{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:15:18Z","timestamp":1787022918925,"version":"build-2736575974"},"reference-count":70,"publisher":"American Academy of Pediatrics (AAP)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>We describe congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency, which is the most common primary adrenal insufficiency in children and adolescents. In this comprehensive review of CAH, we describe presentations at different life stages depending on disease severity. CAH is characterized by androgen excess secondary to impaired steroidogenesis in the adrenal glands. Diagnosis of CAH is most common during infancy with elevated 17-hydroxyprogesterone levels on the newborn screen in the United States. However, CAH can also present in childhood, with late-onset symptoms such as premature adrenarche, growth acceleration, hirsutism, and irregular menses. The growing child with CAH is treated with hydrocortisone for glucocorticoid replacement, along with increased stress doses for acute illness, trauma, and procedures. Mineralocorticoid and salt replacement may also be necessary. Although 21-hydroxylase deficiency is the most common type of CAH, there are other rare types, such as 11\u03b2-hydroxylase and 3\u03b2-hydroxysteroid dehydrogenase deficiency. In addition, classic CAH is associated with long-term comorbidities, including cardiometabolic risk factors, impaired cognitive function, adrenal rest tumors, and bone health effects. Overall, early identification and treatment of CAH is important for the pediatric patient.<\/jats:p>","DOI":"10.1542\/pir.2022-005617","type":"journal-article","created":{"date-parts":[[2024,1,31]],"date-time":"2024-01-31T22:07:51Z","timestamp":1706738871000},"page":"74-84","source":"Crossref","is-referenced-by-count":23,"title":["Congenital Adrenal Hyperplasia"],"prefix":"10.1542","volume":"45","author":[{"given":"Nicole R.","family":"Fraga","sequence":"first","affiliation":[{"name":"*Center for Endocrinology, Diabetes, and Metabolism, Children\u2019s Hospital Los Angeles, Los Angeles, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nare","family":"Minaeian","sequence":"additional","affiliation":[{"name":"*Center for Endocrinology, Diabetes, and Metabolism, Children\u2019s Hospital Los Angeles, Los Angeles, CA"},{"name":"\u2020Keck School of Medicine of University of Southern California, Los Angeles, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mimi S.","family":"Kim","sequence":"additional","affiliation":[{"name":"*Center for Endocrinology, Diabetes, and Metabolism, Children\u2019s Hospital Los Angeles, Los Angeles, CA"},{"name":"\u2020Keck School of Medicine of University of Southern California, Los Angeles, CA"},{"name":"\u2021The Saban Research Institute at Children\u2019s Hospital Los Angeles, Los Angeles, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"417","published-online":{"date-parts":[[2024,2,1]]},"reference":[{"issue":"19","key":"2024020103073725100_B1","doi-asserted-by":"crossref","first-page":"1362","DOI":"10.1056\/NEJM200011093431903","article-title":"Adrenomedullary dysplasia and hypofunction in patients with classic 21-hydroxylase deficiency","volume":"343","author":"Merke","year":"2000","journal-title":"N Engl J 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