Misra Madhusmita, Klibanski Anne
Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Mass., USA.
Horm Res Paediatr. 2016;85(3):147-57. doi: 10.1159/000443735. Epub 2016 Feb 11.
Anorexia nervosa (AN) is a condition of severe undernutrition associated with adaptive changes in many endocrine axes. These changes include hypogonadotropic hypogonadism, acquired growth hormone resistance with low insulin-like growth factor 1 (IGF-1) levels, hypercortisolemia, altered secretion of adipokines and appetite-regulating hormones, and low bone mineral density (BMD). Bone health is impaired subsequent to a low body mass index, decreased lean mass, and the endocrine changes described above. In addition to low areal BMD, AN is characterized by a decrease in volumetric BMD, changes in bone geometry, and reductions in strength estimates, leading to an increased risk for fracture. Weight restoration is essential for restoration of normal endocrine function; however, hypercortisolemia, high peptide YY levels, and ghrelin dynamics may not completely normalize. In some patients, hypogonadotropic hypogonadism persists despite weight restoration. Weight gain and menstrual recovery are critical for improving bone health in AN; however, residual deficits may persist. Physiologic estrogen replacement using transdermal, but not oral, estrogen increases bone accrual in adolescents with AN, while bisphosphonates improve BMD in adults. Recombinant human IGF-1 and teriparatide have been used in a few studies as bone anabolic therapies. More data are necessary to determine the optimal therapeutic strategies for low BMD in AN.
神经性厌食症(AN)是一种严重营养不良的病症,与许多内分泌轴的适应性变化相关。这些变化包括低促性腺激素性性腺功能减退、获得性生长激素抵抗伴胰岛素样生长因子1(IGF-1)水平降低、高皮质醇血症、脂肪因子和食欲调节激素分泌改变以及低骨矿物质密度(BMD)。低体重指数、瘦体重减少以及上述内分泌变化会损害骨骼健康。除了低面积骨密度外,神经性厌食症的特征还包括体积骨密度降低、骨骼几何形状改变以及强度估计值降低,从而导致骨折风险增加。体重恢复对于恢复正常内分泌功能至关重要;然而,高皮质醇血症、高肽YY水平和胃饥饿素动态变化可能无法完全恢复正常。在一些患者中,尽管体重恢复,低促性腺激素性性腺功能减退仍会持续。体重增加和月经恢复对于改善神经性厌食症患者的骨骼健康至关重要;然而,残留缺陷可能仍然存在。使用经皮而非口服的生理雌激素替代疗法可增加神经性厌食症青少年的骨量,而双膦酸盐可改善成年人的骨密度。重组人生长激素和特立帕肽在一些研究中已被用作骨合成代谢疗法。需要更多数据来确定神经性厌食症低骨密度的最佳治疗策略。