Monson J P, Drake W M, Carroll P V, Weaver J U, Rodriguez-Arnao J, Savage M O
Department of Endocrinology, St Bartholomew's Hospital, London, UK.
Horm Res. 2002;58 Suppl 1:52-6. doi: 10.1159/000064765.
Growth hormone (GH) exerts important influences on bone metabolism during lifespan. During childhood, GH is a major determinant of acquisition of bone mass and in adult life, GH partly determines the rate of bone remodelling and therefore influences maintenance of bone mineral density (BMD). Insights into the importance of GH in these respects may be obtained by studies of BMD and indices of bone remodelling in GH deficiency (GHD) of adult-onset and childhood-onset. Adult-onset GHD, usually accompanied by other features of hypopituitarism, may be associated with osteopenia and an increased fracture risk. Postulated mechanisms include GHD and gonadal steroid deficiency of unknown duration; glucocorticoid and thyroxine replacement do not appear to exert a major role. GH replacement in adult-onset GHD results in an early increment in indices of bone remodelling which persists for up to 5 years; BMD increases by 0.5-1.0 SD in males and stabilizes in females over this time period. In adolescents with GHD who traditionally discontinue GH at completion of linear growth, BMD is substantially lower than peak bone mass for a young adult population. Studies addressing the effects of continuation of GH after achievement of final height are currently underway and will provide insights into the possible need to continue GH into adult life. Such studies may confirm a role for GH in promoting continued accrual of bone mass and thereby demonstrate that cessation of GH at achievement of final height, by limiting peak bone mass, may predispose to clinically significant osteoporosis in later life. In addition to the potential importance of GH for achievement of peak bone mass, there may be a superimposed accelerated loss of BMD with advancing age similar to the situation observed in adult-onset GHD. To date, this has been difficult to assess in adult GHD of childhood-onset because the relative contributions of low peak bone mass and increased loss of bone in later life could not be distinguished.
生长激素(GH)在整个生命周期中对骨代谢发挥着重要影响。在儿童期,GH是获取骨量的主要决定因素,而在成年期,GH部分决定骨重塑速率,因此影响骨矿物质密度(BMD)的维持。通过对成年期和儿童期起病的生长激素缺乏症(GHD)患者的BMD及骨重塑指标进行研究,可深入了解GH在这些方面的重要性。成年期起病的GHD通常伴有其他垂体功能减退的特征,可能与骨质减少及骨折风险增加有关。推测的机制包括持续时间不明的GHD和性腺类固醇缺乏;糖皮质激素和甲状腺素替代治疗似乎不起主要作用。成年期起病的GHD患者接受GH替代治疗后,骨重塑指标早期增加,这种增加可持续长达5年;在此期间,男性的BMD增加0.5 - 1.0标准差,女性的BMD则趋于稳定。在传统上在线性生长完成后停止使用GH的青少年GHD患者中,BMD显著低于年轻成年人群的峰值骨量。目前正在进行关于达到最终身高后继续使用GH的影响的研究,这些研究将为成年后可能需要继续使用GH提供见解。此类研究可能证实GH在促进骨量持续积累中的作用,从而表明在达到最终身高时停止使用GH,由于限制了峰值骨量,可能使个体在晚年易患具有临床意义的骨质疏松症。除了GH对达到峰值骨量的潜在重要性外,随着年龄增长,可能还会出现类似于成年期起病的GHD中观察到的BMD加速丢失的情况。迄今为止,由于难以区分儿童期起病的成年GHD患者中低峰值骨量和晚年骨量增加丢失的相对贡献,因此很难对此进行评估。