of which 80% of the cases are of Grave's disease. The activity level of Graves' disease fluctuate during gestation, with exacerbation during the first trimester and improvement by late gestation related to autoimmune process of

the disease affected by gestation. Hyperthyroidism of Graves' disease may also be aggravated by high levels of HCG in the first trimester. Because nonspecific symptoms of hyperthyroidism may be mimicked by normal pregnancy, the presence of a goitre, especially with a bruit or thrill, which may point to a diagnosis of true Graves' disease. One has to be cautious before labelling diagnosis of Grave's disease and should first rule out gestational thyrotoxicosis [36–38].

Patients suspected of having hyperthyroidism require measurement of serum TSH, T4, T3 levels, and TRAb. And it's always necessary to interpret thyroid function tests in relation to the HCG-mediated decrease in serum TSH levels and the increase in T4 binding globulin concentrations that occur during normal pregnancy [39–41].

In a normal pregnancy TSH is typically suppressed specially during late first trimester and last trimester, a lady with Graves' disease, one must anticipate transplacental transfer of TRAB and fetal hyperthyroidism hence adequate treatment of a pregnant woman is necessary to avoid fetal hyperthyroidism. Fetal hyperthyroidism and inadequate treatment is associated with increased risk of medically indicated preterm delivery, intrauterine growth restriction and low birth weight, preeclampsia, congestive heart failure, and fetal death [42]. In addition, overtreatment of the mother with thionamides can result in iatrogenic fetal hypothyroidism [43], but under treatment of maternal hyperthyroidism may lead to central congenital hypothyroidism [44, 45].

Fetal hyperthyroidism is known to be associated with intrauterine growth restriction, fetal tachycardia, fetal goitre, advanced bone age, fetal hydrops, preterm delivery, and fetal death [46]. The diagnosis is suggested by any of these signs or abnormalities. Maternal TRAb levels able to induce fetal hyperthyroidism are usually over three times the upper normal limit. PTU and MMI or its derivative carbimazole are the mainstays of treatment. Recently, the Adverse Event Reporting System of the FDA has focused attention on the relation between hepatotoxicity and PTU [47]. This finding has led to a recommendation that PTU use in pregnancy should be limited to the first trimester, and then treatment must be switched to MMI. Use of MMI during the first trimester has been associated with a possible embryopathy.
