Rivera-Gallardo Ma Teresa, Ma del Socorro Parra-Cabrera, Barriguete-Meléndez Jorge Armando
Grupo Médico Río Mayo, Fundación Ariwá para el Tratamiento, Prevención e Investigación de los Trastornos de la Conducta Alimentaria, Cuernavaca, Morelos, México.
Salud Publica Mex. 2005 Jul-Aug;47(4):308-18. doi: 10.1590/s0036-36342005000400009.
Eating disorders (TCA per its abbreviation in Spanish) are common in young women, with an estimated prevalence of 4-5%. One of the physical complications of eating disorders, especially anorexia nervosa (AN) and eating disorder not otherwise specified (TANE) is bone mass loss, which affects both cortical and trabecular bone. The synergistic effect of malnutrition and estrogen deficiency produces significant bone mass loss, resulting from the uncoupling of bone turnover characterized by a decrease in osteoblastic bone formation and an increase in osteclastic bone resorption. The mechanisms implied in the pathogenesis of bone loss are the hypoestrogenism, hypercortisolism, serum leptin levels and insulin-like growth factor decrease. Severity of bone loss in anorexia nervosa varies depending on duration of illness, the minimal weight ever and sedentarism or strenuous exercise. Long term consequences occur, such as a fracture risk increase in patients who have suffered anorexia nervosa, compared with the general population. The first treatment line to recover bone mass is nutritional rehabilitation together with weight gain. Hormonal replacement therapy may be effective if combined with an anabolic method. Osteopenia and osteoporosis are terms adopted to define the deficiency of bone mass in adults. Authors have used these terms to define densitometric data in young subjects who have not reached their peak bone mass. We suggest the term "hypo-osteogenesia" to define the deficiency in the development of bone mass in adolescents or children.
饮食失调（西班牙语缩写为TCA）在年轻女性中很常见，估计患病率为4%-5%。饮食失调的身体并发症之一，尤其是神经性厌食症（AN）和未另行规定的饮食失调（TANE）是骨质流失，这会影响皮质骨和小梁骨。营养不良和雌激素缺乏的协同作用会导致明显的骨质流失，这是由于骨转换失衡所致，其特征是成骨细胞骨形成减少和破骨细胞骨吸收增加。骨质流失发病机制中涉及的机制包括雌激素水平低下、皮质醇增多、血清瘦素水平和胰岛素样生长因子降低。神经性厌食症中骨质流失的严重程度因病程、最低体重以及久坐或剧烈运动而异。会出现长期后果，例如与普通人群相比，患神经性厌食症的患者骨折风险增加。恢复骨量的一线治疗方法是营养康复并增加体重。如果与合成代谢方法联合使用，激素替代疗法可能有效。骨质减少和骨质疏松是用于定义成人骨量不足的术语。作者已使用这些术语来定义未达到峰值骨量的年轻受试者的骨密度数据。我们建议使用“骨生成不足”一词来定义青少年或儿童骨量发育不足。
