Evidence map›Paper›PMID 8040303›Full record

ArticleThe Journal of clinical investigation1994

Genetic analysis of 29 kindreds with generalized and pituitary resistance to thyroid hormone. Identification of thirteen novel mutations in the thyroid hormone receptor beta gene.

M Adams, C Matthews, T N Collingwood, Y Tone, P Beck-Peccoz, K K Chatterjee

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

55 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Trial
  3. Article
  4. [Resistance to thyroid hormone syndrome with developmental disorders in two children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Article
  5. Article
  6. Approach to the Patient With Raised Thyroid Hormones and Nonsuppressed TSH.The Journal of clinical endocrinology and metabolism · 2024
    Article
  7. Expanding the phenotype ofFrontiers in cell and developmental biology · 2023
    Article
  8. Article
  9. Resistance to Thyroid Hormones: A Case-Series Study.International journal of molecular sciences · 2022
    Article
  10. Severe Resistance to Thyroid Hormone Beta in a Patient with Athyreosis.Thyroid : official journal of the American Thyroid Association · 2022
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. BRAFOncology letters · 2017
    Article
  18. Article
  19. Review
  20. Review
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

6 authors.

M AdamsDepartment of Medicine, University of Cambridge, Addenbrooke's Hospital, United Kingdom.
C Matthews
T N Collingwood
Y Tone
P Beck-Peccoz
K K Chatterjee

Funding

Wellcome Trust
6 · The paper itself

Abstract

Resistance to thyroid hormone (RTH), with elevated serum free thyroid hormones and nonsuppressed thyrotropin levels, is either relatively asymptomatic, suggesting a generalized disorder (GRTH) or associated with thyrotoxic features, indicating possible selective pituitary resistance (PRTH). 20 GRTH and 9 PRTH cases, sporadic or dominantly inherited, were analyzed. Affected individuals were heterozygous for single nucleotide substitutions in the thyroid hormone receptor beta gene, except for a single case of a seven nucleotide insertion. With one exception, the corresponding 13 novel and 7 known codon changes localized to and extended the boundaries of two mutation clusters in the hormone-binding domain of the receptor. 15 kindreds shared 6 different mutations, and haplotype analyses of the mutant allele showed that they occurred independently. The majority (14 out of 19) of the recurrent but a minority (1 out of 10) of unique mutations were transitions of CpG dinucleotides. Mutant receptor binding to ligand was moderately or severely impaired and did not correlate with the magnitude of thyroid dysfunction. There was no association between clinical features and the nature or location of a receptor mutation. These observations suggest that GRTH and PRTH are phenotypic variants of the same genetic disorder, whose clinical expression may be modulated by other non-mutation-related factors.

Indexed as

MutationAdolescentAdultAmino Acid SequenceBase SequenceChildChild, PreschoolDrug ResistanceFemaleHaplotypesHumansMaleMiddle AgedMolecular Sequence DataPituitary GlandReceptors, Thyroid HormoneReceptors, Thyroid HormoneThyroid Hormones

Identifiers

PMID8040303
PMCPMC296123

What Socratic holds

Textmetadata
Read underepoch 390

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.