Poster Presentation ESA-SRB-ANZBMS 2024 in conjunction with ENSA

Thyrotoxic periodic paralysis: A case series and literature review (#582)

Yuhan A Goh 1 , Krishnamurthy Chikkaveerappa 1
  1. Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Murdoch, Western Australia, Australia

Aims: To describe two cases of thyrotoxic periodic paralysis (TPP) in Asian men with normal TSH receptor antibody (TRAB) levels, and review the literature.

Case 1: A 21-year-old Vietnamese male presented to the emergency department with falls and two-week history of intermittent bilateral lower limb myalgia and weakness. Biochemistry (Table 1) demonstrated severe hypokalaemia and overt thyrotoxicosis with negative TRAB. Power returned to baseline following correction of hypokalaemia. He was discharged on carbimazole and metoprolol, and represented three weeks later with relapsed TPP. Metoprolol was switched to propranolol. Technetium-99m (Tc-99m) pertechnetate thyroid scan demonstrated reduced uptake in keeping with thyroiditis (Figure 1A). Carbimazole was ceased and he was euthyroid on follow-up.

Case 2: A 21-year-old Filipino male presented to the emergency department with falls and two-month history of intermittent lower limb weakness upon waking. Biochemistry (Table 1) demonstrated severe hypokalaemia, overt thyrotoxicosis, elevated thyroid peroxidase (TPO) antibodies and normal TRAB levels. Tc-99m pertechnetate thyroid scan demonstrated diffuse uniform uptake consistent with Graves’ disease (Figure 1B). He was discharged on carbimazole and propranolol.

Discussion: TPP is characterised by periodic paralysis, hypokalaemia and thyrotoxicosis. Although thyroid disease is more common in females, TPP predominantly affects males of Asian descent aged between 20-40years (1), and Graves’ disease is the most common cause (1, 2). Patients typically present with recurrent, transient episodes of muscle weakness that usually affects the lower limb proximal muscles. Pathophysiology involves hormonal stimulation of muscle cell Na/K ATPase pump (influenced by thyroid hormone, insulin, catecholamines and androgens) inducing a massive intracellular shift of potassium (3, 4). Mutations in the gene encoding Kir2.6 potassium efflux channel are associated with TPP (5). Acute management involves cardiac monitoring, prompt potassium supplementation and non-selective beta blockade. Restoring euthyroid eliminates attacks of TPP, and patients should avoid precipitants including carbohydrate-rich meals and strenuous exercise.

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  1. Kung AW. Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge. J Clin Endocrinol Metab. 2006;91(7):2490-5.
  2. Chang CC, Cheng CJ, Sung CC, Chiueh TS, Lee CH, Chau T, et al. A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants. Eur J Endocrinol. 2013;169(5):529-36.
  3. Maciel RM, Lindsey SC, Dias da Silva MR. Novel etiopathophysiological aspects of thyrotoxic periodic paralysis. Nat Rev Endocrinol. 2011;7(11):657-67.
  4. Lin SH, Huang CL. Mechanism of thyrotoxic periodic paralysis. J Am Soc Nephrol. 2012;23(6):985-8.
  5. Ryan DP, Dias da Silva MR, Soong TW, Fontaine B, Donaldson MR, Kung AWC, et al. Mutations in Potassium Channel Kir2.6 Cause Susceptibility to Thyrotoxic Hypokalemic Periodic Paralysis. Cell. 2010;140(1):88-98.