Thyrotoxicosis is defined as elevated serum levels of thyroid hormones, while hyperthyroidism specifically is caused by an active hormone synthesis and secretion from the thyroid gland (or ectopic thyroid tissue). Thyroid scintigraphy can easily differentiate between the two conditions.
In the majority of cases (>90%), the aetiology of hyperthyroidism is either Graves’ disease or toxic nodular goitre (solitary or multinodular). Both conditions are characterized by high uptake and turnover rate of iodine in the actively hormone producing thy roid tissue, and the scintigraphic appearance reflects the differences in tissue texture and functionality. There is no need to discontinue antithyroid drugs prior to 99mTc scintigraphy, as these agents do not affect the NIS function.
Graves’ Disease
In Graves’ disease, the entire gland, and the pyramidal lobe if pre sent, shows a scintigraphically uniform thyroid isotope uptake. The size of the gland may range from normal to grossly enlarged. In some cases, superimposed activity in the central part of the thyroid lobes due to the greater depth of thyroid tissue may raise suspicion of thyroid nodules, but this can easily be ruled out by an ultrasound examination.
Thyroid scintigraphy can be omitted in patients with a clinical presentation typical of Graves’ disease, and in the presence of TSH- receptor antibodies in serum. If a measure for the thyroid volume is needed, thyroid ultrasound is more accurate than scintigraphy.
Toxic nodular Goitre
In patients with autonomously functioning thyroid nodules, the thyroid scintigraphy shows one or more marked areas with high isotope uptake. Uptake in the normal paranodular thyroid tissue depends on the thyroid status. In patients with moderately hyper active ‘warm’ nodules, leading to subnormal serum TSH levels, some isotope uptake may be seen in the paranodular thyroid tissue (Figure 1a). In very hyperfunctioning ‘hot’ nodules, completely suppressing serum TSH, the remaining part of the thyroid may not be scintigraphically visualized. Thus, a toxic multinodular goitre (Figure 1b), sometimes being disconfigured due to nodular degeneration, may harbour coexisting hyperactive (warm/ hot) and hypoactive (cold) nodules, as well as hypofunctioning normal thy roid tissue. If the patient has been treated with antithyroid drugs for some time, achieving a normal serum TSH level, the isotope may be more uniformly distributed within the gland.
Fig1. Examples of thyroid scintigrams in various disorders. (a) Solitary warm nodule in the right thyroid lobe. (b) Toxic multinodular goitre with several hot nodules and suppression of the paranodular thyroid tissue. (c) Solitary cold nodule in the right thyroid lobe.
Since 131I therapy usually is a first line treatment in patients with one or more thyrotoxic nodules, scintigraphy is always indicated in such cases to confirm the presence of nodular functional autonomy. Importantly, Graves’ disease may develop de novo in a patient with nodular goitre. In fact, such a coexistence occurs in as many as 10– 15% of unselected hyperthyroid patients. Based on thyroid ultrasound only, the clinician may get the impression that the hyperthyroidism is due to a multinodular goitre rather than Graves’ disease (Figure 2). However, the presence of TSH- receptor antibodies, and a thyroid scintigraphy showing a more diffuse distribution of the isotope throughout the thyroid gland, will clarify the aetiology of the hyperthyroidism.
Fig2. Thyroid scintigraphy in a 57- year- old woman with Graves’ disease and coexisting multinodular goitre. From a euthyroid state 6 months earlier the woman became severely hyperthyroid due to Graves’ disease, which was confirmed by high serum levels of TSH- receptor autoantibodies. Thyroid ultrasound showed a classical bilateral multinodular configuration. The isotope is irregularly distributed as the immune stimulation affects nodular and paranodular tissue to a different extent.
Other Thyrotoxic conditions
Thyrotoxicosis characterized by a low thyroid isotope uptake is most often caused by subacute, silent, or postpartum thyroiditis. These conditions are discussed in section 3.3.
Exposure to excess iodine (e.g. X- ray contrast media) or amiodarone (an antiarrhythmic drug with high iodine content) sometimes leads to thyrotoxicosis. The very high whole- body iodine pool and the iodine load of the gland block for further thy roid iodine uptake. Therefore, the scintigraphy shows low or no thyroid isotope uptake. In fact, knowing that the patient has been exposed to iodine- containing agents, there is rarely indication for thyroid scintigraphy. The clearance of excess iodine, and especially of amiodarone, may take several months, with slow recovery of a normal thyroid function. If the thyrotoxicosis persists, thyroid scintigraphy may be indicated, provided the iodine exposure has ceased.
In patients who factitiously ingest thyroid hormones in excessive amounts, the thyrotoxic state and a faint thyroid scintigram will raise suspicion of thyroiditis. However, excess exogenous thyroid hormone leads to suppression and inactivation of the thyroid gland, reflected by low levels of serum Tg, while this biomarker is usually high in conditions with thyroiditis.
