{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T23:57:39Z","timestamp":1790035059889,"version":"4.0.1"},"reference-count":35,"publisher":"American Academy of Pediatrics (AAP)","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,1,1]]},"abstract":"<jats:p>OBJECTIVES. Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is the most common inherited disorder of adrenal steroid biosynthesis. Patients with the classic form of CAH show androgen excess, with or without salt wasting. There are few studies reporting on higher rates of overweight and obesity among children with CAH. In addition to its role in the regulation of energy balance, leptin is involved in various endocrine and metabolic pathways. In this context, elevated serum leptin levels were reported recently for patients with CAH and were thought to be involved in the development of obesity among these patients. Therefore, the aim of this study was to analyze BMI values, compared with population-based references, for children and adolescents with CAH. Possible contributing factors, such as glucocorticoid therapy, skeletal maturation, birth weight and length, and parental BMI, were correlated with current BMI SD scores (SDS). In addition, the implications of serum leptin levels, corrected for BMI, gender, and Tanner stage, were investigated.<\/jats:p><jats:p>METHODS. We performed a cross-sectional retrospective study of 89 children and adolescents with cah (48 female and 41 male subjects; age: 0.2-17.9 years) who presented in our outpatient department during 1 year. All individuals had classic cah, confirmed with molecular genetic analyses, and received substitution therapy (glucocorticoids and mineralocorticoids, if necessary). The quality of therapy was monitored in follow-up visits every 3 to 6 months, on the basis of clinical presentation and laboratory measurement findings according to current guidelines. We grouped the patients into salt wasting and simple virilizing groups, as well as according to current metabolic control. Leptin levels were measured with a commercial radioimmunoassay and calculated as sds. For statistical analyses, standard parametric and nonparametric methods were used.<\/jats:p><jats:p>RESULTS. The chronologic ages of the children with CAH were between 0.20 and 17.9 years (mean \u00b1 SD: 8.9 \u00b1 4.6 years). The BMI SDS of the whole group ranged from \u22122.7 to 4.3 (mean \u00b1 SD: 0.88 \u00b1 1.3) and was significantly elevated above 0. Fifteen subjects (16.8%) had BMI SDS of &amp;gt;2.0, which indicated a significantly greater frequency of obesity among patients with CAH than expected for the normal population (expected: 2.27%). There was no significant difference in age and BMI between genders and clinical forms (salt wasting versus simple virilizing). BMI SDS was correlated positively with chronologic age. The BMI SDS did not differ significantly between children receiving hydrocortisone, prednisone, or dexamethasone. Hydrocortisone dosages (including equivalent dosages of prednisone and dexamethasone) ranged from 6.2 to 30.1 mg\/m2 body surface area (mean \u00b1 SD: 14.7 \u00b1 4.8 mg\/m2 body surface area). Hydrocortisone dosages were correlated positively with BMI SDS. The relative risk of having a BMI SDS of &amp;gt;2.0 was not significantly elevated among children with prednisone\/dexamethasone medication, compared with those with hydrocortisone treatment. In contrast to this, fludrocortisone dosage was not correlated with BMI SDS. Bone age delay, as calculated from the difference of bone age and chronologic age, ranged from \u22122.9 years to 5.6 years (mean \u00b1 SD: 1.11 \u00b1 1.8 years) and was significantly elevated; it was correlated positively with BMI SDS. The BMI of parents ranged from 17.8 to 39.0 kg\/m2 (median: 24.2 kg\/m2). Median BMI values did not differ significantly between fathers and mothers. The relative risk for obesity among our children (BMI SDS of &amp;gt;2.0) was significantly elevated for children with obese parents, compared with those with nonobese parents (relative risk: 4.86). There was no significant correlation of birth length, birth weight, or gestational age with BMI SDS. Serum leptin values ranged from 0.10 to 32 \u03bcg\/L (median: 4.4 \u03bcg\/L); they were correlated positively with BMI SDS, chronologic age, and Tanner stage. After transformation into leptin concentration SDS values, the median SDS of 0.42 (range: \u22125.4 to 3.1) did not differ significantly from 0.