Congenital Thyrotropin Deficiency-From Discovery to Molecular Biology, Postgenome and Preventive Medicine-
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If untreated within a few weeks of postnatal life, patients with biallelic TSHβ mutations develop cretinism comparable to patients with severe primary congenital hypothyroidism.
“If untreated within a few weeks of postnatal life, these patients develop cretinism comparable to patients with severe primary congenital hypothyroidism [26, 27].”
From 2018 European Thyroid Association (ETA) Guidelines on the Diagnosis and Management of Central Hypothyroidism (2018) · cites this paper as [27]
Section 1.2 (page unavailable) reports that severe cases of congenital isolated TSH deficiency showed signs of nongoitrous cretinism; section 1.3 identifies homozygous or compound-heterozygous TSHβ mutations in this condition. Section 4 says early treatment can prevent irreversible effects of congenital hypothyroidism, but the copy does not specify a window of a few postnatal weeks or compare these patients’ outcomes directly with severe primary congenital hypothyroidism. (LLM, conf=0.85)
Experimental — accuracy not yet measuredHeritable forms of central hypothyroidism due to biallelic TSHβ mutations are associated with severe neonatal onset and characterized by typical manifestations of congenital primary hypothyroidism.
“Heritable forms of CeH due to biallelic TSHβ mutations are associated with severe neonatal onset and characterized by the typical manifestations of congenital primary hypothyroidism (e.g., jaundice, macroglossia, hoarse cry, failure to thrive and retarded growth, umbilical hernia, hypotonia).”
From 2018 European Thyroid Association (ETA) Guidelines on the Diagnosis and Management of Central Hypothyroidism (2018) · cites this paper as [27]
Section 1.3 (page unavailable) reports homozygous and compound-heterozygous TSHβ mutations in congenital isolated TSH deficiency. Section 1.2 says severe cases showed typical signs of nongoitrous cretinism, supporting the broad comparison with congenital hypothyroidism. It does not establish severe neonatal onset for all biallelic cases or specify the listed manifestations. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe most frequently identified mutations associated with multiple pituitary hormone deficiency are in PROP1.
“The most frequently identified mutations associated with MPHD are in PROP1 [27, 34-37].”
From 2018 European Thyroid Association (ETA) Guidelines on the Diagnosis and Management of Central Hypothyroidism (2018) · cites this paper as [27]
Section 2.2 reports PROP1 mutations in cases of combined pituitary hormone deficiency. It does not say they are the most frequently identified mutations or provide a frequency comparison with other genes. (LLM, conf=0.85)
Experimental — accuracy not yet measured
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Central Hypothyroidism: Pathogenic, Diagnostic, and Therapeutic Challenges
Persani, L. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2012-1616 · Cited by 295 · see citing works
Persani, L., Brabant, G., Dattani, M., Bonomi, M., Feldt-Rasmussen, U., Fliers, E., Gruters, A., Maiter, D., Schoenmakers, N., & van Trotsenburg, A. S. P. (2018) · European Thyroid Journal · doi:10.1159/000491388 · Cited by 222 · see citing works
Central hypothyroidism — a neglected thyroid disorder
Beck-Peccoz, P., Rodari, G., Giavoli, C., & Lania, A. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2017.47 · Cited by 140 · see citing works
A Family with Complete Resistance to Thyrotropin-Releasing Hormone
Bonomi, M., Busnelli, M., Beck-Peccoz, P., Costanzo, D., Antonica, F., Dolci, C., Pilotta, A., Buzi, F., & Persani, L. (2009) · New England Journal of Medicine · doi:10.1056/nejmc0808557 · Cited by 122 · see citing works
Mechanisms related to the pathophysiology and management of central hypothyroidism
Yamada, M., & Mori, M. (2008) · Nature Clinical Practice Endocrinology & Metabolism · doi:10.1038/ncpendmet0995 · Cited by 114 · see citing works
The multiple genetic causes of central hypothyroidism
Persani, L., & Bonomi, M. (2017) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2017.04.003 · Cited by 46 · see citing works
- Authors
- MIYAI, K.
- Affiliations
- The University of Osaka (JP)
- Corresponding author
- MIYAI, Kiyoshi
- Venue
- Endocrine Journal
- Publisher
- Japan Endocrine Society
- Published
- 2007
- Volume
- 54
- Issue
- 2
- Pages
- 191-203
- ISSN
- 0918-8959 (ISSN-L)
- 1348-4540
- OpenAlex
- W2067735693
- Cited by
- 28
- References
- 82
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 4 · 2015: 3 · 2014: 2 · 2012: 1
- FWCI
- 0.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Journal (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomics and Rare Diseases
- Keywords
- congenital hypothyroidism, thyrotropin deficiency, TSH receptor, TSH beta subunit, molecular genetics, preventive medicine
- MeSH terms
- Endocrinology, Humans, Mass Screening, Metabolism, Inborn Errors, Molecular Biology, Mutation, Primary Prevention, Thyrotropin, Amino Acid Motifs, Thyrotropin, beta Subunit, History, 20th Century
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