Thyroid Protection Gone Awry: Iododerma Following Potassium Iodide Administration Prior to Metaiodobenzylguanidine Scintigraphy

Dear Editor:

Iododerma is a rare cutaneous eruption that usually presents as papulopustular or pustular lesions isolated to the face, neck, back, and extremities. It has been reported following potassium iodide (KI) treatment for asthma, chronic bronchitis, and Graves' disease, iodinated contrast media, and topical povidone-iodine (1). There has been one report of its occurrence after KI for thyroid protection during an iodide fibrinogen uptake test (2). Herein, we report iododerma after an inadvertent high dose of KI for thyroid protection during I¹²³ metaiodobenzylguanidine (MIBG) scintigraphy.

A 34-year-old man with Crohn's disease, who had undergone partial cecectomy and since treated with adalimumab, was referred for a nonfunctioning adrenal mass that had grown from 1.7 to 2.9 cm in 5 years. His history was negative for reactions to multiple computed tomographic scans with intravenous radiopaque contrast media, topical povidone-iodine, and food allergies. For thyroid protection, he was instructed to take two drops orally twice daily of KI, 1 g/mL, for 3 days prior to I¹²³ MIBG. He erroneously took 0.6 mL for two doses as it was the stated “usual dosage” on the manufacturer's bottle label. The next day, he noticed pustular lesions on his chest and back, associated with a subjective swelling of the throat without dyspnea or wheezing.

He had a pustular acneiform eruption on his chest but was otherwise unremarkable (Supplementary Fig. S1; Supplementary Data are available online at www.liebertonline.com/thy) with normal blood chemistries and complete blood count. Cessation of KI was accompanied by regression of skin lesions within 72 hours. Suspecting an additive in the KI to be responsible, prophylaxis was continued with two drops twice daily of Lugol's solution (containing both KI 100 mg/mL and iodine 50 mg/mL). The next day, I¹²³ MIBG scintigraphy was suggestive of a benign adrenal adenoma. Lugol's solution was continued for 3 days. Four days after imaging, the acneiform skin rash recurred and Lugol's was discontinued with resolution of the skin lesions. As the patient desired a definitive diagnosis, 3 weeks later he was challenged with three drops KI and within 6 hours the rash recurred. A skin biopsy (Supplementary Fig. S2) was performed. The clinical diagnosis of iododerma was made.

Saturated solution of potassium iodide is packaged with instructions for pulmonary indications suggesting doses as high as 300–600 mg three to four times daily. Such doses exceed those for any endocrine indication. Here, the clearly printed pharmacy drug label was ignored, and the manufacturer label was alternatively followed.

Previous reports vary in the time of occurrence after exposure to iodides. There is a 1936 case report and review of 10 fatal episodes by Hollander and Fetterman, and time to symptom onset was as early as after one dose. In contrast, symptoms have been delayed by up to a year of starting oral therapy with KI. The reported dosage and time of exposure are highly variable. There are varying manifestations of cutaneous reactions ranging from vegetating to ulcerating or blistering lesions. Following iodide prophylaxis in Poland after the Chernobyl reactor accident in 1986, only 1% of the population developed skin rashes. There were no reported cases of iododerma. However, these subjects received only a small dose of KI compared with our patient. Control values for the skin rash side-effect in a population not receiving KI were not studied (3).

Iodine is largely bound to protein in the blood, and this complex acts as a foreign antigen that induces what is thought to be a hypersensitivity reaction. A frequent presence of eosinophils in both cutaneous lesions and the peripheral blood in patients with iododerma has led to the hypothesis that an allergic mechanism underlies this disorder (1). However, these findings are not present in the majority of cases. The reason why this patient tolerated dietary iodine in common food items is unclear. Perhaps, an acute iodide load, as contained in KI or Lugol's, may precipitate iododerma in susceptible individuals. Alternatively, normal food consumption may complex low amounts of dietary iodine, preventing this reaction even in susceptible individuals.

No laboratory or histopathological finding is pathognomonic. Upon discontinuation of iodine use, skin lesions typically resolve in days to weeks, leaving only mild postinflammatory changes and possibly dermal atrophy (4). Systemic corticosteroids have been also used (5).

This case not only illustrates an adverse effect rarely encountered by endocrinologists but also reiterates the need for clear dosing instructions. Patients should receive explicit KI solution dosing instructions, because the manufacturer label states an alternate dose that exceeds any common endocrine indication.

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The views expressed in this article are those of the authors and do not reflect the official policy of the Department of the Army, Department of Defense, or U.S. Government.