Key result
Amiodarone-induced thyrotoxicosis can present as hypokalemic periodic paralysis, as demonstrated in a 34-year-old man whose weakness resolved immediately after potassium replacement therapy.
Case Report (n=1)
This case highlights that amiodarone-induced thyrotoxicosis can rarely present as hypokalemic periodic paralysis, which resolves with potassium replacement and antithyroid therapy.
Clinicians should consider thyrotoxicosis in amiodarone patients with acute weakness; single case leaves open true incidence and management.
Thyroid disorder is a well-recognized side effect of amiodarone therapy. Thyrotoxicosis is less common than hypothyroidism. Hypokalemic periodic paralysis is one manifestation of thyrotoxicosis, and is more often seen in Oriental and Latin American men than in other demographic groups. This phenomenon, however, has not been previously described in thyrotoxicosis due to amiodarone usage. We describe a case of amiodarone-induced thyrotoxicosis in a 34-year-old man who presented with sudden lower extremity weakness, heat intolerance, and weight loss. Physical examination demonstrated fine tremors. Serum potassium level was 2.2 mEq/L on admission. Gastrointestinal and renal causes of potassium loss were excluded by history and physical examination. Further biochemical testing demonstrated abnormal thyroid function. The urinary potassium and serum bicarbonate, magnesium, and calcium levels were within normal limits. Lower extremity weakness resolved immediately after potassium replacement therapy. Methimazole therapy was initiated, and the patient was clinically euthyroid on discharge.
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Laroia et al. (2002) conducted a case report in Amiodarone-induced thyrotoxicosis presenting as hypokalemic periodic paralysis (n=1). Amiodarone was evaluated on Hypokalemic periodic paralysis. Amiodarone-induced thyrotoxicosis can present as hypokalemic periodic paralysis, as demonstrated in a 34-year-old man whose weakness resolved immediately after potassium replacement therapy.
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