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Iodide‐induced hypothyroidism in patients after thyroid resection
Author(s) -
CLARK O. H.,
CAVALIERI R. R.,
MOSER C.,
INGBAR S. H.
Publication year - 1990
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1990.tb01903.x
Subject(s) - euthyroid , iodine , medicine , endocrinology , basal (medicine) , thyroid , iodide , hormone , wolff–chaikoff effect , thyroidectomy , chemistry , organic chemistry , insulin
. The purpose of this investigation was to determine whether an intrinsic defect in thyroid hormone production is required for the development of iodide‐induced hypothyroidism or does it also develop in TSH‐stimulated normal thyroid tissue. To answer this question, we studied the response to iodine administration (180 mg iodide daily for 3–4 months) in eight euthyroid patients who had had partial thyroidectomies 2 months to 10 years previously for benign thyroid nodules, and in three euthyroid control subjects. In all 11 euthyroid patients, basal serum TSH concentrations increased during iodide administration. In six of the eight patients who had previous thyroid operations and in two of the three control patients, basal serum TSH concentrations increased into the abnormal range (greater than 6 U ml ‐1 ). Increased serum TSH concentrations were noted as early as 1 week after potassium iodide had been started and the increased levels persisted during the period of iodide administration. Although basal values for serum TSH concentration were initially within the normal range, those patients with highest basal serum TSH values developed the greatest increase in TSH in response to potassium iodine. Among the eight patients treated by partial thyroidectomy, serum T 4 concentrations decreased in five, serum T 3 concentration decreased in three and all five developed mild symptoms of hypothyroidism while receiving iodide. Serum T 4 concentrations also decreased slightly in two of the three control patients. Serum total iodine levels increased from 70pM 0.5 to 315.7 pM 108.6 g dl ‐1 (mean‐pM standard error) during potassium iodide administration, but there was no correlation between the level of serum iodide concentration achieved and inhibition of thyroid function. When iodide was discontinued, symptoms disappeared and thyroid function tests returned to baseline levels within 1 month in all patients, It thus appears that a restricted thyroid mass and/or a mild increase in TSH stimulation is all that is required for the development of hypothyroidism in man when exposed to excessive iodide.