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Effect of Iodine Restriction on Thyroid Function

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In This Article

Abstract and Introduction

Patients and Methods

Results

Discussion

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Figures

Tables

References

Discussion Iodine excess is a well-known exogenous factor that

causes hypothyroidism. Iodine induces suppression of TSH-stimulated cyclic AMP

production and protein iodination in vitro.[12] Administration of excessive

amounts of iodine induces thyroiditis in genetically susceptible animal

strains.[13,14] Sundick et al.[15] reported that highly iodinated thyroglobulin

synthesized by animals fed a high iodine diet was more immunogenic than

thyroglobulin containing fewer iodine atoms.

According to Braverman et al.,[6] four of seven euthyroid patients with

Hashimoto's thyroiditis who were given a solution of potassium iodide (180 mg of

iodine) daily developed hypothyroidism after 4-8 weeks. Reinhardt et al.[7]

reported that seven of 40 patients with underlying Hashimoto's thyroiditis

living in an area of mild iodine deficiency given small amounts of iodine (250

µg daily) developed hypothyroidism.

The frequency of Hashimoto's thyroiditis in the reversible hypothyroidism

group 1 (11 of 21, 52.3%) determined on the basis of TgAb or TPOAb detection is

much higher than in healthy controls. Thus, patients with Hashimoto's

thyroiditis appear susceptible to the development of iodine-induced

hypothyroidism.[6]

As to the effect of administration of excess iodine to euthyroid subjects,

supplementary doses of 1,500 µg daily for 2 weeks caused a subtle but

significant increase in TSH concentrations.[16,17] In Japan, an area with high

dietary iodine, serum TSH concentrations increased significantly in response to

the administration of 27 mg of iodide for 28 days.[18]

In 1965, endemic goiter due to excessive intake of iodine was reported to

occur in coastal regions of Hokkaido, Japan.[19] Recently, iodine-induced

reversible hypothyroidism has been well documented mostly by Japanese

investigators.[1-5,8]

Reversible hypothyroidism occurs occasionally at the recovery phase of

postpartum hypothyroidism, subacute thyroiditis, and painless thyroiditis. Such

cases were excluded by the patients' history. Furthermore, in order to prove

that the iodine restriction was responsible for the recovery of the thyroid

function, we confirmed that all patients had persistent hypothyroidism by

evaluating thyroid functions at least twice before iodine restriction.

It is well known that the thyroid function in hypothyroid patients with

detectable TSH receptor antibodies, especially those with the blocking type, is

changeable.[11,20] There was one patient who was positive for TBII. She had

detectable TSAb and undetectable TSBAb, indicating that TSH receptor antibodies

do not appear to be involved in the manifestation of hypothyroidism.

In the present study, 21 of 33 patients (63.6%) with primary hypothyroidism

showed recovery of thyroid function. The frequency was similar to that reported

by other investigators: 12 of 22 (54.5%);[1] 49 of 116 (42.2%);[2] and 143 of

245 (58.4%).[3] It is very important for patients themselves to know whether

they have irreversible hypothyroidism, requiring life-long thyroid hormone

replacement therapy, or not. If they have permanent hypothyroidism, iodine

restriction, which may not be beneficial for their health, is not necessary.

Thus, we have focused on the possible parameters that were predictive of the

development of iodine-induced hypothyroidism. There was a good correlation

between 99mTc uptake values and aTSH/bTSH ratios. 99mTc uptake values were

significantly higher in group 1 (reversible) than in group 2 (irreversible). In

accordance with the previous studies in which radioactive iodine uptake was

measured,[1,2] determination of 99mTc uptake also predicted the patients'

prognosis. The radioactive iodine uptake test is usually carried out after 1

week of restriction of iodine intake, when the thyroid function of the patients

with iodine-induced hypothyroidism may be partially recovered. In contrast, the

99mTc uptake test can be carried out even at the patients' first visit. The

significant correlation of 99mTc uptake with initial TSH values and with

aTSH/bTSH values indicates that the responsiveness of the thyroid gland to

endogenous TSH is preserved in spite of the impaired intrathyroidal

synthesis of thyroid hormone in reversibly hypothyroid patients with increased

99mTc uptake. In contrast, it is conceivable that autoimmune destruction of the

thyroid is severe enough to cause an impaired response to TSH in irreversibly

hypothyroid patients with decreased 99mTc uptake.[1] In the present study, seven

of 12 (58.3%) patients in group 2 (irreversible hypothyroidism) had Hashimoto's

thyroiditis as judged from TgAb and TPOAb titers. Although it is inexplicable

why the remaining five patients, especially patients 29 and 31, had irreversible

hypothyroidism, undetectable TgAb and TPOAb in serum do not appear to be

predictive of favorable response to iodine restriction, in agreement and

disagreement with the previous studies [Tajiri et al.[1] and Okamura et al.,[2]

respectively].

Hypoechogenicity of the thyroid is known to be a marker of autoimmune

destruction,[21] supporting the diagnosis of Hashimoto's thyroiditis in most

patients with irreversible hypothyroidism. However, there was no significant

difference between the reversible and irreversible hypothyroid groups, in

disagreement with the previous study,[5] since there were a considerable number

of patients with hypoechogenicity in the reversible hypothyroid group,

presumably due to hyperplastic epithelial changes.[8] Thus, the echogenicity

does not appear to predict the spontaneous recovery of thyroid functions.

The free iodine measurement may be helpful for prediction of prognosis of

reversible hypothyroidism to some extent, since the free iodine levels roughly

correlated with aTSH/bTSH values, and they were significantly higher in group 1

(reversible) than in group 2 (irreversible). However, the iodine measurement can

be replaced by inquiring of the patients whether they habitually ingest seaweed

products or not. What is important is that the thyroid function recovered

spontaneously irrespectively of the initial free iodine levels, since the

seaweed had been ingested occasionally or every day and was restricted strictly

in patients with reversible hypothyroidism.

We assume that escape of the Wolff-Chaikoff effect (inhibition of organic

binding of iodide in the thyroid by excess iodide intake) may not occur or the

serum iodine levels to cause escape may be elevated, at 5-100 µg/dL in our

cases, for unknown reasons. This phenomenon does not necessarily relate to

Hashimoto's thyroiditis, since 10 of 21 (47.6%) patients in group 1 had no

findings to support the clinical diagnosis of Hashimoto's thyroiditis. In this

regard, Mizokami et al.[8] proposed a new type of hypothyroidism, which is

pathophysiologically similar to adenomatous goiter.

In conclusion, hypothyroidism observed in patients with high 99mTc uptake and

non-hormonal iodine levels and undetectable or low titers of TgAb and TPOAb can

be reversed, and we recommend starting thyroid hormone replacement therapy in

those who are considered to have advanced Hashimoto's thyroiditis and history of

infrequent ingestion of iodine-containing foods.

R

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