Treatment of Hyperthyroid Disease

Klein, Irwin; Becker, David V.; Levey, Gerald S.

doi:10.7326/0003-4819-121-4-199408150-00010

Cited by 100 publications

(56 citation statements)

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“…5,10,52 This can be accomplished with one of a variety of ␤1-selective or nonselective agents, and can be accomplished rapidly with oral drug administration, whereas treatments such as antithyroid therapy or radioiodine, which lead to a restoration of a chemical euthyroid state, require more time. 85 Although digitalis has been used in hyperthyroidism-associated atrial fibrillation, the increased rate of digitalis clearance as well as the decreased sensitivity of the hyperthyroid heart to this drug results in the need for higher doses of this medication with less predictable responses. 86 Treatment with calcium channel blockers, especially when administered parenterally, should be avoided because of the potential unwanted effects of blood pressure reduction through effects on the smooth muscle cells of the resistance arterioles.…”

Section: Atrial Fibrillationmentioning

confidence: 99%

“…4,74 Although initially thought to be contraindicated, treatment of the thyrotoxic cardiac patient with ␤-adrenergic blockade to reduce heart rate should be first-line therapy. 52,85 In patients with overt heart failure involving pulmonary congestion, the use of digitalis and diuretics is appropriate. 54 The definitive treatment of choice for the hyperthyroidism is with 131 I-radioiodine.…”

Section: Heart Failurementioning

confidence: 99%

“…54 The definitive treatment of choice for the hyperthyroidism is with 131 I-radioiodine. 85,92 This is both safe and effective especially when used in conjunction with ␤-adrenergic blockade. Cure of the hyperthyroidism and a restoration of the euthyroid state frequently results in a reversion of the atrial fibrillation to sinus rhythm and a resolution of the cardiac manifestations (Table 3).…”

Section: Heart Failurementioning

confidence: 99%

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Thyroid Disease and the Heart

Klein¹,

Danzi²

2016

Current Problems in Cardiology

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152

104

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Abstract-The cardiovascular signs and symptoms of thyroid disease are some of the most profound and clinically relevant findings that accompany both hyperthyroidism and hypothyroidism. On the basis of the understanding of the cellular mechanisms of thyroid hormone action on the heart and cardiovascular system, it is possible to explain the changes in cardiac output, cardiac contractility, blood pressure, vascular resistance, and rhythm disturbances that result from thyroid dysfunction. The importance of the recognition of the effects of thyroid disease on the heart also derives from the observation that restoration of normal thyroid function most often reverses the abnormal cardiovascular hemodynamics. In the present review, we discuss the appropriate thyroid function tests to establish a suspected diagnosis as well as the treatment modalities necessary to restore patients to a euthyroid state. We also review the alterations in thyroid hormone metabolism that accompany chronic congestive heart failure and the approach to the management of patients with amiodarone-induced alterations in thyroid function tests.

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Section: Atrial Fibrillationmentioning

confidence: 99%

Section: Heart Failurementioning

confidence: 99%

Section: Heart Failurementioning

confidence: 99%

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Thyroid Disease and the Heart

Klein¹,

Danzi²

2016

Current Problems in Cardiology

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152

104

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“…Propylthiouracil (PTU) is used routinely in the treatment of hyperthyroidism, a common endocrine condition, which may result from various disorders of the thyroid gland, the most prevalent of which is Graves disease (Klein et al, 1994). In addition to the excessive thyroid hormone concentrations associated with this condition, Graves disease has also been found to result in increased stimulation of the adrenergic nervous system.…”

Section: Introductionmentioning

confidence: 99%

Effects of oral propylthiouracil treatment on nitric oxide production in rat aorta

Grieve

Fletcher

Pitsillides

et al. 1999

British J Pharmacology

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1 The eects of oral propylthiouracil (PTU) treatment on vascular nitric oxide (NO) production were studied in the rat aorta. 2 Rats were fed a standard low fat diet with or without 0.1% PTU, for 2 or 4 weeks, or for 2 weeks with additional thyroxine injections. Concentration response curves were then constructed to phenylephrine (PE) in both endothelium-intact and denuded aortic rings from these animals and after incubation with 0.1 mM L-N G nitroarginine (L-NOARG). In addition, expression of nitric oxide synthase (NOS) was analysed in sections of aorta from PTU-treated and control rats using rabbit polyclonal antibodies to both inducible NOS (iNOS) and endothelial NOS (eNOS). to PE in endothelium-intact vessel rings, as compared to controls (P50.05). Both endothelial removal and incubation with L-NOARG restored the maximum response after 2, but not 4 weeks, although, in general, vessel sensitivity was not altered by either treatment. Vessels from PTU-treated rats given thyroxine injections showed no signi®cant dierences between any of the dose response curve parameters. Immunohistochemical analysis suggested that labelling for eNOS may be increased after PTU treatment as compared to control animals, whereas iNOS antibody immunoreactivity was not dierent between the two groups. 4 These results suggest that the hyporesponsiveness to PE observed after oral PTU treatment is, in part, due to enhanced nitric oxide (NO) production by the endothelium, and demonstrate for the ®rst time that thyroid hormones may play a role in the regulation of eNOS activity in the rat aorta.

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“…A significant disadvantage of this therapeutic approach is the variable response, which results in a relatively high frequency of treatment failure, and in overtreatment (1). Much effort has been devoted to the improvement of 131 I dosage by the development of compensatory models that take into account goitre volume and thyroid iodine uptake (2,3).…”

Section: Introductionmentioning

confidence: 99%

Serum TSH and the response to radioiodine treatment of toxic multinodular goitre

Pedersen‐Bjergaard¹,

Kirkegaard²

1997

European Journal of Endocrinology

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A retrospective analysis of data from 73 consecutive patients with toxic multinodular goitre treated with iodine-131 ( 131 I) during a 2-year period was performed to investigate if serum TSH at the time of 131 I treatment influences the outcome. The dose of 131 I was calculated according to a model compensating for thyroid size estimated by palpation and 24-h 131 I uptake. Serum TSH was determined by a third-generation assay with a functional sensitivity of 0.03 mU/l. A significantly more pronounced response to 131 I treatment was observed in patients with TSH > 0.0 mU/l than in patients with TSH=0.0 mU/l (P ¼ 0.0006). This difference resulted in a threefold lower frequency of non-responders and a fivefold higher rate of early hypothyroidism in the group with detectable serum TSH. While the high frequency of hypothyroidism among patients with measurable serum TSH can be explained by destruction of normal thyroid tissue, the high frequency of treatment failure in the group with serum TSH ¼ 0.0 mU/l suggests that autonomous thyroid tissue may also be sensitized to a deleterious effect of 131 I through stimulation by TSH. We conclude that serum TSH has a significant influence on the outcome of 131 I treatment of toxic multinodular goitre. The results of 131 I treatment may be improved by adjustment of the dose of 131 I according to the serum TSH level, in addition to adjustment for goitre size and 24-h 131 I uptake.

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Treatment of Hyperthyroid Disease

Cited by 100 publications

References 0 publications

Thyroid Disease and the Heart

Thyroid Disease and the Heart

Effects of oral propylthiouracil treatment on nitric oxide production in rat aorta

Serum TSH and the response to radioiodine treatment of toxic multinodular goitre

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