title: Lower body weight and BMI at birth were associated with early adiposity rebound in 21-hydroxylase deficiency patients.
abstract: 21-hydroxylase deficiency (21-OHD) is the most common type of congenital adrenal hyperplasia. In addition to the clinical problems caused by adrenal insufficiency and androgen excess, a risk for obesity and metabolic syndrome during young adulthood is a major ramification of the disease. Although glucocorticoid therapy is very likely to be one of the contributory factors, the precise causes of the metabolic status of adult 21-OHD patients remain to be clarified. Previously we reported that 21-OHD patients developed early onset AR, a condition which might create a risk for obesity and metabolic syndrome in adulthood. In order to elucidate the association between the onset of AR and factors during the fetal period to early infancy, we conducted a retrospective longitudinal analysis of 29 21-OHD patients (male: 14 cases, female: 15 cases, salt wasting type: 16, simple virilizing type: 13), who were identified by newborn screening and followed up at least until the age 10 years. Body size at birth, lower body weight, and lower BMI were found to precipitate the timing of AR. On the other hand, no significant association was observed between the timing of AR and sex, gestational age, treatment regimen (including cumulative dose of HDC), and disease severity (the type of the disease, the value of DHEA-S and 17-OHP). There are two points to consider: first, in 21-OHD patients treated with glucocorticoid substitution therapy, the risk for early AR cannot be reduced by adjusting the dose of glucocorticoid; second, fetal factors might affect the metabolic status of 21-OHD patients.
authors.affiliation: Department of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Shigeru
authors.initials: S
authors.lastname: Takishima
authors.forename: Keisuke
authors.initials: K
authors.lastname: Nakajima
authors.forename: Risa
authors.initials: R
authors.lastname: Nomura
authors.forename: Atsumi
authors.initials: A
authors.lastname: Tsuji-Hosokawa
authors.forename: Nozomi
authors.initials: N
authors.lastname: Matsuda
authors.forename: Yohei
authors.initials: Y
authors.lastname: Matsubara
authors.forename: Makoto
authors.initials: M
authors.lastname: Ono
authors.forename: Kentaro
authors.initials: K
authors.lastname: Miyai
authors.forename: Kei
authors.initials: K
authors.lastname: Takasawa
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Morio
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Hasegawa
authors.forename: Kenichi
authors.initials: K
authors.lastname: Kashimada
mesh_terms: D050154:Adiposity; D000312:Adrenal Hyperplasia, Congenital / Q000150:complications / Q000378:metabolism; D001724:Birth Weight / Q000502:physiology*; D015992:Body Mass Index; D002657:Child Development / Q000502:physiology; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007230:Infant, Low Birth Weight / Q000254:growth & development*; D007231:Infant, Newborn; D008137:Longitudinal Studies; D008297:Male; D063766:Pediatric Obesity / Q000209:etiology / Q000378:metabolism; D012189:Retrospective Studies