Prolactinomas in Adolescents: Persistent Bone Loss After 2 Years of Prolactin Normalization

Effect of 2 years of cortisol normalization on the impaired bone mass and turnover in adolescent and adult patients with Cushing's disease: a prospective study

“…Interestingly, earlier studies have shown that young/adolescent patients undergoing glucocorticoid therapy may lose bone mass more rapidly than older patients do (Ruegsegger et al ., 1983). In addition, osteopenic disorders in children with CD may be further worsened by concomitant hypogonadism and GH deficiency, both of which are associated with decreased BMD (Kaufmann et al ., 1992; De Boer et al ., 1994; Canalis, 1996; Leong et al ., 1996; Matkovic, 1996; Di Somma et al ., 1998a,b; Colao et al ., 1999b, 2000b; Soika et al ., 2000).…”

“…Any impairment in bone maturation occurring during childhood can cause severe derangement of bone mass (Soika et al ., 2000). Remarkably, young patients with hyperprolactinaemia (Di Somma et al ., 1998b; Colao et al ., 2000b) or GH deficiency (Kaufmann et al ., 1992; De Boer et al ., 1994; Colao et al ., 1999b) have a greater bone loss than adult patients. In a previous study, we demonstrated that patients with childhood‐onset CD have a similar impairment of bone loss, evaluated by Z score at lumbar spine, with an increased resorption, evaluated by urinary cross‐linked N‐telopeptides of type I collagen (Ntx), as compared to adult patients (Di Somma et al ., 2001).…”

Severe impairment of bone mass and turnover in Cushing’s disease: comparison between childhood‐onset and adulthood‐onset disease

“…Small differences (of 5 -10%) in bone mass and density at maturity are likely to contribute to substantial differences in the occurrence of osteoporotic fractures (Matkovic, 1996). In this regard, it has been shown that bone impairment in young hyperprolactinaemic patients (Greenspan et al, 1986;Biller et al, 1992; Somma et al, 1998a,b;Colao et al, 2000) and childhood-onset GH deficiency (Kaufmann et al, 1992;De Boer et al, 1994;Colao et al, 1999a,b) is more severe than in adult patients, a phenomenon explained by the reduced peak bone mass observed in these patients.…”

Antipsychotics and hyperprolactinaemia: mechanisms, consequences and management

“…36,37 The degree of osteopaenia is related to hyperprolactinaemia duration, especially where the onset was during adolescence, rather than absolute prolactin concentration; 38 treatment of the prolactinoma improves BMD. 39 Longstanding gonadal axis suppression is the most important mechanism linking hyperprolactinaemia with reduced BMD 40 , but prolactin may also have a direct inhibitory effect upon osteoblasts, at least in rats. 41 The molecular mechanisms underlying these direct effects are not fully understood but may involve activation of nuclear factor j B ligand (RANKL), an important regulator of osteoclast differentiation and function.…”