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An atypical case of periodic paralysis
Q1: What is the diagnosis?
Episodic weakness beginning after age 25 is almost never due to primary periodic paralysis.1 Furthermore, the absence of a similar family history raises a strong suspicion of a secondary disorder rather than the primary form.2 Tachycardia and a wide pulse pressure in a nervous individual are suggestive of thyrotoxicosis, which can precipitate hypokalaemia and periodic paralysis by enhancing Na+K+-ATPase activity. The most likely diagnosis, therefore, is hypokalaemic periodic paralysis secondary to thyrotoxicosis.
Q2: How did we confirm it?
Thyroid function tests confirmed the thyrotoxicosis: triiodothyronine 6 nmol/l (1.1–2.9 nmol/l), thyroxine 240 nmol/l (64–154 nmol/l), and thyroid stimulating hormone 0.03 mU/l (0.4–5 mU/l). On careful examination, a barely visible goitre was detected and an ultrasound study established its multinodular nature.
Q3: How should the patient be managed?
Treatment is that of thyrotoxicosis. The attacks cease when the euthyroid state is restored.
Thyrotoxic periodic paralysis is six times more common in males than in females. It is usually seen in orientals, especially between the ages of 20 and 39 years.2 Occasionally, it is the presenting symptom of thyrotoxicosis.3 Episodes of muscle weakness can be precipitated in susceptible thyrotoxic patients by the ingestion of ethanol or carbohydrate, and by strenuous physical exercise in hot humid weather. Despite these precipitating factors, the episodes occur erratically in most patients.4 This condition can occur in patients with thyrotoxicosis of any cause, and the thyrotoxicosis may be clinically mild. The episodes of muscle weakness are invariably associated with a decrease in serum potassium concentration, although it may not always be subnormal. Hypokalaemia alone is not the only cause because potassium levels sufficient to provoke paralysis in a thyrotoxic patient has no effect when the same patient is euthyroid. The exact cause of susceptibility of some thyrotoxic patients to periodic paralysis is not known.4 Whatever the mechanism, the attacks cease in all the patients when the euthyroid state is restored.2 Therefore, it is important that clinicians consider the diagnosis of thyrotoxicosis in any patient with atypical hypokalaemic periodic paralysis.
Episodic weakness beginning after age 25 is almost never due to primary periodic paralysis.
Periodic paralysis can occur in patients with thyrotoxicosis of any cause, and the thyrotoxicosis may be clinically mild.
In all the patients the attacks cease when the euthyroid state is restored.
Hypokalaemic periodic paralysis secondary to thyrotoxicosis.
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