JRSM >
Volume 94, Number 5 >
Pp. 241-242
Departments of Medicine, Llandough Hospital, Vale of Glamorgan,
Wales
1
University of Wales College of Medicine, Heath Park, Cardiff CF64 4XN, Wales,
UK
Correspondence to: Dr J H Lazarus
In a patient with recurrent attacks of muscular weakness, the first diagnosis that springs to mind is familial periodic paralysis. But the function of the thyroid gland deserves thought.
CASE HISTORY
A female Asian student aged 26, domiciled in the UK since childhood, returned from a two-week Mediterranean holiday feeling unwell. After three days of profuse diarrhoea, lethargy and heat intolerance she required admission to hospital. Four months previously she had missed an appointment to a hospital clinic where she was being treated with carbimazole and thyroxine for Graves' thyrotoxicosis. A month before the current admission she had run out of medication. She also had a history of asthma, well controlled with inhaled beclomethasone and salbutamol.
At the time of admission, blood pressure was 110/60 mmHg, heart rate 120/min. She had moderate flaccid proximal muscle weakness, worse in the lower limbs; the rest of the clinical examination was unremarkable. Laboratory results at this stage were: plasma sodium 140 mmol/L, potassium 2.1 mmol/L, urea 7.2 mmol/L and creatinine 100 µmol/L; haemoglobin was 13.2 g/dL and white cell count 9.6 x 109/L, repeated stool examination and cultures were negative, as were blood cultures; liver function tests were normal. Thyroid function tests were: thyroxine (FT4), 54.2 pmol/L (normal 9.8-23.1), tri-idiothyronine (FT3) 30.2 pmol/L (3.50-6.5), thyrotropin (TSH) < 0.02 mU/L (0.35-5.50), TSH receptor antibodies 34% (<10), thyroid peroxidase antibody 88 kU/L (<18.0). She was managed with potassium supplements, intravenous fluids and carbimazole 40 mg daily. On discharge four days later her muscle weakness had resolved and plasma potassium was 4.2mmol/L. Her antithyroid medication was continued at the same dose. Four weeks after discharge she was readmitted complaining of leg weakness of two hours' duration. The pattern of proximal muscle weakness was as before. Plasma potassium was 2.4 mmol/L and the electrocardiogram showed flat T waves; FT4 was 27.2 pmol/L, FT3 8.5 pmol/L and TSH < 0.02 mU/L. Hypokalaemia was corrected with potassium supplements, the muscle weakness improved and she was discharged after five days. At an outpatient clinic two weeks later she had no apparent muscular weakness, plasma potassium was 4.2 mmol/L and she was euthyroid (FT4 14.0 pmol/L, TSH 0.5 mU/l). Thyroxine 100 µg daily was added to her medication.
COMMENT
This patient had thyrotoxic periodic paralysis—a condition characterized by transient localized or generalized muscle weakness or flaccid paralysis which may be of sudden onset and recurrent. It is most serious when respiratory muscles are involved. This complication of thyrotoxicosis is most common in oriental men, but can occur in men of other racial backgrounds and also in women (sex ratio 20:1)1. In Japan the incidence is decreasing: in 1957 it was seen in 8.6% of thyrotoxic men and 0.4% of thyrotoxic women, in 1991 4.3% and 0.4%, respectively2. The clinical and biochemical features of thyrotoxicosis may be subtle at the time of presentation3. The special susceptibility of people of Asian descent is so far unexplained. Episodes of paralysis are most common in hot humid weather. Precipitating factors include high carbohydrate foods, alcohol ingestion, strenuous exercise followed by rest, emotional stress, and treatment with insulin or acetazolamide4,5.
The weakness is usually symmetrical and more obvious in the lower than the upper limbs. Attacks last from a few hours to several days. The condition is customarily associated with hypokalaemia but plasma potassium may be normal6. In our patient, the episode of diarrhoea may have precipitated the initial episode by a hypokalaemic effect. Plasma potassium is normal between attacks. Periodic paralysis may occur with thyrotoxicosis of any cause4. Thyroid hormone excess is thought to increase the activity of Na+/K+-ATPase, either directly or by way of enhanced ß-adrenergic activity, resulting in an intracellular shift of potassium7. The principal differential diagnosis is familial periodic paralysis, and the mainstay of treatment is rapid correction of thyrotoxicosis. Beta-adrenoceptor blocking drugs reduce the frequency and severity of attacks whilst potassium supplements can shorten their duration4. Once a euthyroid state is established, complete recovery of muscular function can be expected.
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