Displaying publications 1 - 20 of 30 in total

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  1. Tan HT, Tan CY, Teong CS, Ratnasingam J, Goh KJ
    J Clin Neurophysiol, 2020 Aug 05.
    PMID: 32773648 DOI: 10.1097/WNP.0000000000000766
    PURPOSE: Thyrotoxic periodic paralysis is characterized by recurrent episodes of reversible, severe proximal muscle weakness associated with hypokalemia and hyperthyroidism. Prolonged exercise test is an easy, noninvasive method of demonstrating abnormal muscle membrane excitability in periodic paralyses. Although abnormal in thyrotoxic periodic paralysis patients, the effects thyroid hormone levels in non-thyrotoxic periodic paralysis thyrotoxicosis patients have not been well studied. The study aims to evaluate thyrotoxicosis patients (regardless of thyrotoxic periodic paralysis history) with prolonged exercise test and correlate it with their thyroid status.

    METHODS: This is a prospective, cross-sectional study of consecutive thyrotoxicosis patients seen at the endocrine clinic of a tertiary medical center. Thyroid status was determined biochemically before prolonged exercise test. Compound muscle action potential (CMAP) amplitudes postexercise were compared against pre-exercise amplitudes and recorded as percentage of mean baseline CMAP amplitude. Comparisons of time-dependent postexercise CMAP amplitudes and mean CMAP amplitude decrement were made between hyperthyroid and nonhyperthyroid groups.

    RESULTS: Seventy-four patients were recruited, 23 (31%) men, 30 (41%) Chinese, and the mean age was 48.5 ± 16.8 years. Of 74 patients, 32 (43%) were hyperthyroid and 42 (57%) were nonhyperthyroid viz. euthyroid and hypothyroid. Time-dependent CMAP amplitudes from 10 to 45 minutes after exercise were significantly lower in hyperthyroid patients compared with nonhyperthyroid patients (P < 0.01). Mean CMAP amplitude decrement postexercise was significantly greater in hyperthyroid than nonhyperthyroid patients (23.4% ± 11.4% vs. 17.3% ± 10.5%; P = 0.02).

    CONCLUSIONS: Compound muscle action potential amplitude declines on prolonged exercise test were significantly greater in hyperthyroid patients compared with nonhyperthyroid patients. Muscle membrane excitability is highly influenced by thyroid hormone level. Thyrotoxic periodic paralysis occurs from increased levels of thyroid hormone activity in susceptible patients.

    Matched MeSH terms: Thyrotoxicosis
  2. Cheah JM, Ng D, Low MY, Foo SH
    J ASEAN Fed Endocr Soc, 2019;34(2):206-209.
    PMID: 33442157 DOI: 10.15605/jafes.034.02.12
    Thyroid crisis is a life-threatening form of thyrotoxicosis characterized by multi-system dysfunction. Therapeutic plasma exchange has been reported to be effective in removing excessive circulating thyroid hormones. We present a 46-year-old female with recently diagnosed Graves' disease associated with thyrotoxic cardiomyopathy admitted for thyroid crisis complicated by propranolol-induced circulatory collapse, acute kidney injury and ischemic hepatitis. The tachyarrhythmia was refractory to conventional therapy. Initiation of TPE resulted in rapid clinical and biochemical stabilization.
    Matched MeSH terms: Thyrotoxicosis
  3. Khoo SSK, Chu CM, Fung YK
    Case Rep Cardiol, 2018;2018:4827907.
    PMID: 29713551 DOI: 10.1155/2018/4827907
    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.
    Matched MeSH terms: Thyrotoxicosis
  4. Singarayar CS, Siew Hui F, Cheong N, Swee En G
    PMID: 29785271 DOI: 10.1530/EDM-18-0012
    Thyrotoxicosis is associated with cardiac dysfunction; more commonly, left ventricular dysfunction. However, in recent years, there have been more cases reported on right ventricular dysfunction, often associated with pulmonary hypertension in patients with thyrotoxicosis. Three cases of thyrotoxicosis associated with right ventricular dysfunction were presented. A total of 25 other cases of thyrotoxicosis associated with right ventricular dysfunction published from 1994 to 2017 were reviewed along with the present 3 cases. The mean age was 45 years. Most (82%) of the cases were newly diagnosed thyrotoxicosis. There was a preponderance of female gender (71%) and Graves' disease (86%) as the underlying aetiology. Common presenting features included dyspnoea, fatigue and ankle oedema. Atrial fibrillation was reported in 50% of the cases. The echocardiography for almost all cases revealed dilated right atrial and or ventricular chambers with elevated pulmonary artery pressure. The abnormal echocardiographic parameters were resolved in most cases after rendering the patients euthyroid. Right ventricular dysfunction and pulmonary hypertension are not well-recognized complications of thyrotoxicosis. They are life-threatening conditions that can be reversed with early recognition and treatment of thyrotoxicosis. Signs and symptoms of right ventricular dysfunction should be sought in all patients with newly diagnosed thyrotoxicosis, and prompt restoration of euthyroidism is warranted in affected patients before the development of overt right heart failure.

