SUN-581 An Unusual Presentation of Hypothyroidism

Introduction:  Hashimoto’s thyroiditis (HT) rarely presents with clinical myopathy, with elevated muscle enzymes and acute kidney injury (AKI) due to rhabdomyolysis. A pilot study has suggested an increased prevalence of subclinical hypothyroidism in patients with unprovoked deep venous thrombosis (DVT). We report a case of HT presenting with asymmetric myopathy, AKI, and bilateral lower extremity DVTs, who responded well to thyroid hormone replacement.  Case Description:  A 58-year-old man with history of psoriasis presented with new erythematous plaques over the trunk and extremities for one month. He had episodic numbness and heaviness in the arms, thighs, and hands, especially when he held objects for sometime (e.g. steering wheel or holding a cell phone). He had difficulty in getting up from a sitting position. He also felt that his calves were swollen. He experienced stiffness in the hands. On examination, he had an asymmetric decrease in muscle power (4/5) in the proximal muscles of the upper and lower extremities. He had small circumscribed psoriatic plaques on the elbows, knees, and trunks. In addition, bilateral pitting edema was noted. Laboratory evaluation was remarkable for elevated creatinine phosphokinase 2310 IU/L, aldolase 15.6 U/L, elevated serum creatinine at 1.34 mg/dl, and elevated CRP at 9.5 mg/dl.  Serological tests for connective tissue disease were all negative. Myositis associated and specific antibodies were negative. Electromyography was consistent with myopathic process with changes in numerous muscle groups bilaterally, most prominent in gluteus medius, lumbar, thoracic and cervical paraspinals. Nerve conduction study showed bilateral carpal tunnel syndrome.  Three weeks later, his lower extremity swelling worsened. Ultrasound venous dopplers revealed bilateral DVT in the posterior tibial and peroneal veins. Thyroid function tests revealed elevated TSH (103.26 micro-IU/mL) and low free T4 (0.22 ng/dl). He has elevated thyroid peroxidase and thyroglobulin antibodies. He was hospitalized for management of unprovoked DVT and severe hypothyroidism secondary to HT. He was started on levothyroxine. Four weeks later, the myopathy resolved and muscle enzymes normalized. TSH improved to 35 micro-IU/ML. Discussion:  HT presenting with clinical myopathy and DVT is extremely rare. Few features in this case raised the question of an alternative etiology for the myopathy – asymmetric proximal muscle involvement, acute to subacute course, and absence of myositis specific antibodies. In a pilot cross sectional study, increased prevalence of subclinical hypothyroidism was found in patients with unprovoked DVT, as noted in our case.  This case highlights the atypical presentation of hypothyroidism due to HT. The identification of the hypothyroidism and initiation of thyroid hormone replacement improved the quality of life and physical function in our patient.