[Iodine-induced subclinical hyperthyroidism in a patient with Hashimoto's disease].

Iodine is a particularly relevant element in thyroid gland physiology. Although healthy follicular cells have several mechanisms which allow them to adapt to marked changes in iodine provision, both iodine deficiency and excess may cause dysfunction in a diseased thyroid gland. A 26-year-old female patient with an unremarkable history attended her family physician reporting fatigue for several weeks previously. Her clinical symptoms spontaneously resolved, but a blood test showed subclinical hyperthyroidism, with TSH 0.258 U/mL and FT4 1.68 ng/100 mL. Diagnosis was confirmed one month later by values of TSH 0.015 and FT4 1.94 (Table 1). A physical examination at the endocrinology clinic revealed a palpable but not visible and nontender goiter of an elastic consistency. Ultrasound examination performed at this same time showed a slightly enlarged gland with no nodules or adjacent adenopathies. The patient had no exophthalmos or signs of eye inflammation, nor edema in the lower limbs, hands, or face. The examination was otherwise unremarkable. The patient had not had recent contact with iodinecontaining products, except that she usually consumed iodinated salt (approximately 3 g/day since the age of 18). She was recommended to stop using iodinated salt and a new test was performed two months later. This test showed subclinical hypothyroidism with elevated anti-peroxidase antibodies (Hashimoto’s disease). The persistence of this subclinical hypothyroidism was confirmed one month later (Table 1). The minimum daily iodine intake recommended for adults is 150 g (220 g for pregnant women).1 This amount is usually provided by diet in coastal areas, but daily intake is frequently lower in inland areas. Salt iodination (with 76 g iodine per gram) is a public health measure aimed at