Evidence map›Paper›PMID 32099819›Full record

ArticleJournal of clinical & translational endocrinology2020

Heterogenous biochemical expression of hormone activity in subclinical/overt hyperthyroidism and exogenous thyrotoxicosis.

Rudolf Hoermann, John E M Midgley, Rolf Larisch, Johannes W Dietrich

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical & translational endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 37% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The various faces of hyperthyroidism.Journal of clinical & translational endocrinology · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Rudolf HoermannDepartment for Nuclear Medicine, Klinikum Lüdenscheid, Paulmannshöherstr. 14, 58515 Lüdenscheid, Germany.
John E M MidgleyNorth Lakes Clinical, 20 Wheatley Avenue, Ilkley LS29 8PT, UK.
Rolf LarischDepartment for Nuclear Medicine, Klinikum Lüdenscheid, Paulmannshöherstr. 14, 58515 Lüdenscheid, Germany.
Johannes W DietrichMedical Department I, Endocrinology and Diabetology, Bergmannsheil University Hospitals, Ruhr University of Bochum, Buerkle-de-la-Camp-Platz 1, D-44789 Bochum, Germany.
Klinikum Lüdenscheid · DEBG University Hospital Bergmannsheil Bochum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSubclinical hyperthyroidism/thyrotoxicosis originates from different causes and clinical conditions, sharing the laboratory constellation of a suppressed TSH in the presence of thyroid hormone concentrations within the reference range.

aimPresentation of hyperthyroidism can manifest itself in several ways. We questioned whether there is either a consistent biochemical equivalence of thyroid hormone response to these diagnostic categories, or a high degree of heterogeneity may exist both within and between the different clinical manifestations.

methodsThis secondary analysis of a former prospective cross-sectional trial involved 461 patients with untreated thyroid autonomy, Graves' disease or on levothyroxine (LT4) after thyroidectomy for thyroid carcinoma. TSH response and biochemical equilibria between TSH and thyroid hormones were contrasted between endogenous hyperthyroidism and thyrotoxicosis (LT4 overdose).

resultsConcentrations of FT4, FT3, TSH, deiodinase activity and BMI differed by diagnostic category. Over various TSH strata, FT4 concentrations were significantly higher in LT4-treated thyroid carcinoma patients, compared to the untreated diseases, though FT3 levels remained comparable. They were concentrated in the upper FT4- but low deiodinase range, distinguishing them from patients with thyroid autonomy and Graves' disease. In exogenous thyrotoxicosis, TSH and FT3 were less responsive to FT4 concentrations approaching its upper normal/hyperthyroid range.

conclusionsThe presence or lack of TSH feedforward activity determines the system response in the thyroid-active (hyperthyroidism) and no-thyroid response to treatment (thyrotoxicosis). This rules out a consistent thread of thyroid hormone response running through the different diagnostic categories. TSH measurements should therefore be interpreted conditionally and differently in subclinical hyperthyroidism and thyrotoxicosis.

Indexed as

DeiodinaseSubclinical hyperthyroidismThyrotoxicosis

Identifiers

PMID32099819
PMCPMC7031309
OpenAlexW3005404756

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.