Poster Presentation The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2017

Thyrotoxic periodic paralysis: an under-recognised complication of thyrotoxicosis (#248)

Senthil Thillainadesan 1 , Shamasunder Acharya 1
  1. John Hunter Hospital, New Lambton, NSW, Australia

Thyrotoxic Periodic Paralysis(TPP) remains an under-recognised complication of thyrotoxicosis marked by episodes of severe hypokalaemia associated with profound weakness. If undiagnosed and untreated it can have fatal outcomes. 

Case 1: A 19-year-old Caucasian male presented with recurrent episodes of sudden severe weakness resulting in paralysis. He was extensively investigated previously with MRI spine and nerve conduction studies.  On his 3rd presentation, his potassium was found to be 1.8mmol/l. Thyroid function test demonstrated severe thyrotoxicosis(TSH-<0.03mIU/L, FT4-61.7pmol/l, FT3- >46.1pmol/l). TSH Receptor antibody(TRAB) level was >40U/L, with diffuse increased uptake(ratio–66) on Technetium scan.  He was promptly treated with potassium replacement, carbimazole and propranolol with good recovery.

Case 2: A 39-year-old Polynesian male presented with acute onset weakness at 2am resulting in a fall whilst getting out of bed. Potassium level was 1.8mmol/l initially, Weakness recovered after potassium replacement. He represented a week later with periodic paralysis(potassium-2.4mmol/l) and was noted to be thyrotoxic(TSH-<0.03mIU/L, T4-26.5pmol/l, T3-10pmol/l). TRAB level was 2.3U/L(reference<2.0) in keeping with Graves’ disease. He was treated with Carbimazole and then radioiodine ablation. He never had further episodes of periodic paralysis.

TPP is seen more frequently in Asian populations but has been reported across the world.(1,2) Graves’s disease is the most common cause.(1) TPP often occurs on walking from sleep after triggers such as carbohydrate ingestion, infections and strenuous exercise.(3,4) Severe hypokalaemia in TPP, can precipitate life threatening arrhythmias. Hypokalaemia in TPP may be caused by increased intracellular potassium influx via the Na+/K+-ATPase and reduced efflux through potassium channels due to effects of thyroid hormone, catecholamines and insulin.  Management of TPP requires potassium replacement with close monitoring due to risk of overcorrection. Non-selective betablockers appear to be beneficial in preventing episodes of TPP while thyrotoxicosis is being treated.(3) Definitive treatment of hyperthyroidism is indicated in most cases to prevent recurrence of TPP.


  1. Chang C-C, Cheng C-J, Sung C-C, Chiueh T-S, Lee C-H, Chau T, Lin S-H. A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants. European Journal of Endocrinology 2013; 169:529-536
  2. Kung AW. Thyrotoxic periodic paralysis: a diagnostic challenge. The Journal of Clinical Endocrinology & Metabolism 2006; 91:2490-2495
  3. Falhammar H, Thorén M, Calissendorff J. Thyrotoxic periodic paralysis: clinical and molecular aspects. Endocrine 2013; 43:274-284
  4. Manoukian MA, Foote JA, Crapo LM. Clinical and metabolic features of thyrotoxic periodic paralysis in 24 episodes. Archives of Internal Medicine 1999; 159:601-606