Hyperthyroidism and Other Causes of Thyrotoxicosis: Management Guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists

Bahn, Rebecca S.; Burch, Henry B.; Cooper, David S.; Garber, Jeffrey R.; Greenlee, M. Carol; Klein, Irwin; Laurberg, Peter; McDougall, I. Ross; Montori, Víctor M.; Rivkees, Scott A.; Ross, Douglas S.; Sosa, Julie Ann; Stan, Marius N.

doi:10.4158/ep.17.3.456

Cited by 589 publications

(340 citation statements)

References 351 publications

(466 reference statements)

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“…Both GD and SPT can present with the same symptoms but differentiating between the two causes of thyrotoxicosis is essential as the treatment differs. 9 Subacute painless thyroiditis is typically a self-limiting disease while GD is not and will progress causing more severe disease unless treated with appropriate therapy.…”

Section: Common Causes Of Thyrotoxicosismentioning

confidence: 99%

“…9 Subacute painless thyroiditis causes an initial thyrotoxic phase secondary to the release of preformed thyroid hormones due to autoimmune thyroid destruction of thyroid follicles. Over weeks to months thyroid function recovers with the possibility of a hypothyroid phase during recovery.…”

Section: Differences Between Gd and Spt As A Cause Of Thyrotoxicosismentioning

confidence: 99%

“…12 The American Thyroid Association Practice Guidelines states that in a patient with a symmetrically enlarged thyroid, recent onset of ophthalmopathy, and persistent, high levels of thyroid hormone for weeks to months, the diagnosis of GD is sufficiently likely that further evaluation of hyperthyroidism causation is unnecessary. 9 The absence of classical GD physical findings in the setting of thyrotoxicosis necessitates further investigations to distinguish between GD and SPT and to further guide treatment. A radioactive iodine uptake (RAIU) test should be performed (except during pregnancy when it is contraindicated).…”

Section: Differences Between Gd and Spt As A Cause Of Thyrotoxicosismentioning

confidence: 99%

“…Radioactive iodine uptake, a measure of thyroid hormone synthesis, will be elevated and occasionally normal in cases of GD but extremely low in cases of SPT. 9 However, normal or even elevated RAIU has been reported in patients with SPT if RAIU is carried out during the recovery phase of SPT. 13,14 Therefore, the earlier the RAIU is carried out at the time of diagnosis of thyrotoxicosis, the more accurate the interpretation.…”

Section: Differences Between Gd and Spt As A Cause Of Thyrotoxicosismentioning

confidence: 99%

“…Rarely, corticosteroids have been used to ameliorate the severity and to shorten the course of thyrotoxicosis due to SPT, but they should be reserved only for severe cases. 9 It is possible that some patients will have recurrent episodes of SPT, separated by years, 10 requiring a similar treatment strategy.…”

Section: Management Of Spt Versus Gd In Generalmentioning

confidence: 99%

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Alemtuzumab Induced Thyroid Disease in Multiple Sclerosis: A Review and Approach to Management

Mahzari

Arnaout

Freedman

2015

Can. J. Neurol. Sci.

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Alemtuzumab, an anti-CD52 monoclonal antibody, was recently approved for treatment of MS in Canada, having shown to significantly reduce relapses and disability in patients, particularly those who relapsed despite first line treatment. Offsetting its benefit however, is the development of novel secondary autoimmune disease, particularly affecting the thyroid gland in up to 36% of patients. The incidence of Alemtuzumab induced thyroid dysfunction (AITD) will likely rise as alemtuzumab becomes more widely used for treating MS. We review the clinical and investigational cues that help delineate the aetiology and management of thyrotoxicosis and hypothyroidism in ATID. AITD can be easily managed and we present a simple approach for its evaluation and management by neurologists that should be implemented prior to considering a referral to an internist or endocrinologist for further opinion or treatment.RÉSUMÉ: Maladie thyroïdienne induite par l'alemtuzumab dans la sclérose en plaques: revue et traitement. L'alemtuzumab, un anticorps monoclonal dirigé contre CD52, a récemment été approuvé pour le traitement de la sclérose en plaques (SP) au Canada. Les études ont démontré qu'il diminuait significativement les rechutes et l'invalidité chez les patients, particulièrement chez ceux qui avaient eu des rechutes malgré le traitement de première intention. Cependant, l'apparition d'une nouvelle maladie auto-immune secondaire à ce traitement, touchant la glande tyroïde chez 36% des patients, en amoindrit les bénéfices. L'incidence de la dysfonction thyroïdienne induite par l'alemtuzumab (DTIA) augmentera vraisemblablement à mesure que l'alemtuzumab sera plus fréquemment prescrit pour traiter la SP. Nous revoyons les indices cliniques et biochimiques qui aident à définir l'étiologie et le traitement de la thyrotoxicose et de l'hypothyroïdie dans la DTIA. La DTIA peut être traitée facilement et nous présentons une approche simple de son évaluation et son traitement par des neurologues. Cette approche devrait être utilisée avant d'envisager de référer le patient à un interniste ou à un endocrinologue pour connaître son opinion ou pour prescrire un traitement.

