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Constitutional delay in growth and puberty (CDGP) is associated with hypoleptinaemia
Author(s) -
Gill Matthew S.,
Hall Catherine M.,
Tillmann Vallo,
Clayton Peter E.
Publication year - 1999
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.1999.00736.x
Subject(s) - leptin , medicine , endocrinology , prepuberty , bone age , body mass index , morning , radioimmunoassay , delayed puberty , hormone , obesity
OBJECTIVE Serum leptin concentrations are higher in early adolescence compared with childhood and may play a facilitatory role in pubertal development. Constitutional delay in growth and puberty (CDGP) is a disorder of the tempo of physical maturation and may be associated with relative hypoleptinaemia. We have therefore compared serum leptin concentrations in normal boys with those in boys exhibiting constitutional delay of growth, controlling for pubertal status, age and body mass index (BMI). PATIENTS 23 boys with constitutional delay in growth ( n = 17, prepubertal) and puberty ( n = 6, early pubertal) and 88 normal boys ( n = 64 prepubertal, n = 24 Tanner stage 2). MEASUREMENTS Serum leptin was measured in a single, non‐fasted morning serum sample by radioimmunoassay. Using the data from normal boys, leptin standard deviation scores (sds) were calculated, to account for the independent influences of age and body mass index (BMI) sds. Both chronological age and bone age were used in the calculation of leptin sds in those with delay. RESULTS BMIsds was significantly lower in prepubertal delays compared with controls but was not different in pubertal subjects. Leptin concentrations were higher in early puberty compared with prepuberty ( P < 0.001) in normal boys but were not significantly elevated in pubertal boys with delay compared with prepubertal delays. Although leptin sds, for both chronological age and bone age, was similar in prepubertal controls and delays, it was significantly lower in the pubertal delay group ( P < 0.05). In controls leptin sds did not correlate with age. However, in delays leptin sds was negatively correlated with both chronological age ( r = − 0.43, P < 0.05) and bone age ( r = − 0.68, P < 0.01), indicating that in the older delays leptin levels were lower than expected given their age and BMIsds. CONCLUSIONS These data indicate that significantly higher leptin levels in Tanner stage 2 compared with prepuberty are not a prerequisite for progression into puberty. However, the absence of elevated leptin concentrations may be associated with delayed puberty in boys.