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Cited by 37Thyroid Disorders and TreatmentsPituitary Gland Disorders and TreatmentsGrowth Hormone and Insulin-like Growth Factors

Bioactivity of thyrotropin (TSH) in patients with central hypothyroidism: comparison between in vivo 3,5,3'-triiodothyronine response to TSH and in vitro bioactivity of TSH.

Horimoto, M, Nishikawa, M, Ishihara, T, Yoshikawa, N, Yoshimura, M, Inada, M·1995·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jcem.80.4.7714080
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Abstract

To investigate the cause(s) of central hypothyroidism with normal or elevated TSH concentrations, we evaluated the bioactivity of serum TSH as well as pituitary and thyroid function. Seven hypothyroid patients had documented deficiencies of anterior pituitary hormones other than TSH. Basal TSH concentrations ranged from 2.2-14.8 microU/mL. Six patients had low T4 and free T4 concentrations; the remaining patient had a low free T4 and a low normal T4 level with an elevated TSH concentration of 14.4 microU/mL. The mean increment in TSH 30, 60, and 90 min after TRH administration (mean delta TSH) in these patients was 13.5 +/- 9.1 microU/mL (mean +/- SD), which was not significantly different from the value in controls (9.2 +/- 3.5 microU/mL). However, the ratio of the T3 increment at 120 min (delta T3) to mean delta TSH (delta T3/mean delta TSH) in patients was 53.9 +/- 29.3 ng/microU, significantly lower than the control value of 239.5 +/- 97.5 ng/microU (P < 0.01), suggesting that the thyroid response to endogenous TSH was blunted. The serum T4 concentration correlated with the mean delta TSH in these patients (r = 0.78; P < 0.05), suggesting that hypothyroidism is dependent on conserved pituitary function. The mean bioactivity to immunoreactivity ratio of basal TSH in patients was 0.97 +/- 0.27 and was not significantly different from the normal value of 1.05 +/- 0.22. One of the two patients with high basal TSH (> 10 microU/mL) had a ratio of 0.59, which is just below the mean +/- SD of normal subjects (0.61), suggesting that most patients had normal TSH bioactivity in vitro. Our findings suggest that in vivo bioactivity of TSH is decreased because of a pituitary disorder, but in vitro bioactivity of TSH is variable in patients with central hypothyroidism.

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Crossref · 10.1210/jcem.80.4.7714080

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  • Poor intrinsic biological activity of secreted TSH molecules is a pathological mechanism accounting for central hypothyroidism.

    “(c) poor intrinsic biological activity of secreted TSH molecules [14-18].”

    From 2018 European Thyroid Association (ETA) Guidelines on the Diagnosis and Management of Central Hypothyroidism (2018) · cites this paper as [16]

  • In central hypothyroidism patients with high immunoreactive TSH, TSH elevations are similar to those generally found in subclinical or mild primary hypothyroidism and may lead to misdiagnosis.

    “In these cases, TSH elevations are similar to those generally found in subclinical or mild primary hypothyroidism and may lead to misdiagnosis [14-17, 30, 42].”

    From 2018 European Thyroid Association (ETA) Guidelines on the Diagnosis and Management of Central Hypothyroidism (2018) · cites this paper as [16]

  • In this subgroup, TSH levels are superimposable to those generally found in subclinical or mild primary hypothyroidism, although the molecule is devoid of full biological activity and FT4 is already in the hypothyroid range.

    “In this subgroup of patients, TSH levels are superimposable to those generally found in subclinical or mild primary hypothyroidism, although the molecule is devoid of full biological activity and the FT4 is already in the hypothyroid range (13, 14, 16, 17).”

    From The diagnosis and management of central hypothyroidism in 2018 (2019) · cites this paper as [16]

  • The three mechanisms of impaired thyrotrope stimulation, reduced pituitary TSH reserve, and impaired intrinsic bioactivity of secreted TSH frequently coexist as a consequence of expansive lesions of the sella region.

    “The three mechanisms are frequently coexisting as a consequence of the expansive lesions of the sella region (16, 17).”

    From The diagnosis and management of central hypothyroidism in 2018 (2019) · cites this paper as [16]

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Authors
Horimoto, M., Nishikawa, M., Ishihara, T., Yoshikawa, N., Yoshimura, M., & Inada, M.
Affiliations
Kansai Medical University (JP)
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
1995-04
Volume
80
Issue
4
Pages
1124-1128
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jcem.80.4.7714080
OpenAlex
W2069192757
Cited by
37
References
16
Citations by year
2025: 1 · 2024: 1 · 2023: 2 · 2021: 1 · 2019: 2 · 2018: 4 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 2 · 2012: 1
FWCI
1.32
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
Keywords
central hypothyroidism, thyroid-stimulating hormone, TSH receptor, thyrotropin-releasing hormone stimulation, pituitary function, free thyroxine, TSH resistance
MeSH terms
Adult, Aged, Female, Humans, Hypothalamic Diseases, Hypothyroidism, Middle Aged, Pituitary Diseases, Thyrotropin, Thyrotropin-Releasing Hormone, Triiodothyronine

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