Poyrazoglu, S., Darendeliler, F., Ahmed, S.F. et al. (17 more authors) (2017) Birth weight in different etiologies of disorders of sex development. Journal of Clinical Endocrinology and Metabolism, 102 (3). pp. 1044-1050. ISSN 0021-972X
Abstract
Context: It is well established that boys are heavier than girls at birth. Although the cause of birth weight (BW) difference is unknown, it has been proposed that it could be generated from prenatal androgen action. Objective: The aim of the current study was to determine the BW of children with disorders of sex development (DSD) of different etiologies and to evaluate the effects of androgen action on BW. Methods: Data regarding diagnosis, BW, gestational age, karyotype, and concomitant conditions were collected from the InternationalDisorders of SexDevelopment (I-DSD) Registry (www.i-dsd).BWstandard deviation score was calculated according to gestational age. Cases were evaluated according to disorder classification in I-DSD (i.e., disorders of gonadal development, androgen excess, androgen synthesis, androgen action, nonspecific disorder of undermasculinization groups, and Leydig cell defect). Results: A total of 533 cases were available; 400 (75%) cases were 46,XY, and 133 (25%) cases were 46,XX. Eighty cases (15%) were born small for gestational age (SGA). Frequency of SGA was higher in the 46,XY group (17.8%) than in the 46,XX (6.7%) group (P = 0.001). Mean BW standard deviation scores of cases with androgen excess and androgen deficiency [in disorders of gonadal development, androgen synthesis, and Leydig cell defect groups and androgen receptor gene (AR)mutation-positive cases in disorders of androgen action groups]were similar to normal childrenwith the same karyotype. SGA birth frequency was higher in the AR mutation-negative cases in disorders of androgen action group and in the nonspecific disorders of the undermasculinization group. Conclusions: BWdimorphism is unlikely to be explained by fetal androgen action per se. 46,XY DSDs due to nonspecific disorders of undermasculinizationare more frequently associatedwithfetal growth restriction, SGA, and concomitant conditions.
Metadata
Item Type: | Article |
---|---|
Authors/Creators: |
|
Copyright, Publisher and Additional Information: | © 2017 The Endocrine Society. This is an author produced version of a paper subsequently published in Journal of Clinical Endocrinology and Metabolism. Uploaded in accordance with the publisher's self-archiving policy. |
Dates: |
|
Institution: | The University of Sheffield |
Academic Units: | The University of Sheffield > Faculty of Medicine, Dentistry and Health (Sheffield) > The Medical School (Sheffield) > Division of Genomic Medicine (Sheffield) > Department of Oncology and Metabolism (Sheffield) |
Depositing User: | Symplectic Sheffield |
Date Deposited: | 12 Apr 2017 08:49 |
Last Modified: | 12 Apr 2017 08:55 |
Published Version: | https://doi.org/10.1210/jc.2016-3460 |
Status: | Published |
Publisher: | Endocrine Society |
Refereed: | Yes |
Identification Number: | 10.1210/jc.2016-3460 |
Related URLs: | |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:114461 |