Premium
Pubertal development and its influences on bone mineral density in Australian children and adolescents with cystic fibrosis
Author(s) -
Buntain Helen M,
Greer Ristan M,
Wong Joseph CH,
Schluter Philip J,
Batch Jennifer,
Lewindon Peter,
Bell Scott C,
Wainwright Claire E
Publication year - 2005
Publication title -
journal of paediatrics and child health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.631
H-Index - 76
eISSN - 1440-1754
pISSN - 1034-4810
DOI - 10.1111/j.1440-1754.2005.00635.x
Subject(s) - medicine , menarche , bone mineral , bone age , breast development , endocrinology , peak bone mass , population , bone density , short stature , lean body mass , anthropometry , testosterone (patch) , young adult , physiology , osteoporosis , hormone , body weight , environmental health
Background: Pubertal delay is thought to contribute to suboptimal peak bone mass acquisition in young people with cystic fibrosis (CF), leading to an increased fracture incidence. This study aims to compare pubertal development in young people with CF with that of a local healthy population and assess the influence it has on areal bone mineral density (aBMD). Methods: Tanner stage, age of menarche, bone age (BA), sex hormone levels and aBMD were examined in 85 individuals with CF (aged 5.3–18.1 years, 39 females) and 100 local controls (5.6–17.9 years, 54 females). Results: Tanner stage and age of menarche were not significantly different between controls and CF. Tanner stage‐adjusted mean values for follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T) were lower in males with CF (FSH: P = 0.004, LH: P = 0.01 and T: P = 0.002). Bone age was delayed in adolescents with CF compared to controls (chronological age–BA: controls = 0.13 years (SE = 0.16), CF = 0.95 years (SE = 0.22), P = 0.003). Areal bone mineral density (adjusted for age, sex, height and lean tissue mass) was not significantly different between CF and controls. Moderate negative correlations were found between delayed BA and weight ( r = −0.41, P < 0.001) and height ( r = −0.41, P < 0.001). Conclusions: There was no evidence of clinical pubertal delay or low aBMD (adjusted for short stature and lean tissue mass) in young people with CF when compared with a local population, despite lower nutritional markers, height and weight and delayed skeletal maturation.