LAUSR

Thyrotoxic hypokalemic periodic paralysis (THPP) is an uncommon disease characterized by acute onset of lifethreatening hypokalemia and disabling muscle weakness due to the excessive release of thyroid hormone [1]. In Caucasians, the prevalence is very low, about 0.1% of hyperthyroid patients [2]. THPP is more common in Asians with a prevalence of 2% of hyperthyroid patients [3]. Hypokalemia is due to potassium shift into the cells by Na–K–ATPase activity increased during thyrotoxicosis [1]. THPP could be misdiagnosed in Western countries because of its similarities to familial hypokalemic periodic paralysis (FHPP), a disorder caused by a genetic defect of a calcium channel subunit [2]. We describe a case of an Italian Asian male with periodic paralysis as early manifestation of thyrotoxicosis. A 23-year-old man was admitted to the emergency room of our Hospital for a complete flaccid quadriparesis arising during the night. No significant familial and personal past medical history was reported. At physical examination, pulmonary and abdominal systems were normal and only tachycardia was found. An electrocardiogram showed a regular sinus tachycardia. A head CT-scan was negative for any acute cerebral injury. Laboratory investigations revealed a potassium of 1.64 mmol/L (reference range 3.5–5), everything else was normal; an intravenous administration of potassium chloride was immediately started. The day after, the patient was admitted to our Internal Medicine and Endocrinology Department. Vomiting, diarrhoea, drug, and alcohol abuse were excluded. He reported a 40 lbs weight loss in the last 5 months despite an increased appetite. Laboratory assays showed no general and electrolyte abnormalities. Thyroid function testing revealed a suppressed thyroidstimulating hormone (TSH) (< 0.005 μIU/L; 0.25–5) with elevated-free T3 (23.4 pg/mL; 2–3.85) and free T4 (6.64 ng/ dL; 0.93–1.7). Thyroid autoantibodies’ assays showed an elevated TSH-receptor antibody (> 40 IU/L; < 0.55), thyroglobulin antibody (247 UI/mL; < 115), and thyroid peroxidase antibody (382 UI/mL; < 34). Finally, a Thyrotoxic periodic hypokalemic paralysis associated with Graves’ thyrotoxicosis was diagnosed. The ultrasound scan revealed a heterogeneous enlarged thyroid gland without masses confirming Graves’s disease. The patient was started on methimazole 30 mg/die and propranolol therapy; he was discharged 3 days later without recurrence of weakness. The patient was euthyroid 1 month after methimazole was started and had no other paralysis episodes. Subsequent analysis of the most common mutations in the gene coding for the calcium channel 1-subunit (CACNA1S), responsible for the FHPP, was normal as expected. THPP is a potentially life-threatening disorder and can be the only initial presentation of thyrotoxicosis. THPP is a very rare condition in Western countries, but it has to be considered in the differential diagnosis of acute paralysis with preserved consciousness, to rapidly administer definitive treatment and improve patients’ outcome. In consideration of the constant increase of Asian population in Western countries, we think that it is important to be aware of this rare condition to correctly diagnose and treat THPP and prevent associated mortality and morbidity, mainly due to cardiac arrhythmias.