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“Introduction Young adults with childhood-onset

growth hormone deficiency (CO GHD) have lower bone mineral density than healthy controls [1, 2], displaying IKBKE reduced cortical thickness, cortical cross-sectional area and overall cortical mineral content [3]. Accordingly, an increased susceptibility to fractures compared to population controls has been described in young adults with CO GHD [4–6]. Until recently, patients with CO GHD were only treated with growth hormone (GH) until final adult height was attained, usually up until the age of 15–20 years. The achievement of final adult height, however, occurs much earlier than the acquisition of peak bone mass and muscle strength in both genders, with males achieving these milestones later than females [7]. During the last few years, it has been shown that in addition to stimulating linear growth, GH therapy has important beneficial effects on the accrual of lean body mass and bone mineralisation, past the years of achieving adult height [8]. Indeed, the impact of GH on bone mass accrual can continue even after discontinuation of therapy for over 1.5 years [9]. These observations suggest that GH treatment should be continued up to the achievement of peak bone mass. An increase in bone mass in young adults with GHD following GH treatment has been reported in several but not all studies [10, 11]. In adolescents with GHD, Drake et al.