Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Absence of mutation in the follicle-stimulating hormone receptor gene in severe primary hypothyroidism associated with gonadal hyperstimulation.

Journal of pediatric endocrinology & metabolism : JPEM - 1 Aug 2007

Suarez Elizabeth A, d'Alva Catarina B, Campbell Andrew, Miller-Horn Jill, Dever Maureen, Faerber Eric, Medonca Berenice B, Latronico Ana Claudia, De Luca Francesco

Abstract excerpt

BACKGROUND: Severe hypothyroidism can cause a distinct form of precocious puberty in children, characterized by delayed skeletal maturation, predominance of FSH-mediated effects over LH-mediated function, and reversal of sexual precocity upon thyroid hormone replacement. The etiology of this unusual form of precocious puberty in children remains poorly understood. Recently, three mutations of the FSH receptor...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Child
Share to Hypothyroidism

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Pituitary Gland

Share to Puberty, Precocious

Share to Radiography

Share to Receptors, FSH

Share to Severity of Illness Index

Share to Thyrotropin

Source

Identifiers

PMID: 17937064
DOI: 10.1515/jpem.2007.20.8.923

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Absence of mutation in the follicle-stimulating hormone receptor gene in severe primary hypothyroidism associated with gonadal hyperstimulation.PMID 17937064Read ↗

Evaluating the roles of follicle-stimulating hormone receptor polymorphisms in gonadal hyperstimulation associated with severe juvenile primary hypothyroidism.Semantic proximity Read ↗

Presence and absence of follicle-stimulating hormone receptor mutations provide some insights into spontaneous ovarian hyperstimulation syndrome physiopathology.Semantic proximity Read ↗

Delayed puberty and primary amenorrhea associated with a novel mutation of the human follicle-stimulating hormone receptor: clinical, histological, and molecular studies.Semantic proximity Read ↗

Mutations and polymorphisms of the FSH receptor (FSHR) gene: clinical implications in female fecundity and molecular biology of FSHR protein and gene.Semantic proximity Read ↗

Molecular characterization and phenotypic expression of mutations in genes for gonadotropins and their receptors in humans.Semantic proximity Read ↗

A novel phenotype related to partial loss of function mutations of the follicle stimulating hormone receptor.Semantic proximity Read ↗

Identification of the first germline mutation in the extracellular domain of the follitropin receptor responsible for spontaneous ovarian hyperstimulation syndromeSemantic proximity Read ↗

Clinical manifestations of genetic defects affecting gonadotrophins and their receptors.Semantic proximity Read ↗

A Novel mutation in the FSH receptor inhibiting signal transduction and causing primary ovarian failure.Semantic proximity Read ↗

A Novel Mutation in the FSH Receptor Inhibiting Signal Transduction and Causing Primary Ovarian FailureSemantic proximity Read ↗

Structural analysis of the thyrotropin receptor in four patients with congenital hypothyroidism due to thyroid hypoplasia.Semantic proximity Read ↗

Two different entities of spontaneous ovarian hyperstimulation in a woman with FSH receptor mutation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.