The presenting features of 236 thyrotoxic patients seen in the thyroid clinic were reviewed. 18.65% of these patterns had one or more dermatological complaints at presentation. There was no specific difference in this group of patients when compared with the general hyperthyroid population with regard to age, race, sex, duration of hyperthyroidism or biochemical indices of thyrotoxicosis. The two major complaints were itching and alopecia. The prevalence of pruritus at 6.4% in our series was identical to that of other workers, but we had a much lower occurrence of alopecia at 2.6%. The diagnosis of thyrotoxicosis was delayed in two patients in whom the only major complaint was pruritus. These symptoms cleared quickly when these patients became euthyroid. However there were other patients who noted hair loss with anti-thyroid medications. The incidence of vitiligo, eczema, onycholysis in our series was much lower those quoted in the Western literature The occurrence of pretibial myoxoedema in our series is similar to that of other workers from this region. The other miscellaneous manifestations include urticaria, xanthelasma and systemic lupus erythematosis. In conclusion we feel the cutaneous manifestations of hyperthyroidism are common in our patients.
Many neurological diseases like myopathy, periodic paralysis, ophthalmoplegia, and myasthenia gravis are known associations of thyrotoxicosis. However the association of neuropathy with thyrotoxicosis is not frequently recognized. First described by Charcot in 1889, thyrotoxic neuropathy or 'Basedow's Paraplegia' is a rarely reported entity. We describe here a case of a young woman with subacute distal neuropathy as the presenting manifestation of thyrotoxicosis. The neuropathy improved on antithyroid treatment. A careful literature search leads us to believe that peripheral neuropathy in thyrotoxicosis is under recognised. Thyroid function tests can be helpful in the diagnosis of this treatable neuropathy and should be included in the routine work up.
Thyrotoxicosis gives rise to a high output cardiac failure. Rarely, it can cause a dilated cardiomyopathy with severe impairment of myocardial function which improves significantly following treatment.
A total of 23 patients with psychoses associated with thyrotoxicosis were admitted to the psychiatric unit of a University Hospital over a 13-year period, of which 20 patients were included in this retrospective study. It was found that a parallel relationship between thyrotoxicosis and psychosis appears to exist in six patients, while in the remaining 14 patients, the course of the two disease processes were largely independent of each other. Paranoid delusions and auditory hallucinations were the most prominent psychiatric symptoms. Depression was commonly seen even in patients who were not having an affective illness. In four patients, a mixed schizo-affective psychosis was seen, suggesting that the diagnostic distinction between the affective and schizophrenic reactions are often blurred in psychosis associated with thyrotoxicosis.
This report deals with a middle aged man in whom the presenting symptom of the disorder was dysphagia. The clinical approach to the final diagnosis of thyrotoxic myopathy causing dysphagia is outlined and the pathophysiology of dysphagia then discussed. The need to include thyrotoxicosis in the differential diagnosis of an otherwise unexplained case of dysphagia is stressed.
A 35-year-old Malaysian man presented with rapid onset of flaccid quadriparesis associated with nausea and vomiting. General blood tests revealed severe hypokalaemia (serum potassium 1.5 mmol/L) and hypophosphataemia (serum phosphate 0.29 mmol/L) as a potential cause of the flaccid paralysis. Arterial blood gases showed mixed acid base disturbance of respiratory alkalosis and metabolic acidosis with hyperlactataemia. Thyrotoxic periodic paralysis (TPP) was suspected as the underlying cause of this presentation and thyroid function tests showed severe hyperthyroid results (free T4 > 77.2 pmol/L, free T3 19.3 pmol/L, thyroid-stimulating hormone [TSH] < 0.05 mIU/L). Treatment with intravenous potassium and phosphate infusion and oral propranolol resulted in rapid resolution of his symptoms. A discussion of the clinical and pathophysiological features and treatment of TPP (a very rare encounter in UK clinical practice) is presented, and to our knowledge associated hyperlactataemia has not been previously described.
A 27-year-old male of Malaysian descent presented to the Emergency Department (ED) with rapidly progressive flaccid paralysis that quickly compromised his respiratory effort. The patient was found to have a serum potassium of 1.9 meq/L, and was diagnosed as having an acute paralytic episode secondary to thyrotoxic periodic paralysis. The paralytic attack was aborted with a combination of potassium replacement and parenteral propranolol in large doses. We report the use of a rarely described, yet possibly more effective, therapy for an acute attack of thyrotoxic periodic paralysis.