**3. Procedures for radioiodine whole body imaging**

#### **3.1 Patients preparation**

Thyroid hormone replacement must be withheld for a sufficient time to permit an adequate rise of TSH (>30 uIU/mL). This is at least 2 weeks for triiodothyronine (T3) and 3–4 weeks for thyroxine (T4). This is also achieved by the administration of recombinant human TSH (rhTSH, Thyrogen®, given as two injections of 0.9 mg intramuscularly on each of two consecutive days) without stopping thyroid hormone replacement. rhTSH must be used in patients who may not have an elevation of TSH to the adequate level due to a large residual volume of functioning thyroid tissue or pituitary abnormalities, which precludes elevation of TSH. rhTSH might be used to prevent severe hypothyroidism related to the stopping of thyroid hormone replacement.(Silberstein, Alavi et al. 2005; Silberstein, Alavi et al. 2006)

All patients must discontinue eating/using iodide-containing foods or preparations, and other medications that could potentially affect the ability of thyroid cancer tissue to accumulate iodide for a sufficient time before radioiodine administration. A low-iodine diet is followed for 7–14 days before the radioiodine is given, as it significantly increases the uptake of radioiodine by the well differentiated thyroid cancer tissue. The avoided or permitted food items are summarized in table 1. The recommended time interval of drug withdrawal is summarized in

Ingested iodides are rapidly and nearly completely absorbed (>90%) from the duodenum into the blood and most of the iodides are excreted by kidneys. Sodium iodide symporter (NIS) on the apical membrane of enterocytes mediates active iodide uptake. Normally about one fifth of absorbed iodides are taken up by thyroid follicular cells and this is used for thyroid hormone synthesis, yet the clearance of circulating iodide varies with iodine intake. In the condition of an adequate iodine supply, ≤10% of absorbed iodides are taken up by the thyroid and in chronic iodine deficiency, this fraction can exceed 80%.(Zimmermann and Crill) The basal membrane of the thyroid follicular cell is able to actively transport iodide to the interior of the cell against a concentration gradient by the action of the NIS, which co-transports one iodide ion along with two sodium ions. The process of concentrating iodide in the thyroid follicular cells is called iodide trapping and presence of the NIS is essential for the process.(Hall 2011) Thyroid hormones are produced by oxidation, organification and coupling processes in

the thyroid gland and they are finally released into the blood stream for their action.

The rat NIS gene and the human NIS gene were cloned in 1996.(Dai, Levy et al. 1996; Smanik, Liu et al. 1996) NIS is a 13 transmembrane domain protein with an extracellular amino- and intracellular carboxyl-terminus and the expression of the NIS gene is mainly regulated by thyroid stimulating hormone (TSH). Binding of TSH to its receptor activates the NIS gene transcription and controls translocation and retention of NIS at the plasma

In addition to its expression in the thyroid follicular cells, NIS is detectable and active in some extrathyroidal tissues such as the salivary glands, gastric mucosa, lactating mammary glands, etc. Therefore, these tissues are able to take up iodide by the action of the NIS. However, contrary to thyroid follicular cells, there are no long-term retention of iodide and TSH dependency. (Baril, Martin-Duque et al. 2010) The physiologic function of the NIS in

Thyroid hormone replacement must be withheld for a sufficient time to permit an adequate rise of TSH (>30 uIU/mL). This is at least 2 weeks for triiodothyronine (T3) and 3–4 weeks for thyroxine (T4). This is also achieved by the administration of recombinant human TSH (rhTSH, Thyrogen®, given as two injections of 0.9 mg intramuscularly on each of two consecutive days) without stopping thyroid hormone replacement. rhTSH must be used in patients who may not have an elevation of TSH to the adequate level due to a large residual volume of functioning thyroid tissue or pituitary abnormalities, which precludes elevation of TSH. rhTSH might be used to prevent severe hypothyroidism related to the stopping of thyroid hormone replacement.(Silberstein, Alavi et al. 2005; Silberstein, Alavi et al. 2006) All patients must discontinue eating/using iodide-containing foods or preparations, and other medications that could potentially affect the ability of thyroid cancer tissue to accumulate iodide for a sufficient time before radioiodine administration. A low-iodine diet is followed for 7–14 days before the radioiodine is given, as it significantly increases the uptake of radioiodine by the well differentiated thyroid cancer tissue. The avoided or permitted food items are summarized in table 1. The recommended time interval of drug withdrawal is summarized in

**2.1 Iodine absorption and metabolism** 

**2.2 Sodium iodide symporter** 

membrane, and so this increases iodide uptake.

the extrathyroidal tissues is not yet clear.

**3.1 Patients preparation** 

**3. Procedures for radioiodine whole body imaging** 

table 2. Imaging should be delayed for a long enough period to eliminate the effects of these interfering factors. The goal of a low iodine diet and the drug withdrawal is to make a 24-hour urine iodine output of about 50 ug.(Silberstein, Alavi et al. 2006).


Table 1. Food guide for a low iodine diet. Some items on the allowed list may not be low in iodine in some forms or merchandise brands. The labels must be checked to be sure that the items meet the requirements of the low-iodine diet. (Amin, Junco et al.; Nostrand, Bloom et al. 2004)
