{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:35:51Z","timestamp":1787016951409,"version":"build-2736575974"},"reference-count":91,"publisher":"BMJ","issue":"6","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["Arch Dis Child"],"published-print":{"date-parts":[[2017,6]]},"abstract":"<jats:p>After the introduction of replacement therapy with glucocorticoids and mineralocorticoids in the 1950s, congenital adrenal hyperplasia (CAH) is no longer a life-limiting condition. However, due to the successful introduction of medical steroid hormone replacement, CAH has become a chronic condition, with associated comorbidities and long-term health implications. The aim of treatment is the replacement of mineralocorticoids and glucocorticoids and the normalisation of elevated androgen concentrations. Long-term consequences of the condition and current treatment regimens include unfavourable changes in the cardiovascular risk profile, impaired growth, testicular adrenal rest tumours (TART) in male and subfertility in both male and female patients with CAH. Optimising replacement therapy in patients with CAH remains challenging. On one hand, treatment with supraphysiological doses of glucocorticoids might be required to normalise androgen concentrations and decrease size or presence of TARTs. On the other hand, treatment with supraphysiological doses of glucocorticoids is associated with an increased prevalence of unfavourable cardiovascular and metabolic risk profiles as well as impaired longitudinal growth and gonadal function. Therefore, treatment of children and adults with CAH requires an individualised approach. Careful monitoring for early signs of complications is already warranted during paediatric healthcare provision to prevent and reduce the impact of comorbidities in later life.<\/jats:p>","DOI":"10.1136\/archdischild-2016-311910","type":"journal-article","created":{"date-parts":[[2016,12,14]],"date-time":"2016-12-14T23:27:11Z","timestamp":1481758031000},"page":"578-584","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":30,"title":["Cardiovascular health, growth and gonadal function in children and adolescents with congenital adrenal hyperplasia"],"prefix":"10.1136","volume":"102","author":[{"given":"Christiaan F","family":"Mooij","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emma A","family":"Webb","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hedi L","family":"Claahsen van der Grinten","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nils","family":"Krone","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2016,12,14]]},"reference":[{"key":"key-10.1136\/archdischild-2016-311910-1","first-page":"245","article-title":"Congenital adrenal hyperplasia due to 21-hydroxylase deficiency","volume":"21","author":"White","year":"2000","journal-title":"Endocr Rev"},{"key":"key-10.1136\/archdischild-2016-311910-2","doi-asserted-by":"crossref","first-page":"E367","DOI":"10.1210\/jc.2011-1997","article-title":"Increased activation of the alternative \u201cbackdoor\u201d pathway in patients with 21-hydroxylase deficiency: evidence from urinary steroid hormone analysis","volume":"97","author":"Kamrath","year":"2012","journal-title":"J Clin Endocrinol Metab"},{"key":"key-10.1136\/archdischild-2016-311910-3","doi-asserted-by":"crossref","first-page":"181","DOI":"10.1016\/j.beem.2008.10.014","article-title":"Genetics of congenital adrenal hyperplasia","volume":"23","author":"Krone","year":"2009","journal-title":"Best Pract Res Clin Endocrinol Metab"},{"key":"key-10.1136\/archdischild-2016-311910-4","doi-asserted-by":"crossref","first-page":"2611","DOI":"10.1073\/pnas.1300057110","article-title":"Genotype-phenotype correlation in 1,507 families with congenital adrenal hyperplasia owing to 21-hydroxylase deficiency","volume":"110","author":"New","year":"2013","journal-title":"Proc Natl Acad Sci USA"},{"key":"key-10.1136\/archdischild-2016-311910-5","doi-asserted-by":"crossref","first-page":"427","DOI":"10.1111\/j.1365-2265.2011.04123.x","article-title":"Steroid 21-hydroxylase gene mutational spectrum in 454 Argentinean patients: genotype-phenotype correlation in a large cohort of patients with congenital adrenal hyperplasia","volume":"75","author":"Marino","year":"2011","journal-title":"Clin Endocrinol (Oxf)"},{"key":"key-10.1136\/archdischild-2016-311910-6","doi-asserted-by":"crossref","first-page":"1059","DOI":"10.1210\/jcem.85.3.6441","article-title":"Predicting phenotype in steroid 21-hydroxylase deficiency? 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