Thyrotoxic hypokalaemic periodic paralysis in a man from Nepal

Abstract

A case is presented of a rare complication of hyperthyroidism, known as thyrotoxic hypokalaemic periodic paralysis, in a man from Nepal. A 26-year-old Nepalese man, with known hypokalaemia, was referred to the clinical laboratory services for electrolyte analysis. Results showed Na⁺ 120 mmol/l and K⁺ 2.8 mmol/l, and he was prescribed potassium chloride. In fact, he had previously been receiving potassium supplementation periodically and his history revealed that he had experienced the same type of attack and was hospitalised 6 months earlier. He had profound tremor and was agitated and irritable during his visit to this hospital. Thyroid function testing showed high T3 (tri-iodothyronine) and T4 (thyroxine) with low thyroid stimulating hormone (TSH) concentration in the serum, indicating thyrotoxic hypokalaemic periodic paralysis. Treatment with neomercazole resulted in an improvement during the follow up visit. Hypokalaemia is believed to be a consequence of a massive shift due to increased sodium–potassium–adenosine triphosphatase (Na⁺K⁺ATPase ) pump activity in the presence of elevated thyroid hormones.

BACKGROUND

This is a rare case and it has not been reported from Nepal until now. This case is important because this information will help the clinician look for the cause of hypokalaemia rather than implement symptomatic treatment of hypokalaemia.^1,2

CASE PRESENTATION

A 26-year-old Nepalese man with known hypokalaemia was referred to the clinical laboratory services department for electrolyte estimation. Results showed values of Na⁺ 120 mmol/l and K⁺ 2.8 mmol/l, and he was prescribed supplemental potassium chloride.

The patient’s history revealed that he had previously been admitted to a hospital in Kathmandu for acute onset of severe weakness of his lower limbs 6 months earlier. He was paralysed and his movement was restricted. Investigations revealed a hypokalaemic status and a diagnosis of acute hypokalaemic periodic paralysis was made. Potassium chloride supplementation returned the serum K⁺ value to normal and the patient regained some of his strength in his limbs. Subsequently, the potassium chloride supplementation was stopped, but the patient was advised to take it intermittently when signs and symptoms of hypokalaemia developed.

The patient had lost approximately 15 kg in weight during the previous 6 months. He appeared agitated and irritable during his visit to the hospital. He had profound tremor which was pronounced during discussion with the laboratory personnel.

INVESTIGATIONS

Blood analysis revealed: haemoglobin 12.5 g/dl; glucose 112 mg/dl; urea 34 mg/dl; creatinine 1.2 mg/dl (all within reference range). Thyroid function test (enzyme linked immunosorbent assay (ELISA) method) revealed: T3 (tri-iodothyronine) 7.0 ng/ml (reference range 0.69–2.02 ng/ml); T4 (thyroxine) 12.0 μg/dl (reference range 4.4–11.6 μg/dl); thyroid stimulating hormone (TSH) 0.2 mIU/l (reference range 0.4–6.2 mIU/l). There was high T3 and T4 with low TSH in serum, indicating hyperthyroidism. Finally, after thorough clinical examination and laboratory work up, a diagnosis of thyrotoxic hypokalaemic periodic paralysis (THPP) was reached. In fact, this patient had classic features of THPP.

TREATMENT

The patient was treated with neomercazole (5 mg twice daily), an anti-thyroid drug that depresses the formation of thyroid hormone.

OUTCOME AND FOLLOW-UP

Thyroid function test and serum electrolyte values returned to normal and were maintained within normal reference ranges during the follow up visits.

DISCUSSION

Thyroid function test revealed an elevation of T3 and T4 and a low value of TSH in the patient’s serum, confirming hyperthyroidism. The hallmark of THPP is hypokalaemia with serum potassium concentration usually <3.0 nmol/l and even as low as 1.1 nmol/L.³ Hypokalaemia occurs due to a massive shift of potassium into the cells rather than net loss from the body.⁴ This is the consequence of a rapid and massive shift of potassium from the extracellular into the intracellular compartment, mainly into the muscles. This is believed to be related to increased sodium–potassium–adenosine triphosphatase (Na⁺K⁺ATPase) pump activity in the presence of elevated hormone concentration.⁵ T3, the biologically most active thyroid hormone, can enter mitochondria freely and generate ATP that fuels the Na⁺K⁺ATPase pump located in cell membranes. Potassium flux and sodium transport as well as Na/K-ATPase pump activity have been elevated in patients with THPP.⁵ This hyperthyroid state might have caused increased gastrointestinal motility, resulting in the patient having diarrhoea when he attended the hospital. He also had mild dehydration, and as a result his Na+ value was lower than the reference range. All these problems might have caused severe weakness during his visit to the hospital.

Though THPP is common in Asian males of Mongoloid origin, this is the first case reported from this Himalayan nation, although five Nepalese patients were diagnosed and treated in Qatar.⁶ In fact, this complication of hyperthyroidism has now been reported in many Asian males, with reports from Malaysia, China, and India.^7–9 It seems that this condition is not confined to Asian countries only, as there have also been reports from the USA¹⁰ and many other countries. This complication of hyperthyroidism manifests as hypokalaemia as the main presenting feature, and can create a diagnostic dilemma as happened in this case. Treatment with neomercazole normalised the thyroid function test parameters.¹¹ Serum electrolyte status also returned to normal and stabilised. The signs and symptoms of hyperthyroidism disappeared and there was rapid improvement in the general health status of the patient.

LEARNING POINTS

• Thyrotoxic hypokalaemic periodic paralysis is a rare but well documented complication of hyperthyroidism.

• Hypokalaemia should be investigated thoroughly to find the cause instead of implementing symptomatic treatment.

• If the patient is a Nepalese male of Mongoloid origin, he should be investigated for thyrotoxic hypokalaemic periodic paralysis.

• The diagnosis is easily missed since the signs and symptoms are non-specific.

• With documentation of hypokalaemia, careful correlation of clinical features with thyroid function test results is helpful for arriving at the diagnosis