A case of psoriasis exacerbated by radioactive iodine therapy.

Dear Editor:

Psoriasis is a chronic inflammatory skin disease that is characterized by erythematous, sharply demarcated papules and plaques covered by scales. Although the exact causes of psoriasis still remains obscure, it is known that genetic, immunological, and environmental factors contribute to its etiopathogenesis. Several factors such as trauma, stress, infections, and medications may exacerbate psoriasis. The most common medications known to trigger or worsen existing psoriasis include lithium, gold salts, beta blockers, and antimalarials. Exacerbation of psoriasis due to medications such as adrenergic antagonists, interferon, gemfibrozil, iodine, digoxin, and chlonidine has also been observed1. Radioactive iodine (RAI) therapy has been used for the remnant ablation and adjuvant therapy of thyroid cancer. The mechanism of RAI treatment is as follows: the thyroid gland needs iodine and absorbs it from the bloodstream, and then radiation destroys both cancerous and normal thyroid cells. Herein, we report the first case of psoriasis exacerbated by RAI therapy.

A 32-year-old Korean woman presented with a 5-day history of erythroderma with papules and pustules on the whole body. On general inspection, generalized, scaly erythroderma with papules and pustules was observed (Fig. 1). She had a history of psoriasis for about 20 years and had undergone systemic narrow band ultraviolet (UV)-B phototherapy.

Fig. 1

Generalized, scaly erythroderma with papules and pustules was observed on the arm (A) and abdomen (B) 5 days after radioactive iodine therapy.

She received a diagnosis of papillary thyroid cancer and underwent total thyroidectomy 14 months previously. She was scheduled to have RAI therapy for thyroid cancer and was treated with phototherapy for psoriasis for up to 2 days before RAI therapy. Since then, she had applied topical steroid and calcipotriol ointment for the treatment of psoriasis. Five days after RAI therapy, erythroderma with papules and pustules developed over her whole body. Thus, this case was diagnosed as psoriasis exacerbated by RAI therapy. She applied topical desonide lotion and calcipotriol cream for 3 weeks, and clinical improvement was observed. She restarted to undergo systemic narrow band UV-B phototherapy for the treatment of psoriasis.

Shelley2 reported two cases of generalized pustular psoriasis induced by potassium iodide. Kaufman3 observed that iodine/iodides specifically activate the enzyme dihydrofolic reductase. Methotrexate and aminopterin, as folic acid analogues, bind this enzyme, which blocks the metabolic steps in the synthesis of deoxyribronucleic acid and also blocks cell division4,5. Thus, activation of dihydrofolic reductase is associated with aggravation of the disease and inactivation associated with remission. This suggests that dihydrofolic reductase plays an important role in the pathogenesis of pustular psoriasis.

We suspected that the mechanism in this case was related to the activation of dihydrofolic reductase through RAI. Further study about the folic acid pathway in psoriasis and the connection between RAI and psoriasis may be necessary.