<\/jats:p><jats:p>CONCLUSIONS. Children and adolescents with CAH have a higher risk of obesity. Glucocorticoid dosage, chronologic age, advanced bone age maturation, and parental obesity contributed to elevated BMI SDS, whereas birth weight and length, serum leptin levels, used glucocorticoid, and fludrocortisone dosage were not associated with obesity. Therefore, children with CAH who become obese should be tightly monitored and should participate concurrently in weight management programs that include obese family members.<\/jats:p>","DOI":"10.1542\/peds.2005-1005","type":"journal-article","created":{"date-parts":[[2006,1,5]],"date-time":"2006-01-05T02:28:34Z","timestamp":1136428114000},"page":"e98-e105","source":"Crossref","is-referenced-by-count":141,"title":["Obesity Among Children and Adolescents With Classic Congenital Adrenal Hyperplasia Due to 21-Hydroxylase Deficiency"],"prefix":"10.1542","volume":"117","author":[{"given":"Thomas M. K.","family":"Vo\u0308lkl","sequence":"first","affiliation":[{"name":"Division of Pediatric Endocrinology, Hospital for Children and Adolescents, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diemud","family":"Simm","sequence":"additional","affiliation":[{"name":"Division of Pediatric Endocrinology, Hospital for Children and Adolescents, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoph","family":"Beier","sequence":"additional","affiliation":[{"name":"Division of Pediatric Endocrinology, Hospital for Children and Adolescents, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helmuth G.","family":"Do\u0308rr","sequence":"additional","affiliation":[{"name":"Division of Pediatric Endocrinology, Hospital for Children and Adolescents, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"417","published-online":{"date-parts":[[2006,1,1]]},"reference":[{"key":"2021120819444404300_R1","doi-asserted-by":"crossref","unstructured":"Hughes IA. Congenital adrenal hyperplasia: a continuum of disorders. Lancet.\u20081998;352:752\u2013754","DOI":"10.1016\/S0140-6736(98)22037-X"},{"key":"2021120819444404300_R2","doi-asserted-by":"crossref","unstructured":"New MI. An update of congenital adrenal hyperplasia. Ann NY Acad Sci.\u20082004;1038:14\u201343","DOI":"10.1196\/annals.1315.009"},{"key":"2021120819444404300_R3","unstructured":"Knorr D, Hinrichsen-de-Lienau SG. Persistent obesity and short final height after corticoid overtreatment for congenital adrenal hyperplasia (CAH) in infancy. Acta Paediatr Jpn.\u20081988;30(suppl):89\u201392"},{"key":"2021120819444404300_R4","doi-asserted-by":"crossref","unstructured":"Cornean RE, Hindmarsh PC, Brook CG. Obesity in 21-hydroxylase deficient patients. Arch Dis Child.\u20081998;78:261\u2013263","DOI":"10.1136\/adc.78.3.261"},{"key":"2021120819444404300_R5","doi-asserted-by":"crossref","unstructured":"Blum WF, Kiess W, Rascher W. Leptin: The Voice of Adipose Tissue. Heidelberg, Germany: Johann Ambrosius Barth Verlag; 1997","DOI":"10.1159\/000191303"},{"key":"2021120819444404300_R6","unstructured":"Poyrazoglu S, Gunoz H, Darendeliler F. Serum leptin levels in patients with 21-hydroxylase deficiency before and after treatment. Turk J Pediatr.\u20082003;45:33\u201338"},{"key":"2021120819444404300_R7","doi-asserted-by":"crossref","unstructured":"Charmandari E, Weise M, Bornstein SR, et al. Children with classic congenital adrenal hyperplasia have elevated serum leptin concentrations and insulin resistance: potential clinical implications. J Clin Endocrinol Metab.\u20082002;87:2114\u20132120","DOI":"10.1210\/jcem.87.5.8456"},{"key":"2021120819444404300_R8","doi-asserted-by":"crossref","unstructured":"Clayton PE, Miller WL, Oberfield SE, Ritzen EM, Sippell WG, Speiser PW. Consensus statement on 21-hydroxylase deficiency from the European Society for Paediatric Endocrinology and the Lawson Wilkins Pediatric Endocrine Society. Horm Res.\u20082002;58:188\u2013195","DOI":"10.1159\/000065490"},{"key":"2021120819444404300_R9","doi-asserted-by":"crossref","unstructured":"Hauffa BP, Winter A, Stolecke H. Treatment and disease effects on short-term growth and adult height in children and adolescents with 21-hydroxylase deficiency. Klin Padiatr.