Endocrine Abstracts

Thyrotoxic periodic paralysis (TPP) is a rare endocrine emergency where early diagnosis of both hypokalaemia and thyrotoxicosis are vital to allow prompt treatment to prevent life-threatening complications and prevent recurrences. We present the first reported case of TPP in which four known stimulants of Na–K–ATPase acted simultaneously to produce profound hypokalaemia. A 32 year-old competitive body-builder took thyroxine supplements & a long-acting β2 agonist, Clenbuterol and followed a strict diet, in preparation for a body-building competition. Following this, he went on an extreme food-binge lasting several hours. Several hours later, he developed bilateral lower limb weakness, which progressed over the next 15 hours. He attended the emergency department 24 hours after the onset of symptoms, with severe bilateral, symmetrical weakness of the lower limbs. He had no family history of thyroid disease or intermittent paralysis. Hypokalaemia of 2.3 mmol/l was found, dropping to 1.9 mmol/l in the presence of primary respiratory alkalosis (pH-7.44, pCO2-5.2). ECG showed features of hypokalaemia, including prolonged QT/QTc-intervals of 520 msec/640 msec, respectively. Hyperinsulinaemia was confirmed (276 pmol/l), with blood glucose of 7.4 mmol/l. TSH was suppressed (<0.02 mIU/l) indicating biochemical thyrotoxicosis, with normal free-T4 (12 pmol/l) and slightly reduced total-T3 (1.02 nmol/l). FSH & LH were both suppressed (<0.5 IU/l), total testosterone was normal (23.7 nmol/l) but oestradiol was elevated (224 pmol/l. Urine was screened using ultra-performance-liquid-chromatography, mass-spectrometry (UPLC-TOF-MS) for over 1300 drugs and metabolites & was positive for Clenbuterol & the anabolic steroids Trenbolone and Oxandrolone. From simultaneous samples we were thus able to document that hyperthyroidism, hyperinsulinaemia, β-agonist activity and alkalosis were all acting in concert in this patient, to stimulate Na-K-ATPase and cause significant hypokalaemia and profound muscle weakness. All four elements were entirely self-induced. Serum potassium normalised within 12-hours with parenteral potassium and fluid replacement, with return of full muscle power and normalisation of the ECG. The patient discontinued his thyroxine supplements and at outpatient review 1 month later, his thyroid-function tests were normal. This case outlines the vital necessity of checking thyroid-function tests & doing full medicines reconciliation in any patient presenting with hypokalemia and muscle weakness. It also highlights the possibility that competitive bodybuilders may constitute a unique ‘at-risk’ group for TPP by virtue of the supplements they take, which often include thyroxine and β-agonists.