Department of rheumatology, hôpital Roger-Salengro, CHRU de Lille, 59000 Lille, France; EA4490, PMOI, pathophysiology of inflammatory bone diseases, université de Lille, université Littoral Côte d'Opale, 59000 Lille, France.
Department of addiction medicine, hôpital Fontan, CHRU de Lille, 59000 Lille, France.
Joint Bone Spine. 2019 Jan;86(1):95-101. doi: 10.1016/j.jbspin.2018.03.014. Epub 2018 Apr 10.
Bone loss in anorexia nervosa (AN) is multifactorial; its mechanisms are not yet clearly understood and may vary depending on disease duration and severity. To determine to what extent adipokines may be involved in the bone alterations found in anorexic patients, we evaluated plasma levels for leptin, adiponectin and Pref-1 against other clinical and biological parameters in a population of anorexic patients split according to weight and bone status.
Plasma concentrations of leptin, total adiponectin, high molecular weight (HMW) adiponectin, and Pref-1 were measured. The ratio of HMW adiponectin to total adiponectin - HMW (percentage) - was calculated. We divided our population into 5 groups with different phenotypes characterizing the severity of the disease and/or the severity of bone involvement: 1 - Normal BMD and body mass index (BMI): recovery from AN; 2 - Osteopenia (-2<Z-score<-1) and BMI>17kg/m; 3 - Osteopenia and BMI≤17kg/m; 4 - Osteoporosis (Z-score≤-2) and BMI>17kg/m; 5 - Osteoporosis and BMI≤17kg/m.
The study involved 80 anorexia nervosa patients. Mean BMI was 16.8±2.4kg/m. No significant difference was found in total and HMW adiponectin plasma concentrations between the 5 groups. HMW (percentage) was significantly higher in group 5 compared to group 1. Leptin was significantly lower in groups 3 and 5 compared to the other groups. For the whole group femoral neck and hip BMD correlated negatively with total adiponectin and HMW adiponectin. No correlation was found between BMD (whatever the site) and plasma leptin. Multivariate analysis revealed that 2 factors - leptin and BMI - explained 10% of the variance in spine BMD. For femoral neck BMD, the 2 explanatory factors were BMI and total adiponectin which explained 14% of the variance in BMD. For total hip BMD, 27% of the variance in BMD was explained by 3 factors: leptin, BMI, and total adiponectin.
Bone status in anorexia nervosa is mainly determined by BMI, leptin and adiponectin.
厌食症（AN）患者存在多种原因的骨质流失，其发病机制尚不完全清楚，可能因疾病持续时间和严重程度而有所不同。为了确定脂肪细胞因子在厌食症患者骨骼改变中可能发挥的作用，我们评估了不同体重和骨骼状态的厌食症患者群体的血浆瘦素、脂联素和 Pref-1 水平，并将其与其他临床和生物学参数进行了比较。
测量了血浆中瘦素、总脂联素、高分子量（HMW）脂联素和 Pref-1 的浓度。计算了 HMW 脂联素与总脂联素的比值（HMW/总脂联素的百分比）。我们将患者分为 5 组，每组的表型不同，特征为疾病严重程度和/或骨骼受累严重程度不同：1. 正常骨密度和体重指数（BMI）：从 AN 中恢复；2. 骨量减少（-2<Z 评分<-1）且 BMI>17kg/m；3. 骨量减少且 BMI≤17kg/m；4. 骨质疏松（Z 评分≤-2）且 BMI>17kg/m；5. 骨质疏松且 BMI≤17kg/m。
该研究共纳入 80 例 AN 患者，平均 BMI 为 16.8±2.4kg/m。5 组患者之间总脂联素和 HMW 脂联素的血浆浓度无显著差异。与组 1 相比，组 5 的 HMW（百分比）显著更高。与其他组相比，组 3 和组 5 的瘦素明显更低。对于整个研究人群，股骨颈和髋部 BMD 与总脂联素和 HMW 脂联素呈负相关。无论在何处（股骨颈或髋部），BMD 均与血浆瘦素无相关性。多元分析显示，2 个因素——瘦素和 BMI——可解释脊柱 BMD 变异的 10%。对于股骨颈 BMD，2 个解释因素为 BMI 和总脂联素，可解释 BMD 变异的 14%。对于全髋 BMD，3 个因素（瘦素、BMI 和总脂联素）可解释 BMD 变异的 27%。
厌食症患者的骨骼状态主要由 BMI、瘦素和脂联素决定。