    Learning points: Thyrotoxicosis is associated with right ventricular dysfunction and pulmonary hypertension apart from left ventricular dysfunction described in typical thyrotoxic cardiomyopathy.Symptoms and signs of right ventricular dysfunction and pulmonary hypertension should be sought in all patients with newly diagnosed thyrotoxicosis.Thyrotoxicosis should be considered in all cases of right ventricular dysfunction or pulmonary hypertension not readily explained by other causes.Prompt restoration of euthyroidism is warranted in patients with thyrotoxicosis complicated by right ventricular dysfunction with or without pulmonary hypertension to allow timely resolution of the abnormal cardiac parameters before development of overt right heart failure.

    Matched MeSH terms: Thyrotoxicosis
  5. Idrose AM
    Acute medicine & surgery, 2015 07;2(3):147-157.
    PMID: 29123713 DOI: 10.1002/ams2.104
    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.
    Matched MeSH terms: Thyrotoxicosis
  6. Yeap LL, Lim KS, Ng CC, Hui-Ping Khor A, Lo YL
    Ther Drug Monit, 2014 Feb;36(1):3-9.
    PMID: 24342894 DOI: 10.1097/FTD.0000000000000024
    The authors describe a case of a 37-year-old Malay lady with an unusually slow carbamazepine clearance, which may be related to genetic polymorphisms of drug metabolizing enzymes and transporters. When given a small daily dose of 200 mg immediate-release carbamazepine, this patient experienced drowsiness. Subsequently, she reduced her carbamazepine dose to 200 mg twice a week (on Mondays and Fridays), resulting in poor seizure control. At the same time, the patient was diagnosed with hyperthyroidism and was given carbimazole and propranolol. Hyperthyroidism and the concurrent use of these antihyperthyroid agents may have further slowed down the metabolism of carbamazepine. Therapeutic drug monitoring of carbamazepine was carried out, and a slow carbamazepine clearance of 1.45 L·h⁻¹ per 70 kg was observed. Genotyping of selected genetic variants in CYP3A4, CYP3A5, EPHX1, ABCB1, and ABCC2 revealed that she has CYP3A5*3/*3 and ABCB1 3435-CC genotypes. Both genotypes have been shown to be associated with higher adjusted mean serum carbamazepine concentration in Chinese and Korean patients with epilepsy. Physicians should be vigilant about the risk of adverse effects among patients with a slow carbamazepine clearance, especially in Malays. Simulations of carbamazepine dosing regimen based on the pharmacokinetic parameters of this patient were performed to allow individualization of drug therapy.
    Matched MeSH terms: Thyrotoxicosis/drug therapy; Thyrotoxicosis/physiopathology*
  7. Yahaya N, Din SW, Ghazali MZ, Mustafa S
    Singapore Med J, 2011 Sep;52(9):e173-6.
    PMID: 21947158
    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.
    Matched MeSH terms: Thyrotoxicosis/blood; Thyrotoxicosis/diagnosis
  8. Sahni V, Gupta N, Anuradha S, Tatke M, Kar P
    Med J Malaysia, 2007 Mar;62(1):76-7.
    PMID: 17682580
    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.
    Matched MeSH terms: Thyrotoxicosis/complications*; Thyrotoxicosis/physiopathology
  9. Al-Jubouri MA, Inkster GD, Nee PA, Andrews FJ
    Ann. Clin. Biochem., 2006 Jul;43(Pt 4):323-5.
    PMID: 16824287 DOI: 10.1258/000456306777695681
    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.
    Matched MeSH terms: Thyrotoxicosis/complications; Thyrotoxicosis/diagnosis*; Thyrotoxicosis/ethnology
  10. Sthaneshwar P, Prathibha R, Yap SF
    Malays J Pathol, 2005 Jun;27(1):29-32.
    PMID: 16676690
    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.
    Matched MeSH terms: Thyrotoxicosis/diagnosis; Thyrotoxicosis/pathology*; Thyrotoxicosis/physiopathology
  11. Zainurrashid Z, Shaker AaRH
    Family Physician, 2005;13:2-4.
    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
    Matched MeSH terms: Thyrotoxicosis
  12. Zainuddin Z, Shaker AAH
    Family Physician, 2005;13(3):2-4.
    MyJurnal
    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
    Matched MeSH terms: Thyrotoxicosis
  13. Wan Nazaimoon WM, Siaw FS, Sheriff IH, Faridah I, Khalid BA
    Ann. Clin. Biochem., 2001 Jan;38(Pt 1):57-8.
    PMID: 11270843
    Matched MeSH terms: Thyrotoxicosis/diagnosis*; Thyrotoxicosis/enzymology*
  14. Birkhahn RH, Gaeta TJ, Melniker L
    J Emerg Med, 2000 Feb;18(2):199-202.
    PMID: 10699522
    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.
