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.
Thyroid diseases are common in women, including at the time of pregnancies. Many typical features of hyperthyroidism are common in normal pregnancies and this may delay or mask the diagnosis. Uncontrolled thyrotoxicosis increases the rate of miscarriage, intrauterine growth restriction (IUGR), premature labour and perinatal mortality. Multi-disciplinary efforts are required to achieve optimal control of thyrotoxicosis. Anti-thyroid drugs are safe and should be used with the lowest possible doses. Radioiodine treatment is contraindicated during pregnancy and lactation. Indications of surgery include: compression symptoms, thyroid malignancy, non-compliance to medications or when the patient develop drugs side effects. Keywords: Hyperthyroidism, pregnancy
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 the problems of a young man who was clinically euthyroid but biochemically hyperthyroid. The possibility of peripheral resistance to thyroid hormones to explain this paradoxical state is discussed. The importance of recognising this condition to avoid the erroneous diagnosis of thyrotoxicosis and inappropriate therapy 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.
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.
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.
Thirty-eight normal volunteers and 10 patients with untreated thyrotoxicosis were each given 0.5 ml of Lugol's solution daily for 10 days. On days 0, 5, 10, 15 and 20, serum levels of T4, free T4, T3 and TSH (by sensitive immunoradiometric assay) were measured. In normal subjects, the serum concentrations of free T4 declined significantly at day 10 while TSH levels were significantly increased at days 5, 10 and 15. Serum levels of T4 and T3 did not change significantly. All the observed changes took place within the limits of normal ranges for the hormones mentioned. In contrast, in the thyrotoxic subjects, both T4 and T3 were significantly decreased at days 5 and 10, while serum TSH remained below detection limit (0.14 mU/l) throughout the study. Short exposure to excessive iodide in normal subjects affects T4 and T3 release and this effect could be partially overcome by compensatory increase in TSH. In thyrotoxicosis, lack of compensatory increase in TSH results in rapid decreases in T4 and T3 levels. The integrity of the hypothalamo-pituitary-thyroidal axis may be effectively assessed by measuring TSH response to iodide suppression, using a highly sensitive immunoradiometric assay.
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.
Twenty eight patients with hyperthyroidism complicating their pregnancies were seen at the Obstetrics and Gynaecology Department, University Hospital, Kuala Lumpur, Malaysia in a six-year period. All patients were treated with antithyroid drugs, carbimazole being the mainstay of treatment. The incidence of the disease was 0.9 per 1000 births and was similar with other series. No cases of fetal goitre were noted. The mean birth weight was 2952 g; there was no significant difference in the birth weight of term live births in patients treated with carbimazole alone or carbimazole combined with propranolol.
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.
Severe thyrotoxicosis can present with a myriad of cardiovascular complications. It may be mild features such as palpitations, tachycardia, and exertional dyspnea or may progress to life-threatening consequences such as atrial fibrillation, tachyarrhythmias, heart failure, myocardial infarction, and shock. In rare cases, they may present with myocardial ischemia secondary to coronary artery vasospasm. We report a case of a 59-year-old Malay gentleman who presented with fast atrial fibrillation and tachycardia-mediated heart failure that evolved to a silent myocardial infarction secondary to severe coronary artery vasospasm with undiagnosed severe thyrotoxicosis. He had complete resolution of heart failure and no further recurrence of coronary artery vasospasm once treatment for thyrotoxicosis was initiated and euthyroidism achieved. This life-threatening consequence has an excellent prognosis if recognised early and treated promptly.
Thyroid hormones affect all organ systems and, in excess, can cause increased metabolic rate, heart rate, ventricle contractility, and gastrointestinal motility as well as muscle and central nervous system excitability. Thyroid storm is the extreme manifestation of thyrotoxicosis with an estimated incidence of 0.20 per 100,000 per year among hospitalized patients in Japan. The mortality of thyroid storm without treatment ranges from 80% to 100%; but with treatment, the mortality rate is between 10% and 50%. The diagnostic strategy for thyroid storm may take into consideration Burch-Wartofsky scoring or Akamizu's diagnostic criteria. Multiple treatment aims need to be addressed in managing thyroid storm effectively. This paper puts together all aspects to be considered for the management of hyperthyroidism and thyroid storm during the acute and emergency phase as well as consideration of special populations.
Carbimazole, in 3 divided daily doses, is commonly prescribed for the treatment of thyrotoxicosis. However, based on its long intra-thyroid half-life, the drug may be effective when used as a single or twice daily dose. This study was undertaken to determine the effect of once, twice or thrice daily doses of carbimazole on thyroid function in patients with thyrotoxicosis. Seventy previously untreated thyrotoxic patients were randomly allocated to receive carbimazole 30 mg once (group 1), 15 mg twice (group 2) and 10 mg thrice (group 3) daily. All patients were also prescribed propranolol 20 mg thrice daily for the first 4 weeks. Blood was taken for total T3, T4, TSH, blood counts and liver enzymes determinations at the beginning and at 6 weeks of treatment. Only 48 (68.6%) patients were included in the analysis, as the rest defaulted follow-up (20.0%) or blood samples were not available at review (11.4%). Of the 48 patients, 17 were in group 1, 16 in group 2 and 15 in group 3. Following 6 weeks of treatment, there was no significant difference in the mean serum levels of total T3 and T4 between the 3 groups. However, there was a significant decrease in the mean serum levels of total T3 and T4 as compared to the start of the treatment. Four patients (23.5%) in group 1, 4 patients (25%) in group 2 and 3 patients (20%) in group 3 were still thyrotoxic at 6 weeks of treatment, whilst 10 patients (58.8%) in group 1, 6 patients (37.5%) in group 2 and 3 (20%) in group 3 were biochemically hypothyroid.(ABSTRACT TRUNCATED AT 250 WORDS)