Paralysed by hyperthyroidism: a rare case of graves

Suhail Abdul-Wahab; Natalie Vanderpant; Beenish Masood; Rishi Iyer; Sulmaaz Qamar; Sam Baxter; Bernard Khoo; Eleni Armeni; Ahmed Yousseif; Efthimia Karra; Dipesh Patel

doi:10.1530/endoabs.109.P269

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Endocrine Abstracts (2025) 109 P269 | DOI: 10.1530/endoabs.109.P269

SFEBES2025 Poster Presentations Thyroid (41 abstracts)

Paralysed by hyperthyroidism: a rare case of graves’ thyrotoxicosis and thyrotoxic periodic paralysis

Suhail Abdul-Wahab ¹ , Natalie Vanderpant ¹ , Beenish Masood ¹ , Rishi Iyer ¹ , Sulmaaz Qamar ¹ , Sam Baxter ¹ , Bernard Khoo ^1,2 , Eleni Armeni ¹ , Ahmed Yousseif ^1,2 , Efthimia Karra ^1,2 & Dipesh Patel ^1,2

Author affiliations

¹Royal Free London NHS Foundation Trust, London, United Kingdom; ²University College London, London, United Kingdom

Background: Thyrotoxic periodic paralysis (TPP), a rare but serious complication of untreated or poorly managed hyperthyroidism, characterized by hypokalaemia and muscular weakness

Case history: A 25 year-old male of mixed White-Asian background presented with 8-10hr history of limb weakness and chest discomfort. His profound limb weakness made him unable to mobilise out of bed. He had a 4-year history of autoimmune thyrotoxicosis, treated with Carbimazole 20 mg OD and Propranolol 40 mg BD. He had stopped treatment 3 weeks prior due to personal stress. On examination, he had fine tremors, irregular pulse, normal JVP without oedema or cardiac murmurs. Neurologically, GCS was 15, with intact cranial nerves, reduced upper limb power (3/5 bilaterally), lower limb power (2/5 bilaterally), exaggerated reflexes, and inability to complete the finger-nose test due to weakness. ECG showed Mobitz type II conduction block and ST depression in lateral leads. He had severe hypokalaemia; K+ 1.8 mmol/l, with sodium 142 mmol/l, magnesium 0.84 mmol/L and glucose 7.4 mmol/l, TSH <0.01 mU/l, freeT4 48.9 pmol/l, and freeT3 15.0 pmol/l. Cardiac markers were normal (troponin 11 ng/l, NT-proBNP < 50 pg/mL). His TSH-RAb and anti-TPO antibodies were elevated at 2.45U/L and 574U/mL respectively. His K+ improved to 2.9 after 40mmol of IV potassium. Further 40mmol of IV made is K+ 4.77, the muscle weakness improved and ECG reverted to normal-sinus-rhythm. Muscle power regained completely within 18-24 hours. His Carbimazole and Propranolol were re-instated.

Discussion: Early recognition and treatment of TPP is critical to prevent cardiac complications. Acute management includes oral or IV potassium with close monitoring of blood levels due to rebound hyperkalaemia risk. Non-compliance is a significant risk factor for the recurrence of thyrotoxicosis and its complications. Long-term management should focus on achieving euthyroidism to prevent recurrence, with discussion of definitive treatments.