Misra Madhusmita, Golden Neville H, Katzman Debra K
Division of Pediatric Endocrinology and the Neuroendocrine Unit, Massachusetts General Hospital, Boston, Massachusetts.
Division of Adolescent Medicine, Stanford University School of Medicine, Palo Alto, California.
Int J Eat Disord. 2016 Mar;49(3):276-92. doi: 10.1002/eat.22451. Epub 2015 Aug 27.
Low bone mineral density (BMD) is a known consequence of anorexia nervosa (AN) and is particularly concerning during adolescence, a critical time for bone accrual. A comprehensive synthesis of available data regarding impaired bone health, its determinants, and associated management strategies in AN is currently lacking. This systematic review aims to synthesize information from key physiologic and prospective studies and trials, and provide a thorough understanding of impaired bone health in AN and its management.
Search terms included "anorexia nervosa" AND "bone density" for the period 1995-2015, limited to articles in English. Papers were screened manually based on journal impact factor, sample size, age of participants, and inclusion of a control group. When necessary, we included seminal papers published before 1995.
AN leads to low BMD, impaired bone quality and increased fracture risk. Important determinants are low lean mass, hypogonadism, IGF-1 deficiency, and alterations in other hormones that impact bone health. Weight gain and menses restoration are critical for improving bone outcomes in AN. Physiologic estrogen replacement as the transdermal patch was shown to increase bone accrual in one study in adolescent females with AN; however, residual deficits persist. Bisphosphonates are potentially useful in adults with AN.
To date, evidence suggests that the safest and most effective strategy to improve bone health in AN is normalization of weight with restoration of menses. Pharmacotherapies that show promise include physiologic estradiol replacement (as the transdermal estradiol patch), and in adults, bisphosphonates. Further studies are necessary to determine the best strategies to normalize BMD in AN.
低骨矿物质密度（BMD）是神经性厌食症（AN）的一个已知后果，在青春期这一骨骼积累的关键时期尤其令人担忧。目前缺乏关于AN患者骨骼健康受损、其决定因素及相关管理策略的现有数据的综合综述。本系统评价旨在综合关键生理学研究、前瞻性研究及试验中的信息，全面了解AN患者的骨骼健康受损情况及其管理方法。
检索词为1995年至2015年期间的“神经性厌食症”和“骨密度”，仅限于英文文章。根据期刊影响因子、样本量、参与者年龄及是否包含对照组对手稿进行人工筛选。必要时，我们纳入了1995年之前发表的重要论文。
AN会导致低BMD、骨质量受损及骨折风险增加。重要的决定因素包括低瘦体重、性腺功能减退、胰岛素样生长因子-1（IGF-1）缺乏以及其他影响骨骼健康的激素变化。体重增加和月经恢复对于改善AN患者的骨骼状况至关重要。在一项针对患有AN的青春期女性的研究中，经皮贴片形式的生理性雌激素替代疗法显示可增加骨量积累；然而，仍存在残余缺陷。双膦酸盐类药物对成年AN患者可能有用。
迄今为止，有证据表明，改善AN患者骨骼健康最安全、最有效的策略是通过恢复月经使体重正常化。显示出前景的药物治疗方法包括生理性雌二醇替代疗法（经皮雌二醇贴片），对于成年人则是双膦酸盐类药物。有必要进行进一步研究以确定使AN患者BMD正常化的最佳策略。
