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. 2023 May 3;94(4):1317–1326. doi: 10.1038/s41390-023-02610-5

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Relative abundance of urinary cortisol and derivatives normalized to cortisone 21-sulfate. Total urine samples = 332; number of urines with steroids detected are shown in each bar. b Cortisol glucuronide vs cortisone sulfate in HC-treated infants. n = 64 for 14 infants while on HC (range 15–63 days); r = 0.70, p = 8.7e–11 by linear regression. c Cortisol glucuronide vs cortisone urinary levels in control infants. n = 80 for 14 infants during a comparable time period to HC-treated infants (range 10–45 days); r = 0.69, p = 4.0e–10. d Comparison of cortisol glucuronide abundance in HC-treated and control infants. Data are for urine samples collected over 10 days before starting HC (Pre) and 10 days during HC therapy (post). Levels in HC-treated infants increased 1.9- (mean)/2.6-fold (median) and were 2.0-fold higher vs control infants. *p = 0.31; **p = 0.006; n = 14/14 infants and 44/53 (post/pre) samples in control infants and 52/38 in HC-treated infants.