The absence of a pathologic medical history, otherwise normal findings on physical examination, and a positive family history of delayed puberty in one or both parents suggest the diagnosis of constitutional delay. However, before making that diagnosis, important pathological conditions (e.g., CNS tumors) must be excluded. Boys with constitutional delay usually have delayed growth in childhood, and, consequently, they are short when compared with their peers. The bone age is retarded from the chronological age, but the developmental milestones are achieved at a normal bone age, i.e., onset of the first signs of pubertal development by a bone age of 14 yr. Gonadotropin and testosterone concentrations increase in concert with the advancement of the bone age. Thus, all stages of pubertal development occur at an age that is later than usual. However, boys with constitutional delay in growth and puberty do not reach their predicted adult height (50). One explanation is that reduced estrogen concentrations for chronological age (but not for bone age), impair growth hormone (GH) secretion functionally and temporally. When this functional GH deficiency lasts for a sufficiently long time, it may also affect negatively on adult height. After the onset of puberty or the initiation of testosterone treatment, growth velocity and GH secretion normalize. Final height cannot be increased with GH or testosterone treatment, although these treatments temporarily increase growth velocity.
Finkelstein and colleagues reported decreased radial (51), spinal (51,52), and femoral (52) bone mineral density (BMD) in otherwise healthy adult men with history of delayed puberty, in comparison with controls (who had a normal onset of puberty). However, another study recently showed that young men with a history of delayed puberty have normal volumetric BMD, and the authors proposed that the reduced apparent BMD is likely the consequence of the influence of bone size on measured bone density (53).
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