Endocrine Abstracts

Case history: Thyrotoxic periodic paralysis (TPP) which was first described in 1902 is characterised by episodes of painless muscle weakness, hypokalaemia and thyrotoxicosis without any total body potassium deficit. It predominantly affects people of Asian descent between 20 and 40 years old with a 2 percent incidence compared to 0.2 percent in non-Asian descent. The pathogenesis of TPP is related to an increase Na+/K+-ATPase activity in the skeletal muscle leading to an influx of potassium into cells. Here we present a rare case of TPP and his progress. A 22 year old Caucasian gentleman presented to Emergency Department (ED) with quadriplegia. He was found to have severe hypokalaemia (1.6 mmols/l) in the context of a normal magnesium/calcium. Despite no signs and symptoms of hyperthyroidism, his thyroid function test (TFT) showed a free T4 of 51 and TSH of <0.01. He was commenced on 30 mg carbimazole once a day. However, he represented 2 days later with paraplegia and his potassium was 2.6 mmols/l. On both occasions, his symptoms improved within 6–8 hours independent of intravenous potassium treatment.

Results and treatment: 16 weeks into his treatment; he remains asymptomatic with no associated symptoms of thyrotoxicosis and further episode of hypokalaemia. His antibodies were positive (both thyroid peroxidase antibodies and TSH receptor antibodies). Thyroid uptake scan showed evidence of generalised overactive thyroid with no focal lesion. With carbimazole treatment, his thyroid function normalised. He eventually underwent a near total thyroidectomy around 8 months into treatment. Currently, he is doing well on 125 micrograms of levothyroxine.

Conclusions and points for discussion: Intravenous (IV) potassium during a crisis is crucial for accelerated recovery. The main concern is rebound hyperkalaemia as the patient is not depleted in total potassium. Beta-blockers such as oral propranolol prevent adrenergic stimulation of Na+/K+-ATPase activity by reducing the influx of potassium into cells. Potassium supplements between attacks as prophylaxis are not useful. Once the thyrotoxicosis is under control, offer definitive treatment options such as radioactive iodine therapy or thyroidectomy to avoid future relapses.

Clinical questions:: A) Considering his hyperthyroidism was fully asymptomatic and only presented with paralysis and the potential genetic cause for TPP, is there any place for family screening?

B) In our case, we offered thyroidectomy as soon as he was euthyroid on medication, was that the right choice, or should we have waited for longer or alternatively with no eye involvement offer him radioactive iodine?