ReviewFrontiers in endocrinology2014
Spreading the clinical window for diagnosing fetal-onset hypogonadism in boys.
Review in Frontiers in endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 56 citations in OpenAlex.
- Incomplete male puberty: a new nosographic entity.Endocrine · 2026Review
- Current landscape of fertility induction in males with congenital hypogonadotropic hypogonadism.Annals of the New York Academy of Sciences · 2024Review
- Mini-Puberty, Physiological and Disordered: Consequences, and Potential for Therapeutic Replacement.Endocrine reviews · 2024Review
- Testicular Sertoli Cell Hormones in Differences in Sex Development.Frontiers in endocrinology · 2022Review
- Recent advancement in the treatment of boys and adolescents with hypogonadism.Therapeutic advances in endocrinology and metabolism · 2022Review
- Correlation Analysis of Genotypes and Phenotypes in Chinese Male Pediatric Patients With Congenital Hypogonadotropic Hypogonadism.Frontiers in endocrinology · 2022Article
- El laboratorio en el diagnóstico multidisciplinar del desarrollo sexual anómalo o diferente (DSD): III) Marcadores bioquímicos y genéticos en los 46,XY IV) Propuestas para el diagnóstico diferencial de los DSD.Advances in laboratory medicine · 2021Review
- The laboratory in the multidisciplinary diagnosis of differences or disorders of sex development (DSD): III) Biochemical and genetic markers in the 46,XYIV) Proposals for the differential diagnosis of DSD.Advances in laboratory medicine · 2021Review
- Biomarkers of male hypogonadism in childhood and adolescence.Advances in laboratory medicine · 2020Review
- Stem Leydig Cells in the Adult Testis: Characterization, Regulation and Potential Applications.Endocrine reviews · 2020Review
- Male Hypogonadism and Disorders of Sex Development.Frontiers in endocrinology · 2020Review
- Puberty and Inhibin B in 35 Adolescents With Pituitary Stalk Interruption Syndrome.Frontiers in pediatrics · 2020Article
- What Does AMH Tell Us in Pediatric Disorders of Sex Development?Frontiers in endocrinology · 2020Review
- Delayed Puberty-Phenotypic Diversity, Molecular Genetic Mechanisms, and Recent Discoveries.Endocrine reviews · 2019Review
- Review
- Paediatric and adult-onset male hypogonadism.Nature reviews. Disease primers · 2019Review
- Early Identification of Isolated Sertoli Cell Dysfunction in Prepubertal and Transition Age: Is It Time?Journal of clinical medicine · 2019Article
- Male Central Hypogonadism in Paediatrics - the Relevance of Follicle-stimulating Hormone and Sertoli Cell Markers.European endocrinology · 2018Review
- Sexual Dimorphism and the Origins of Human Spinal Health.Endocrine reviews · 2018Review
- Anti-Müllerian Hormone and Testicular Function in Prepubertal Boys With Cryptorchidism.Frontiers in endocrinology · 2018Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In early fetal development, the testis secretes - independent of pituitary gonadotropins - androgens and anti-Müllerian hormone (AMH) that are essential for male sex differentiation. In the second half of fetal life, the hypothalamic-pituitary axis gains control of testicular hormone secretion. Follicle-stimulating hormone (FSH) controls Sertoli cell proliferation, responsible for testis volume increase and AMH and inhibin B secretion, whereas luteinizing hormone (LH) regulates Leydig cell androgen and INSL3 secretion, involved in the growth and trophism of male external genitalia and in testis descent. This differential regulation of testicular function between early and late fetal periods underlies the distinct clinical presentations of fetal-onset hypogonadism in the newborn male: primary hypogonadism results in ambiguous or female genitalia when early fetal-onset, whereas it becomes clinically undistinguishable from central hypogonadism when established later in fetal life. The assessment of the hypothalamic-pituitary-gonadal axis in male has classically relied on the measurement of gonadotropin and testosterone levels in serum. These hormone levels normally decline 3-6 months after birth, thus constraining the clinical evaluation window for diagnosing male hypogonadism. The advent of new markers of gonadal function has spread this clinical window beyond the first 6 months of life. In this review, we discuss the advantages and limitations of old and new markers used for the functional assessment of the hypothalamic-pituitary-testicular axis in boys suspected of fetal-onset hypogonadism.
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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.