\u20081997;209:71\u201377","DOI":"10.1055\/s-2008-1043931"},{"key":"2021120819444404300_R10","doi-asserted-by":"crossref","unstructured":"Cunha HM, Elias LLK, Camacho-Hubner C, Moreira AC, Martinelli CE. Different states of clinical control are associated with changes in IGF-I and IGFBPs in children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Clin Endocrinol.\u20082004;61:94\u2013101","DOI":"10.1111\/j.1365-2265.2004.02075.x"},{"key":"2021120819444404300_R11","doi-asserted-by":"crossref","unstructured":"Kru\u0308ger C, Rauh M, Do\u0308rr HG. Immunoreactive renin concentrations in healthy children from birth to adolescence. Clin Chim Acta.\u20081998;274:15\u201327","DOI":"10.1016\/S0009-8981(98)00044-8"},{"key":"2021120819444404300_R12","doi-asserted-by":"crossref","unstructured":"Knorr D, Bidlingmaier F, Kuhnle U. Diagnosis and monitoring of therapy of the various enzymatic defects causing congenital adrenal hyperplasia by semiautomatic capillary gas-liquid chromatography. Horm Res.\u20081982;16:201\u2013208","DOI":"10.1159\/000179503"},{"key":"2021120819444404300_R13","unstructured":"Reinken L, Stolley H, Droese W, van Oost G. Longitudinal data of physical growth of healthy children, II: height, weight, skinfold thickness of children aged 1.5\u201316 years. Klin Padiatr.\u20081980;192:25\u201333"},{"key":"2021120819444404300_R14","doi-asserted-by":"crossref","unstructured":"Kromeyer-Hauschild K, Wabitsch M, Kunze D, et al. Percentiles of body mass index for children and adolescents evaluated from different regional German studies [in German]. Monatsschr Kinderheilkd.\u20082001;149:807\u2013818","DOI":"10.1007\/s001120170107"},{"key":"2021120819444404300_R15","doi-asserted-by":"crossref","unstructured":"Barlow SE, Dietz WH. Obesity evaluation and treatment: Expert Committee recommendations: the Maternal and Child Health Bureau, Health Resources and Services Administration and the Department of Health and Human Services. Pediatrics.\u20081998;102(3). Available at: www.pediatrics.org\/cgi\/content\/full\/102\/3\/e29","DOI":"10.1542\/peds.102.3.e29"},{"key":"2021120819444404300_R16","doi-asserted-by":"crossref","unstructured":"Bellizzi MC, Dietz WH. Workshop on childhood obesity: summary of the discussion. Am J Clin Nutr.\u20081999;70:173S\u2013175S","DOI":"10.1093\/ajcn\/70.1.173s"},{"key":"2021120819444404300_R17","unstructured":"Wabitsch M. Obesity in childhood and adolescence: recommendations of a United States of America Task Force for diagnosis and therapy. Klin Padiatr.\u20082000;212:287\u2013296"},{"key":"2021120819444404300_R18","unstructured":"World Health Organization. Obesity: preventing and managing the global epidemic: report of a WHO consultation. World Health Organ Tech Rep Ser.\u20082000;894:i\u2013253"},{"key":"2021120819444404300_R19","doi-asserted-by":"crossref","unstructured":"Niklasson A, Ericson A, Fryer JG, Karlberg J, Lawrence C, Karlberg P. An update of the Swedish reference standards for weight, length and head circumference at birth for given gestational age (1977\u20131981). Acta Paediatr Scand.\u20081991;80:756\u2013762","DOI":"10.1111\/j.1651-2227.1991.tb11945.x"},{"key":"2021120819444404300_R20","doi-asserted-by":"crossref","unstructured":"Groell R, Lindbichler F, Riepl T, Gherra L, Roposch A, Fotter R. The reliability of bone age determination in central European children using the Greulich and Pyle method. Br J Radiol.\u20081999;72:461\u2013464","DOI":"10.1259\/bjr.72.857.10505010"},{"key":"2021120819444404300_R21","doi-asserted-by":"crossref","unstructured":"Blum WF, Englaro P, Hanitsch S, et al. Plasma leptin levels in healthy children and adolescents: dependence on body mass index, body fat mass, gender, pubertal stage, and testosterone. J Clin Endocrinol Metab.\u20081997;82:2904\u20132910","DOI":"10.1210\/jc.82.9.2904"},{"key":"2021120819444404300_R22","unstructured":"von Kries R. Obesity among Bavarian children: experiences from school admittance examinations. Gesundheitswesen.\u20082004;66(suppl 1):S80\u2013S85"},{"key":"2021120819444404300_R23","doi-asserted-by":"crossref","unstructured":"Cole TJ, Freeman JV, Preece MA. Body mass index reference curves for the UK, 1990. Arch Dis Child.