    Matched MeSH terms: Thyrotoxicosis/complications; Thyrotoxicosis/diagnosis*
  15. Asmah BJ, Wan Nazaimoon WM, Norazmi K, Tan TT, Khalid BA
    Horm. Metab. Res., 1997 Nov;29(11):580-3.
    PMID: 9479560 DOI: 10.1055/s-2007-979105
    The effect of thyroid hormones on the renin-angiotensin-aldosterone system has not been fully resolved. Highly specific immunoassays for measurement of renin, aldosterone, free T4 (fT4), free T3 (fT3) and ultrasensitive TSH enables a direct and more accurate measurement of these hormones. We investigated the relationship between plasma renin, aldosterone and thyroid hormones in the basal state and after intravenous frusemide. This is a cross-sectional study involving 37 patients with thyrotoxicosis, 42 rendered euthyroid with normal fT4, fT3 and TSH levels, 17 with euthyroid levels of fT4 and fT3 but suppressed TSH, and 11 with hypothyroidism. Basal plasma renin was significantly higher in thyrotoxicosis (63.4 +/- 9.8 microU/ml, mean +/- SEM) compared to euthyroid (32.7 +/- 4.4 microU/ml) and hypothyroid (26.7 +/- 9.8 microU/ml). Basal plasma renin for euthyroid with suppressed TSH (41.0 +/- 7.4 microU/ml) was significantly higher than hypothyroid (p = 0.02). Basal plasma aldosterones were not significantly different except for suppressed TSH (157.7 +/- 13 pg/ml), which was higher than normal (109.9 +/- 10.4 pg/ml; p = 0.04). Following frusemide, plasma renin and aldosterone were significantly increased in all groups. Plasma renin was highly correlated to fT3 (r = 0.405, p < 0.001), total T3 (r = 0.359, p < 0.001), fT4 (r = 0.331, p < 0.001) and TSH (r = 0.300, p < 0.001) in the basal state, but less to total T4 (r = 0.248, p < 0.01). Plasma renin correlated poorly to serum aldosterone (r = 0.212, p < 0.03). This study clearly showed that regulation of renin was mainly influenced by fT3, and that aldosterone response to frusemide was blunted in thyrotoxicosis despite normal electrolytes.
    Matched MeSH terms: Thyrotoxicosis/blood
  16. Jeyamalar R, Chan SP
    Int J Cardiol, 1995 Nov 10;52(1):83-4.
    PMID: 8707441
    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.
    Matched MeSH terms: Thyrotoxicosis/complications*; Thyrotoxicosis/therapy
  17. Yusoff K, Khalid BA
    Ann Acad Med Singap, 1993 Jul;22(4):609-12.
    PMID: 8257070
    Cardiac arrhythmias are common in patients with thyrotoxicosis. Conduction abnormalities have been seen in a few thyrotoxic patients, but these, in particular high grade atrioventricular (AV) block, often occur in the presence of other conditions. Three thyrotoxic patients with conduction abnormalities are described: two were associated with severe hypokalaemia and the third had congestive cardiac failure. Conditions predisposing to conduction abnormality should be identified when this occurs in a thyrotoxic patient as their correction may help resolve or explain the conduction abnormality.
    Matched MeSH terms: Thyrotoxicosis/physiopathology*
  18. Mafauzy M, Wan Mohamad WB, Zahary MK, Mustafa BE
    Med J Malaysia, 1993 Mar;48(1):71-5.
    PMID: 8341175
    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)
    Matched MeSH terms: Thyrotoxicosis/drug therapy*
  19. Zaini A, Khir A, Doi SA, Chan SP, Paramsothy M, Khoo BH
    J Int Med Res, 1992 Jun;20(3):279-88.
    PMID: 1397673
    To evaluate the effects of simple compensated fixed-dose iodine-131 therapy for thyrotoxicosis, the long-term results for 74 patients treated with a fixed dose of iodine-131 ranging from 5 to 12 mCi (185 to 444 MBq) were evaluated in the first 2 years of a trial. The dose selected was loosely based on the gross size of the thyroid gland. Routine antithyroid drug therapy was given for a minimum of 3 months after iodine-131 therapy. The mean (+/- SD) duration of follow-up was 74.5 +/- 42 months. The results indicated that roughly 25% of patients treated in this way will become hypothyroid after 5 years and that 85% are cured (need no further therapy during the follow-up period) using a single dose of iodine-131. Of those cured using a single iodine-131 dose, 81% were no longer receiving drugs after 6 months and 85% after 1 year. Such a regimen seems currently to be among the best available where prolonged periods of medication-free euthyroidism after therapy are sought.
    Matched MeSH terms: Thyrotoxicosis/radiotherapy*
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