Increased sensitivity to the inhibitory effect of excess iodide on thyroidfunction in patients with beta-thalassemia major and iron overload and thesubsequent development of hypothyroidism

Objective: Patients with beta-thalassemia frequently develop primary hypoth yroidism and other endocrine disorders due to iron overload. We studied whe ther administration of excess iodide to patients with apparently normal thy roid function could uncover an underlying thyroid disease. Design and methods: Twenty-five patients, 10 prepubertal (mean age 11 +/- 3 years) and 15 adults (mean age 23 +/- 5 years) with normal thyroid hormone and TSH levels, a normal response of TSH to TRH and negative thyroid perox idase antibodies received 20 mg iodide three times daily for three weeks, a nd thyroid hormone and TSH levels were measured weekly during, and for thre e weeks after, iodide administration and every 3 months thereafter for the next 5 years. Results: During iodide administration there was a significant decrease in t hyroid hormone concentrations which remained within normal levels, and a si gnificant increase in TSH concentrations which in 14 out of 25 (56%) patien ts reached the hypothyroid level. Baseline TSH values were higher in those patients who developed subclinical hypothyroidism (2.31 +/- 0.71 mU/l vs 1. 34 +/- 0.64 mU/l, P=0.0016), Subclinical hypothyroidism developed in 70% of prepubertal and in 47% of adult patients. Serum ferritin was elevated in a ll patients. Nine of the fourteen patients (64.3%) who developed subclinica l hypothyroidism during iodide administration developed hypothyroidism duri ng the 5-year follow-up compared with only one of the eleven patients with a normal response to iodide (P=0.004). Conclusions: Patients with beta-thalassemia should not be exposed to excess iodide due to increased sensitivity to its inhibitory effects on thyroid f unction. The susceptible individuals frequently develop permanent hypothyro idism in the following years.