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.
We report a patient with unusual manifestations of hyperthyroidism which initially suggested lymphoma. The pathophysiology of these features in thyrotoxicosis is discussed. The need to consider thyrotoxicosis in an otherwise unexplained case of lymphoid hyperplasia will be stressed.
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.
Primary thyroid lymphoma (PTL) is a rare form of thyroid cancer that is known to be associated with Hashimoto thyroiditis. This association is supported by the presence of elevated titres of both antithyroglobulin and antimicrosomal antibodies in up to 95 percent of patients with PTL. Most patients with PTL present with a rapidly enlarging neck mass and compressive symptoms. The majority of thyroid cancer patients have normal levels of thyroid hormones; they are rarely hyperthyroid, with no obvious clinical features of thyrotoxicosis. We describe a patient who presented with minimal clinical features of thyrotoxicosis despite having markedly elevated serum free thyroxine and suppressed serum thyroid-stimulating hormone levels.
Thyrotoxic periodic paralysis (TPP) is a medical emergency characterised by sudden onset of muscle weakness with hypokalemia that resolves with the treatment of hyperthyroidism. We report three cases of thyrotoxic periodic paralysis seen at the Accident and Emergency Care Department, University of Malaya Medical Centre in a period of four months. We also review the clinical presentation, pathophysiology, biochemical features and management of TPP. All three patients were young Asian males, presenting with muscle weakness of sudden onset. The first patient presented with lower limb weakness and had symptoms of thyrotoxicosis and goitre. He had a previous similar episode which resolved spontaneously. The second patient presented with quadriplegia, respiratory acidosis and had no signs and symptoms of thyrotoxicosis. The electrocardiogram of this patient showed normal sinus rhythm with U wave in V3 and a flat T wave, which are characteristic of hypokalaemia. The third patient, who was a known case of thyrotoxicosis, was admitted thrice for hypokalemic paralysis during the study period. All cases had low serum potassium, suppressed TSH and elevated T4 confirming thyrotoxic periodic paralysis. Potassium therapy was useful during the crisis; however prophylactic potassium has not been shown to prevent attacks as seen in one of our cases.