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Section: Common Causes Of Thyrotoxicosismentioning

confidence: 99%

Section: Differences Between Gd and Spt As A Cause Of Thyrotoxicosismentioning

confidence: 99%

Section: Differences Between Gd and Spt As A Cause Of Thyrotoxicosismentioning

confidence: 99%

Section: Differences Between Gd and Spt As A Cause Of Thyrotoxicosismentioning

confidence: 99%

Section: Management Of Spt Versus Gd In Generalmentioning

confidence: 99%

See 3 more Smart Citations

Alemtuzumab Induced Thyroid Disease in Multiple Sclerosis: A Review and Approach to Management

Mahzari

Arnaout

Freedman

2015

Can. J. Neurol. Sci.

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Subclinical Hyperthyroidism and the Risk of Coronary Heart Disease and Mortality

Collet¹,

Gussekloo²,

Bauer³

et al. 2012

Arch Intern Med

472

378

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Background Data from prospective cohort studies regarding the association between subclinical hyperthyroidism and cardiovascular outcomes are conflicting. We aimed to assess the risks of total and coronary heart disease (CHD) mortality, CHD events, and atrial fibrillation (AF) associated with endogenous subclinical hyperthyroidism among all available large prospective cohorts. Methods Individual data on 52 674 participants were pooled from 10 cohorts. Coronary heart disease events were analyzed in 22 437 participants from 6 cohorts with available data, and incident AF was analyzed in 8711 participants from 5 cohorts. Euthyroidism was defined as thyrotropin level between 0.45 and 4.49 mIU/L and endogenous subclinical hyperthyroidism as thyrotropin level lower than 0.45 mIU/L with normal free thyroxine levels, after excluding those receiving thyroid-altering medications. Results Of 52 674 participants, 2188 (4.2%) had subclinical hyperthyroidism. During follow-up, 8527 participants died (including 1896 from CHD), 3653 of 22 437 had CHD events, and 785 of 8711 developed AF. In age-and sex-adjusted analyses, subclinical hyperthyroidism was associated with increased total mortality (hazard ratio [HR], 1.24, 95% CI, 1.06–1.46), CHD mortality (HR, 1.29; 95% CI, 1.02–1.62), CHD events (HR, 1.21; 95% CI, 0.99–1.46), and AF (HR, 1.68; 95% CI, 1.16–2.43). Risks did not differ significantly by age, sex, or preexisting cardiovascular disease and were similar after further adjustment for cardiovascular risk factors, with attributable risk of 14.5% for total mortality to 41.5% for AF in those with subclinical hyperthyroidism. Risks for CHD mortality and AF (but not other outcomes) were higher for thyrotropin level lower than 0.10 mIU/L compared with thyrotropin level between 0.10 and 0.44 mIU/L (for both, P value for trend, ≤.03). Conclusion Endogenous subclinical hyperthyroidism is associated with increased risks of total, CHD mortality, and incident AF, with highest risks of CHD mortality and AF when thyrotropin level is lower than 0.10 mIU/L.

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Management of Graves Disease

Burch

Cooper

2015

JAMA

280

222

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Management of Graves disease includes treatment with antithyroid drugs, RAI, or thyroidectomy. The optimal approach depends on patient preference and specific patient clinical features such as age, history of arrhythmia or ischemic heart disease, size of goiter, and severity of thyrotoxicosis. Physicians should be familiar with the advantages and disadvantages of each therapy to best counsel their patients.

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Hyperthyroidism and Other Causes of Thyrotoxicosis: Management Guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists

Cited by 589 publications

References 351 publications

Alemtuzumab Induced Thyroid Disease in Multiple Sclerosis: A Review and Approach to Management

Alemtuzumab Induced Thyroid Disease in Multiple Sclerosis: A Review and Approach to Management

Subclinical Hyperthyroidism and the Risk of Coronary Heart Disease and Mortality

Management of Graves Disease

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