**4.1 The major antigen of Graves' disease: the thyrotropin receptor**

The TSHR is a G protein coupled receptor. The TSHR is the primary auto antigen of Graves' disease, experimentally proven with mice antigen antibody studies [18].

**51**

*Hyperthyroidism*

**5. Diagnosis**

affair.

**5.1 Imaging**

grey scale analysis [20].

**6. Medical treatment**

*DOI: http://dx.doi.org/10.5772/intechopen.90314*

is usually suppressed, and T3 is normal or increased.

It is always better to test TSH and T4 rather than testing TSH alone, measuring both T4 & TSH increases diagnostic accuracy. In case of overt hyperthyroidism T3 and T4 are high and TSH is low and in subclinical disease T4 is usually normal TSH

TSH-Receptor-Ab (TRAb) is a specific biomarker for Grave's Disease. Immunoassays used nowadays do competitive assays which measure Thyroid Receptor binding inhibitory immunoglobulins (TBII) [19]. Bioassays can differentiate between blocking and stimulating TRAB but its time consuming and a costly

Most clinicians would request thyroid ultrasound (US) and often isotope scanning is seldom available in India. Imaging tests are investigator dependant and hence experience and qualification of a person doing the test does matter, also matter is instruments used, hence a high-frequency linear probe should be used. GD is often, but not invariably, characterised by diffuse thyroid enlargement and by hypoechogenicity, both of which are assessed by ultra-sonogram and conventional

A colour-flow or power Doppler examination is characterised by vascular patterns and can quantify vascularity of thyroid [21]. Thyroid vascularity is significantly increased in severe Grave's disease and it typically shows a pulsatile pattern in thyroid gland which is called as "thyroid inferno" that is multiple small areas of increased intrathyroidal flow seen throughout the gland [22]. To measure accurately thyroid artery flow velocity and peak systolic velocity (PSV), it requires adjustments of pulse repetition frequency of wall filters and control of the insonation angle between 0 and 60°. The PSV is capable of differentiation between GD related thyrotoxicosis or amiodarone-induced thyrotoxicosis type 2, where the blood flow is reduced [23]. A typical US finding along with TRAB results can make diagnosis almost certain but thyroid scintigraphy is needed prior to Radioactive iodine abla-

There are three ways by which GD is treated. One is by oral treatment with antithyroid drugs which reduces synthesis of thyroid hormones second is Radioactive iodine ablation where radioactive iodine is used to burn thyroid follicles and third one being thyroid surgery where thyroid gland is removed so that thyroid synthesising machinery is taken outside the body [20, 24]. ATD represent the most commonly used therapy in Europe, Asia, and in the meantime in the USA [25, 26]. The main ATD are thionamides, such as propylthiouracil (PTU), carbimazole (CBZ), and the active metabolite of the CBZ as, methimazole (MMI). CBZ is not an active substance; it has to be decarboxylated to MMI in the liver. Thionamides inhibit the coupling of iodothyronines and hence reduce the biosynthesis of TH [27]. These drugs mainly inhibit function of thyroperoxidase, reducing oxidation and the organification of iodide. ATD are indicated as a first-line treatment of GD, particularly in younger subjects, and for short-term treatment of GD before definitive RAI therapy or thyroidectomy [20]. ATD also helps to reduce TRAb levels and rates of remission of GD. PTU at very high doses also inhibits deiodination of T4 to T3 [28]. However, this effect is of use in case of thyrotoxicosis crisis but for long term use

tion so that multinodular goitre can be differentiated [20].
