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Fulltext Acute and emergency care for thyrotoxicosis and thyroid storm

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
Thyrotoxicosis presenting as hypokalaemic paralysis and hyperlactataemia in an oriental man

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
Serum creatine kinase: an adjunct biochemical index of subclinical thyrotoxicosis?

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*
Conduction abnormalities in thyrotoxicosis--a report of three cases

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*
Fulltext A Combination of Tachycardia-Mediated Heart Failure and Coronary Artery Vasospasm-Induced Silent Myocardial Infarction in a Patient with Severe Thyrotoxicosis

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
Effects of Lugol's solution on thyroid function in normals and patients with untreated thyrotoxicosis

Tan TT, Morat P, Ng ML, Khalid BA

Clin Endocrinol (Oxf), 1989 Jun;30(6):645-9.
PMID: 2591064

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.

Matched MeSH terms: Thyrotoxicosis/blood; Thyrotoxicosis/physiopathology*
Thyrotoxicosis after iodine fortification. A 21-year Danish population-based study

Ma ZF

Clin Endocrinol (Oxf), 2018 11;89(5):677-678.
PMID: 30176058 DOI: 10.1111/cen.13846
Matched MeSH terms: Thyrotoxicosis*
Right ventricular dysfunction and pulmonary hypertension: a neglected presentation of thyrotoxicosis

Singarayar CS, Siew Hui F, Cheong N, Swee En G

Endocrinol Diabetes Metab Case Rep, 2018;2018.
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
Hyperthyroidism in pregnancy

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
Hyperthyroidism in pregnancy

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
Thyrotoxicosis in pregnancy

Ong HC

Family Practitioner, 1977;2:25-28.

Matched MeSH terms: Thyrotoxicosis
Plasma renin and aldosterone in thyroid diseases

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
A reversible dilated cardiomyopathy due to thyrotoxicosis

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
Prolonged Exercise Test in Patients With History of Thyrotoxicosis

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
Fulltext Weathering the Crisis: A Case of Thyroid Crisis with Propranolol-Induced Circulatory Collapse Successfully Treated with Therapeutic Plasma Exchange

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
Fulltext Primary thyroid lymphoma with elevated free thyroxine level

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
Fulltext Thyrotoxicosis in pregnancy--a six year review

Lim BH, Raman S, Sivanesaratnam V, Ngan A

Singapore Med J, 1989 Dec;30(6):539-41.
PMID: 2635396

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.

Matched MeSH terms: Thyrotoxicosis/drug therapy*; Thyrotoxicosis/epidemiology
Thyrotoxic periodic paralysis and intravenous propranolol in the emergency setting

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*
Fulltext Results of long-term follow-up after compensated fixed-dose therapy for thyrotoxicosis

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*
Fulltext Thyrotoxic periodic paralysis: a report of 3 Malaysian cases and a review of its pathology

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

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