Abstract

Thyroiditis, or self-limiting inflammation of the thyroid gland consists of 3 phases: hyperthyroidism, from release of hormone from damaged cells; hypothyroidism, when thyroid stores are depleted and euthyroidism with restoration of thyroid function. Etiology can include infectious, drug-induced or autoimmune causes such as multiple sclerosis (MS). In fact, 20-25% of untreated MS patients have autoimmune thyroiditis [1]. Moreover, drugs used to treat MS such as alemtuzumab and interferon have been reported to cause thyroid disease [2]. A 42-year-old female with MS on natalizumab for 10 years presented with right sided neck pain radiating to her jaw for 3 months and difficulty swallowing. Family history was pertinent for hypothyroidism in her father, and MS in her brother. She was exposed to nuclear radiation at age 3 from the Chernobyl disaster. On presentation, vital signs and physical exam were unremarkable. Thyroid ultrasound noted an ill-defined 4.2X1.3X1.9 cm hypoechoic nodule in the right mid-pole. Fine needle aspiration of the nodule showed subacute granulomatous thyroiditis (SAH). Labs showed TSH 0.02mIU/L [0.4-4.5], FT4 1.5ng/dL [0.8-1.8] and elevated total T3 204ng/dL [76-181]. TSI< 89 [140%]. Naproxen was given for pain control. Repeat labs 1 month later showed TSH 0.83mIU/L, FT4 1.1 ng/dL and total T3 196ng/dL, consistent with resolution of thyroiditis and clinically correlated with resolution of her pain. However, a month later she presented with worsening left sided neck pain and left thyromegaly associated with speech difficulty, diaphoresis, and constipation. Repeat thyroid ultrasound showed decreased size of right thyroid nodule 1.1X1.1X0.9cm and findings consistent with thyroiditis. She was treated with prednisone with complete resolution of symptoms. Labs post treatment showed elevated TSH 6.01mIU/L, total T3 106ng/dL, and FT4 0.8ng/dL consistent with the recovery phase of thyroiditis. Anti-TPO antibody level was < 1 [< 9 IU/mL]. Labs 1 month later showed normal TSH and FT4 levels. Natalizumab, a humanized monoclonal antibody commonly used to treat MS, has rarely been associated with thyroid disease. Alterations in thyroid function are thought to be due to direct toxicity on the thyroid, its blood supply or indirectly mediated by the immune system [2]. Although MS can be associated with thyroiditis, our patient did not present with the typical pattern of thyroiditis. Instead, she reported symptoms consistent with inflammation of one lobe of thyroid followed by resolution, and thereafter developed inflammation and pain of the other lobe, raising suspicion of potential involvement of natalizumab due to her atypical presentation.

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