A Treatable Reason of Myopathy: Hypothyroidism

Abstract

Dear Editor, Various neurologic complications may be seen in thyroid disorders. These complications may include cranial and peripheral nerve disorders, cerebellar ataxia, encephalopathy, coma, seizures, sleep disorders and myopathy. Both hyperthyroidism and hypothyroidism may lead to myopathy manifestation. Proximal muscle weakness, muscular pain on exercise, pseudohypertrophy due to muscle edema, decreased deep tendon reflexes, and stiffening in muscles are seen in hypothyroidism myopathy (1). Increased creatine kinase (CK) levels have been reported depending on the severity of the disease (2). The aim of the treatment is euthyroidism of the patient. A complete clinical and biochemical improvement is achieved in most patients. Although occasionally improvement of the myopathy picture takes longer, the average duration of CK levels to return back to the normal values has been reported as 2 to 12 weeks (3,4). A 28-year-old female patient presented with the symptoms of leg pain, fatigue, weakness, and difficulty in climbing up stairs for about 15 days. A neurologic examination revealed mild paresis in proximal muscles. Deep tendon reflexes were hypoactive. Bilateral plantar reflex revealed the Babinski sign. In biochemical examination CK was found as 10535 U/L, and thyroid stimulating hormone (TSH) as 32.38 µIU/mL (Table 1). Electromyography showed findings compatible with mild myogenic exposure in proximal muscles (Table 2). With L-thyroxine therapy, CK and TSH values were dramatically decreased and returned to normal at the second month of treatment as CK: 120 U/L and TSH: 2.68 µIU/ mL, and a complete clinical improvement was observed. Our