\u20081995;73:25\u201329","DOI":"10.1136\/adc.73.1.25"},{"key":"2021120819444404300_R24","doi-asserted-by":"crossref","unstructured":"Roche EF, Charmandari E, Dattani MT, Hindmarsh PC. Blood pressure in children and adolescents with congenital adrenal hyperplasia (21-hydroxylase deficiency): a preliminary report. Clin Endocrinol (Oxf).\u20082003;58:589\u2013596","DOI":"10.1046\/j.1365-2265.2003.01757.x"},{"key":"2021120819444404300_R25","doi-asserted-by":"crossref","unstructured":"Barker DJ. The developmental origins of adult disease. Eur J Epidemiol.\u20082003;18:733\u2013736","DOI":"10.1023\/A:1025388901248"},{"key":"2021120819444404300_R26","doi-asserted-by":"crossref","unstructured":"Sayer AA, Syddall HE, Dennison EM, et al. Birth weight, weight at 1 y of age, and body composition in older men: findings from the Hertfordshire Cohort Study. Am J Clin Nutr.\u20082004;80:199\u2013203","DOI":"10.1093\/ajcn\/80.1.199"},{"key":"2021120819444404300_R27","doi-asserted-by":"crossref","unstructured":"Matthews SG. Early programming of the hypothalamo-pituitary-adrenal axis. Trends Endocrinol Metab.\u20082002;13:373\u2013380","DOI":"10.1016\/S1043-2760(02)00690-2"},{"key":"2021120819444404300_R28","doi-asserted-by":"crossref","unstructured":"Frisch H, Waldhauser F, Lebl J, et al. Congenital adrenal hyperplasia: lessons from a multinational study. Horm Res.\u20082002;57(suppl 2):95\u2013101","DOI":"10.1159\/000058109"},{"key":"2021120819444404300_R29","doi-asserted-by":"crossref","unstructured":"Loos RJ, Bouchard C. Obesity: is it a genetic disorder?J Intern Med.\u20082003;254:401\u2013425","DOI":"10.1046\/j.1365-2796.2003.01242.x"},{"key":"2021120819444404300_R30","doi-asserted-by":"crossref","unstructured":"Snyder EE, Walts B, Perusse L, et al. The human obesity gene map: the 2003 update. Obes Res.\u20082004;12:369\u2013439","DOI":"10.1038\/oby.2004.47"},{"key":"2021120819444404300_R31","doi-asserted-by":"crossref","unstructured":"Beck B. Neuropeptides and obesity. Nutrition.\u20082000;16:916\u2013923","DOI":"10.1016\/S0899-9007(00)00410-X"},{"key":"2021120819444404300_R32","doi-asserted-by":"crossref","unstructured":"Sandoval DA, Davis SN. Leptin: metabolic control and regulation. J Diabetes Complications.\u20082003;17:108\u2013113","DOI":"10.1016\/S1056-8727(02)00167-8"},{"key":"2021120819444404300_R33","doi-asserted-by":"crossref","unstructured":"Masuzaki H, Ogawa Y, Hosoda K, et al. Glucocorticoid regulation of leptin synthesis and secretion in humans: elevated plasma leptin levels in Cushing's syndrome. J Clin Endocrinol Metab.\u20081997;82:2542\u20132547","DOI":"10.1210\/jc.82.8.2542"},{"key":"2021120819444404300_R34","doi-asserted-by":"crossref","unstructured":"Heiman ML, Ahima RS, Craft LS, Schoner B, Stephens TW, Flier JS. Leptin inhibition of the hypothalamic-pituitary-adrenal axis in response to stress. Endocrinology.\u20081997;138:3859\u20133863","DOI":"10.1210\/endo.138.9.5366"},{"key":"2021120819444404300_R35","doi-asserted-by":"crossref","unstructured":"Ahima RS, Prabakaran D, Mantzoros C, et al. Role of leptin in the neuroendocrine response to fasting. Nature.\u20081996;382:250\u2013252","DOI":"10.1038\/382250a0"}],"container-title":["Pediatrics"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/publications.aap.org\/pediatrics\/article-pdf\/117\/1\/e98\/1010462\/zpe00106000e98.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/publications.aap.org\/pediatrics\/article-pdf\/117\/1\/e98\/1010462\/zpe00106000e98.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,6]],"date-time":"2023-05-06T02:35:09Z","timestamp":1683340509000},"score":1,"resource":{"primary":{"URL":"https:\/\/publications.aap.org\/pediatrics\/article\/117\/1\/e98\/67968\/Obesity-Among-Children-and-Adolescents-With"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2006,1,1]]},"references-count":35,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2006,1,1]]},"published-print":{"date-parts":[[2006,1,1]]}},"URL":"https:\/\/doi.org\/10.1542\/peds.2005-1005","relation":{},"ISSN":["0031-4005","1098-4275"],"issn-type":[{"value":"0031-4005","type":"print"},{"value":"1098-4275","type":"electronic"}],"subject":[],"published":{"date-parts":[[2006,1,1]]}}}