ReviewBMJ case reports2013
Elevated free thyroxine and non-suppressed thyrotropin.
Review in BMJ case reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Partial Thyroid Hormone-Binding Globulin Deficiency: A Case Report and Literature Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- TSH adenoma and syndrome of resistance to thyroid hormones-Two cases report of syndrome of inappropriate secretion of thyrotropin.Brain and behavior · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A young man was diagnosed with hyperthyroidism 10 years prior to current presentation after a random health screening revealed an elevated free thyroxine (fT4) of 36.9 pmol/L. During that time, he saw multiple physicians and was treated with carbimazole intermittently. His repeat thyroid function tests showed persistently elevated fT4 ranging 25-35.7 pmol/L and non-suppressed thyroid-stimulating hormone (TSH) concentrations of 6.78-22.1 mIU/L. He had a smooth, firm and non-tender goitre. At our institution, laboratory interference was first excluded by serial dilution study (TSH) and retesting of TSH and fT4 on alternate assay, which gave reproducible results. His normal α-subunit and sex hormone binding globulin, partially suppressed TSH by high dose triiodothyronine (T3), and positive TSH response to thyrotropin-releasing hormone stimulation were consistent with resistance to thyroid hormone syndrome. The diagnosis was confirmed by direct sequencing of thyroid hormone receptor-β gene, revealing a heterozygous R320 L mutation that causes reduced T3 affinity and reduced corepressor dissociation.
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Registered trials
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 OpenQuestion graph.