Cited by 39Thyroid Disorders and TreatmentsThyroid and Parathyroid SurgeryThyroid Cancer Diagnosis and Treatment

A clinical and therapeutic approach to thyrotoxicosis with thyroid-stimulating hormone suppression only

Papi, Giovanni, Pearce, Elizabeth N., Braverman, Lewis E., Betterle, Corrado, Roti, Elio·2005·The American Journal of Medicine

Abstract

Subclinical hyperthyroidism is defined as normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations and persistently suppressed thyroid stimulating hormone (TSH) concentrations. The most common cause of subclinical hyperthyroidism is the use of suppressive doses of L-thyroxine for treatment of hypothyroidism or, less commonly, diffuse nontoxic goiter or thyroid carcinoma (exogenous subclinical hyperthyroidism). Endogenous subclinical hyperthyroidism may be caused by a variety of thyroid disorders that result in overproduction and release of thyroid hormones from the gland with normal/high 24-hour thyroid radioiodine uptake or by inflammation in the thyroid resulting in release of excess thyroid hormones and low 24-hour thyroid radioiodine uptake. Several groups have investigated whether persistent endogenous or exogenous subclinical hyperthyroidism, like overt hyperthyroidism, causes symptoms, adverse effects on the cardiovascular and the skeletal systems, and increased mortality, whether endogenous subclinical hyperthyroidism evolves to overt thyrotoxicosis, and whether or not it should be treated. The present report reviews the most important and recent studies of subclinical hyperthyroidism and attempts to draw conclusions based upon the literature and the authors' experience.

Integrity signals

Registry

Crossref · 10.1016/j.amjmed.2005.01.004

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90 of 90 references verified0 citation errors · 0 not checkable

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  • Suppressed TSH has in population studies consistently been associated with higher mortality and other adverse effects compared to people with normal or even higher TSH concentrations.

    “Thus, suppressed TSH has in population studies consistently been associated with a higher mortality and other adverse effects compared to people with normal or even higher TSH concentrations ( Table 5 ) (87–90).”

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Authors
Papi, G., Pearce, E. N., Braverman, L. E., Betterle, C., & Roti, E.
Affiliations
  • Azienda Unita' Sanitaria Locale Di Modena (IT)
  • Boston University (US)
  • University of Padua (IT)
  • University of Milan (IT)
Corresponding author
Braverman, Lewis E.
Venue
The American Journal of Medicine
Publisher
Elsevier BV
Published
2005-04
Volume
118
Issue
4
Pages
349-361
ISSN
0002-9343 (ISSN-L)
OpenAlex
W2062330332
Cited by
39
References
91
Citations by year
2026: 2 · 2022: 1 · 2021: 1 · 2017: 2 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 3 · 2012: 2
FWCI
0.64
Type
journal article
Language
en
Update notices
erratum (2005-08-01)
Open access
closed
Locations
  • The American Journal of Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Surgery › Thyroid and Parathyroid Surgery
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
Keywords
subclinical hyperthyroidism, thyrotoxicosis, TSH suppression, levothyroxine, hypothyroidism treatment, thyroid inflammation, thyroid radioiodine uptake, cardiovascular effects, skeletal effects, mortality
MeSH terms
Bone and Bones, Cardiovascular System, Humans, Thyrotoxicosis, Thyrotropin, Thyroxine, Triiodothyronine

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