Startseite Medizin Clinical utility of urinary gonadotrophins in hypergonadotrophic states as Turner syndrome
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Clinical utility of urinary gonadotrophins in hypergonadotrophic states as Turner syndrome

  • Alessandra Boncompagni ORCID logo EMAIL logo , Jane McNeilly , Mohammed Murtaza , Laura Lucaccioni , Lorenzo Iughetti , Sze Choong Wong und Avril Mason
Veröffentlicht/Copyright: 23. Oktober 2020

Abstract

Background

Girls with Turner syndrome (TS) are at an increased risk of primary ovarian insufficiency (POI). Good correlation between serum and urinary gonadotrophins exists in children assessed for disorders of puberty, but there is little evidence of their reliability in hypergonadotropic states.

Objectives

To determine whether there was a correlation between serum and urinary Luteinising Hormone (uLH) and Follicle-Stimulating Hormone (uFSH) in hypergonadotrophic states, and whether uFSH could suggest an ovarian failure in TS as Anti-Mullerian Hormone (AMH).

Patients and Methods

Retrospective cohort study of 37 TS girls attending the paediatric TS clinic in Glasgow between February 2015 and January 2019, in whom 96 non-timed spot urine samples were available with a median age at time of sample of 12.89 years (3.07–20.2 years). uLH and uFSH were measured by chemiluminescent microparticle immunoassay. Simultaneous serum gonadotrophins and AMH were available in 30 and 26 girls, respectively. AMH <4 pmol/L was considered indicative of ovarian failure.

Results

A strong correlation was found between serum LH and uLH (r 0.860, P<0.001) and serum FSH and uFSH (r 0.905, p<0.001). Among patients≥10 years not on oestrogen replacement, ROC curve identified uFSH as a reasonable marker for AMH<4 pmol/L uFSH of >10.85 U/L indicates an AMH <4 pmol/L with 75% sensitivity and 100 % specificity (AUC 0.875)with similar ability as serum FSH (AUC 0.906).

Conclusion

uLH and uFSH are non-invasive, useful and reliable markers of ovarian activity in hypergonadotropic states as TS. uFSH could provide an alternative to AMH (in centres which are limited by availability or cost) in revealing ovarian failure and requirement for oestrogen replacement in pubertal induction.


Corresponding author: Alessandra Boncompagni, Departments of Medical and Surgical Sciences of Mothers, Children and Adults, Post-graduate School of Paediatrics, University of Modena & Reggio Emilia, Paediatric Unit, Via del Pozzo 71 41124, Modena, Italy; and Developmental Endocrinology Research Group, Royal Hospital for Children, University of Glasgow, Glasgow, UK, Phone: +393491440692, Fax: +39 0594223072, E-mail: .

Acknowledgments

We want to thank all the paediatric endocrine nurses of the Royal Hospital for Children of Glasgow for their help with samples’ collection.

  1. Research funding: None declared.

  2. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  3. Competing interests: No funding organizations played a role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

  4. Ethical statement: The research presented in the manuscript was conducted ethically in accordance with the World Medical Association Declaration of Helsinki.

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Received: 2020-01-31
Accepted: 2020-08-16
Published Online: 2020-10-23
Published in Print: 2020-11-26

© 2020 Walter de Gruyter GmbH, Berlin/Boston

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