Radioiodine is indicated for the treatment of hyperthyroidism caused by a hyperfunctioning nodule or a toxic MNG (295 [EL

4]). The aims of radioiodine treatment are ablation of the autonomously functioning areas, restoration of euthyroidism, and
reduction of goiter size (296 [EL 4-guidelines],297 [EL 3],298 [EL 4-guidelines]). AFTNs are usually more radioresistant than
toxic diffuse goiters, and greater radiation doses may be needed for successful treatment, especially in countries with iodization
programs leading to decreased radioactive iodine uptake (225 [EL 3],299 [EL 3]).
Radioiodine therapy normalizes thyroid function in 85 to 100% of patients with hyperfunctioning thyroid nodules or toxic
MNGs (295 [EL 4]). After treatment, the thyroid volume generally decreases substantially (median decrease, 35% at 3 months
and 45% at 24 months) (297 [EL 3],300 [EL 2]). Radioiodine treatment is generally thought to be effective and safe. Although
some investigators have indicated that radioiodine treatment may be associated with increased cardiovascular and cancer death
(301 [EL 2]), other large-scale epidemiologic studies have demonstrated discordant results (302 [EL 3]). Based on recent data,
both increased morbidity (303 [EL 2]) and mortality (268 [EL 2]) rates are more likely related to the disease rather than its
therapy.
After ablation of the autonomous tissue, most patients become euthyroid because of residual normal thyroid tissue, which is no
longer suppressed. Nevertheless, depending on the dose of radioiodine used, follow-up of thyroid function, and the possible
presence of autoimmune thyroiditis, postradioiodine hypothyroidism may develop in up to 60% of patients after 20 years (295
[EL 4],304 [EL 3]). In up to 5% of patients, immunogenic hyperthyroidism may result from radioiodine treatment of toxic or
nontoxic nodular goiter (305 [EL 3],306 [EL 3]) because of induction of TRAbs (307 [EL 3]), typically occurring 3 to 6 months
after radioiodine treatment.
Ingestion of drugs with high iodine content (e.g., amiodarone, a saturated solution of potassium iodide) should
Radioiodin diindikasikan untuk mengobati hipertiroid yang disebabkan oleh fungsi nodul yang berlebihan atau toksik dari
MNG. Tujuan dari terapi radioiodin adalah ablasi area yang berfungsi secara otonom, memperbaiki
eutiroidsm, dan mereduksi ukuran struma.
be avoided before radioiodine administration so as not to impair radioiodine uptake by the thyroid. If possible,
antithyroid drugs (especially propylthiouracil) (308 [EL 2]) should be withdrawn at least 1 week before
treatment to prevent radioiodine uptake by normal thyroid tissue and increase uptake in the hot thyroid tissue.
Use of antithyroid drugs during the first week after radioiodine therapy also decreases radioiodine treatment
efficacy. However, it also decreases biochemical and clinical hyperthyroidism and complications such as atrial
fibrillation (309 [EL 1]).
Radioiodine treatment is best suited for small- to medium-sized benign goiters, for patients previously treated
surgically, those with serious comorbid conditions, and those who decline surgery (295 [EL 4]). However,
radioiodine is not suited for large nodules that require high doses of radioiodine and that may be unresponsive to
treatment or for situations when immediate resolution of hyperthyroidism is desired (295 [EL 4]). The only
absolute contraindications to radioiodine treatment are breastfeeding and pregnancy, which should be excluded
by a pregnancy test (295 [EL 4],297 [EL 3],298 [EL 4-guidelines]). There is no consensus on a lowest age limit
for receiving radioiodine treatment (310 [EL 2]).
The use of radioiodine for the treatment of nontoxic nodular goiter has been reported in numerous studies from
geographic areas with relatively low to high-normal dietary intake of iodine (223 [EL 4-review],295 [EL 4],311
[EL 3],312 [EL 4]). No studies comparing radioiodine therapy given with or without dietary iodine restriction
have been published.
