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. 2022 Feb 23;23(3):631–645. doi: 10.1007/s11154-022-09717-w

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Novel therapeutic approaches for patients with 21OHD include the replacement of glucocorticoids (GC) by improved modified-release HC preparations (Plenadren^®, Chronocort^®) or improved modes of GC delivery (CSHI), associated with more efficient suppression of hypothalamic–pituitary–adrenal (HPA)-axis driven adrenal androgen production. This HPA-axis-driven adrenal androgen production may be additionally blocked by corticotropin releasing hormone (CRH) receptor blocking (Tildacerfont, crinecerfont) or ACTH (receptor) blocking. Alternatively, adrenal androgen production may be inhibited by adrenal steroidogenesis blockers (Nevanimibe, abiraterone acetetate), adrenotoxic drugs (mitotane), or bilateral adrenalectomy. Inhibition of the aromatization of adrenal androgens may lower the suppressing effects of estrogens on growth and (co)-administration of anti-androgens may inhibit hyperandrogenic effects. Gene and cell-based therapies anticipate restoring the HPA-axis regulated glucocorticoid and mineralocorticoid production