Vitamin D Deficiency and Secondary Hyperparathyroidism as Potential Causes of Idiopathic Knee Angular Deformity: A Prospective Cross-Sectional Comparative Study.

IF 1.5 3区 医学 Q3 ORTHOPEDICS
Sang Roc Han, Won Ik Lee, Su Yeon Yu, Mi Hyun Song, Tae-Joon Cho, Chang Ho Shin
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引用次数: 0

Abstract

Background: Genu valgum and genu varum have various causes; however, the cause in some children remains unknown, leading to a diagnosis of idiopathic angular deformity. In this study, we investigated whether vitamin D deficiency could lead to idiopathic knee angular deformity in the absence of typical radiographic findings of rickets by examining serum markers in affected children and controls.

Methods: In this prospective cross-sectional comparative study, we evaluated 38 children aged 7 to 14 years with genu valgum or varum without medical conditions or radiographic findings affecting lower limb alignment and 29 controls. Laboratory parameters and the prevalence of vitamin D deficiency (serum 25-hydroxyvitamin D level <20 ng/mL) or hyperparathyroidism [serum parathyroid hormone (PTH) level >60 pg/mL] were compared between the 2 groups. The prevalence of angular deformities was compared among the groups based on the presence of vitamin D deficiency and hyperparathyroidism. Binary logistic regression analysis was used to calculate the odds ratios (ORs) for angular deformities based on vitamin D deficiency and hyperparathyroidism.

Results: The mean serum 25-hydroxyvitamin D levels did not significantly differ between the angular deformity (16.7±6.1 ng/mL) and control groups (19.9±7.1 ng/mL) (P=0.055). However, vitamin D deficiency was more prevalent in the angular deformity group than in the control group (79% vs. 48%, P=0.009). Angular deformities were more prevalent in children with both vitamin D deficiency and hyperparathyroidism than in those without these conditions [11/13 (85%) vs. 5/18 (28%), P=0.012]. The logistic regression analysis-adjusted for age, sex, and weight-showed a higher risk of angular deformity in children with both vitamin D deficiency and hyperparathyroidism (OR: 9.86, 95% CI: 1.36-71.47, P=0.024), but not in children with vitamin D deficiency alone.

Conclusions: Isolated vitamin D deficiency without other laboratory abnormalities or radiographic findings of rickets did not lead to knee angular deformity. However, in cases in which vitamin D deficiency elevates PTH levels, idiopathic genu valgum or genu varum might be observed.

Level of evidence: Level III-prognostic study.

维生素D缺乏和继发性甲状旁腺功能亢进是特发性膝关节角畸形的潜在原因:一项前瞻性横断面比较研究。
背景:膝外翻和膝内翻有多种原因;然而,在一些儿童的原因仍然不明,导致诊断为特发性角畸形。在这项研究中,我们通过检测患病儿童和对照组的血清标志物,研究了维生素D缺乏是否会在没有典型佝偻病影像学表现的情况下导致特发性膝关节角畸形。方法:在这项前瞻性横断面比较研究中,我们评估了38名年龄在7至14岁之间,没有医疗条件或影像学表现影响下肢对齐的膝外翻或内翻儿童和29名对照组。比较两组患者实验室指标及维生素D缺乏症发生率(血清25-羟基维生素D水平60 pg/mL)。根据维生素D缺乏症和甲状旁腺功能亢进的存在,比较各组之间角状畸形的患病率。采用二元logistic回归分析计算因维生素D缺乏和甲状旁腺功能亢进导致的角状畸形的比值比(ORs)。结果:角畸形组血清25-羟基维生素D水平(16.7±6.1 ng/mL)与对照组(19.9±7.1 ng/mL)差异无统计学意义(P=0.055)。然而,维生素D缺乏症在角畸形组比对照组更为普遍(79%对48%,P=0.009)。角状畸形在维生素D缺乏和甲状旁腺功能亢进的儿童中比在没有这些疾病的儿童中更为普遍[11/13(85%)比5/18 (28%),P=0.012]。经年龄、性别和体重调整后的logistic回归分析显示,维生素D缺乏和甲状旁腺功能异常的儿童发生角畸形的风险更高(OR: 9.86, 95% CI: 1.36-71.47, P=0.024),但单独维生素D缺乏的儿童没有发生角畸形的风险。结论:没有其他实验室异常或佝偻病影像学表现的单独维生素D缺乏不会导致膝关节角畸形。然而,在维生素D缺乏升高甲状旁腺激素水平的情况下,可能会观察到特发性膝外翻或膝内翻。证据等级:iii级预后研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.30
自引率
17.60%
发文量
512
审稿时长
6 months
期刊介绍: ​Journal of Pediatric Orthopaedics is a leading journal that focuses specifically on traumatic injuries to give you hands-on on coverage of a fast-growing field. You''ll get articles that cover everything from the nature of injury to the effects of new drug therapies; everything from recommendations for more effective surgical approaches to the latest laboratory findings.
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