In general, a 40 to 50% decrease in thyroid size after 1 year (295 [EL 4],311 [EL 3],313 [EL 3],314 [EL 1]) and
a 50 to 60% decrease after 3 to 5 years can be achieved with radioiodine therapy (315 [EL 4-review]), half of
which is seen within 3 months (295 [EL 4]). The degree to which goiter volume decreases varies greatly, and
20% of patients do not seem to respond at all. In a randomized study (314 [EL 1]), LT 4 had no effect, whereas
radioiodine decreased goiter size by 50% after 1 to 2 years. In very large goiters (>100 mL), volume decreased
by only 30 to 40% after 1 year, and the amount of decrease inversely correlated with initial goiter size (316 [EL
4],317 [EL 3]). Theoretically, the effect of radioiodine depends on the retained dose in the thyroid. Radioiodine
activities have generally been adjusted according to radioiodine uptake, aiming at an absorbed dose of 100 Gy
(295 [EL 4],302 [EL 3],316 [EL 4]), but investigators have questioned whether this adjustment is worthwhile
(318 [EL 3]). Because of regulations regarding allowed radiation doses, which vary considerably between
countries, many physicians use fixed doses limited to the maximum outpatient activity to avoid hospitalization.
Use of radioiodine usually improves symptoms and respiratory function (316 [EL 4],317 [EL 3],318 [EL 3],319
[EL 2]).
Early adverse effects of radioiodine are generally mild and transient (295 [EL 4],312 [EL 4]). They include
radiation thyroiditis in approximately 3% of cases, transient thyrotoxicosis in 5%, and occasionally an increase
in thyroid size of up to 25%. Late adverse effects are currently limited to hypothyroidism in 22 to 58% of cases
within 5 to 8 years after therapy. Although the risk of malignancy is not generally thought to be increased, no
large-scale studies have been conducted in patients with nontoxic goiter as opposed to toxic goiter. No studies
have compared radioiodine therapy with surgery, and there are few quality-of-life studies using a validated
thyroid-specific quality-of-life questionnaire (320 [EL 2], 321 [EL 2], 322 [EL 4]).
The use of recombinant human TSH (rhTSH) for nontoxic goiter is currently off-label. The main reason for
using rhTSH is based on a desire to increase radioiodine uptake in the large number of patients with low uptake
and to decrease extrathyroidal radioiodine uptake, thereby decreasing the risk of malignancy and facilitating a
decrease in goiter size (295 [EL 4],312 [EL 4],323 [EL 1]).
The optimal dose of rhTSH and its timing in relation to subsequent radioiodine therapy are not clear. Recent
data, however, suggest that radioiodine uptake is doubled with use of rhTSH doses as small as 0.03 to 0.1 mg
without an evident dose-response relationship (295 [EL 4],324 [EL 4-review]). Activation of the thyroid
sodium-iodine symporter takes time, and an interval of 24 to 48 hours between rhTSH stimulation and
radioiodine administration seems optimal (295 [EL 4],312 [EL 4],323 [EL 1]). When used in combination with
radioiodine therapy, rhTSH decreases goiter volume 35 to 56% more than nonstimulated radioiodine therapy
(316 [EL 4],325 [EL 1],326 [EL 3]). It also improves respiratory function (315 [EL 4-review],316 [EL 4]).
However, it is unclear whether its use increases patient satisfaction (325 [EL 1]). The goiter-decreasing effect
increases with greater thyroid size, in contrast to the effect without rhTSH prestimulation. Thus, it is possible to
reduce radioiodine activity in correspondence with the increase in radioiodine uptake obtained with rhTSH
stimulation while achieving the same decrease in goiter size. This decreases radioiodine activity and thereby
decreases the theoretical risk of extrathyroidal malignancy. The induction of transient dose-dependent
hyperthyroidism is the main adverse effect, starting 4 to 8 hours after rhTSH injection and peaking after 24 to 48
hours, with normalization within 3 weeks. With rhTSH doses 0.1 mg, thyroid hormone levels are maintained
within the reference range in most patients (321 [EL 2]), with no alterations in structural or functional
parameters of the heart (327 [EL 3]). Acute (within 24-48 hours) dose-related swelling of the normal thyroid has
been demonstrated with an increase in mean thyroid volume of 35% with 0.9 mg rhTSH, 24% with 0.3 mg
rhTSH, and 10% with 0.1 mg rhTSH (319 [EL 2],320 [EL 2]). Therefore, the optimal rhTSH dose seems to be
0.1 mg (328 [EL 1],329 [EL 3]).