Department of Rheumatology Military Hospital, El Manar University of Tunis, Tunis, Tunisia.
Faculty of Medicine of Tunis, Tunis El Manar University, Tunisia.
Curr Rheumatol Rev. 2024;20(5):488-500. doi: 10.2174/0115733971267895231227102539.
Hypoparathyroidism is a rare metabolic disorder that can be responsible for musculoskeletal manifestations.
We present a systematic review of musculoskeletal manifestations of adult-onset nonsurgical nongenetic hypoparathyroidism.
A systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline using the MEDLINE database, including manuscripts describing musculoskeletal manifestations of adult-onset nonsurgical nongenetic hypoparathyroidism.
Musculoskeletal manifestations included myopathy, shoulder disorder, immune-negative non-erosive peripheral arthritis, axial involvement simulating spondylarthritis, and diffuse ligamentous ossifications. An association between hypoparathyroidism and spondyloarthritis or autoimmune diseases is possible. T-cell activation, seen in patients with hypoparathyroidism, may explain the co-occurrence of hypoparathyroidism with other autoimmune diseases. The treatment of these manifestations is based on calcium and active vitamin D supplementation. Parathyroid hormone may have an anabolic effect on muscle atrophy and muscle weakness. Parathyroid hormone can also promote bone formation and bone resorption by stimulating osteoclast differentiation by increasing RANKL (receptor activator for nuclear factor kappa-B ligand) expression. Therefore, hypoparathyroidism can be responsible for an increase in bone mineral density. However, the risk of fractures does not appear to be reduced due to changes in bone microarchitecture and the high risk of falls. Treatment with parathyroid hormone has been shown to improve bone microarchitecture.
Our review showed that musculoskeletal manifestations are frequent in patients with hypoparathyroidism, including muscular, axial, peripheral articular, and entheseal manifestations.
甲状旁腺功能减退症是一种罕见的代谢紊乱,可导致骨骼肌肉表现。
我们对成人非手术非遗传性甲状旁腺功能减退症的骨骼肌肉表现进行了系统回顾。
根据系统评价和荟萃分析的首选报告项目指南,使用 MEDLINE 数据库进行了系统评价,包括描述成人非手术非遗传性甲状旁腺功能减退症骨骼肌肉表现的手稿。
骨骼肌肉表现包括肌病、肩部疾病、免疫阴性非侵蚀性周围关节炎、模拟脊椎关节炎的轴性受累以及弥漫性韧带骨化。甲状旁腺功能减退症与脊椎关节炎或自身免疫性疾病之间可能存在关联。甲状旁腺功能减退症患者中可见 T 细胞激活,这可能解释了甲状旁腺功能减退症与其他自身免疫性疾病的同时发生。这些表现的治疗基于钙和活性维生素 D 的补充。甲状旁腺激素可能对肌肉萎缩和肌无力有合成代谢作用。甲状旁腺激素还可以通过增加 RANKL(核因子 kappa-B 配体受体激活剂)表达来刺激破骨细胞分化,从而促进骨形成和骨吸收。因此,甲状旁腺功能减退症可导致骨密度增加。然而,由于骨微结构的变化和跌倒风险高,骨折风险似乎并未降低。甲状旁腺激素治疗已被证明可以改善骨微结构。
我们的综述表明,骨骼肌肉表现是甲状旁腺功能减退症患者常见的表现,包括肌肉、轴性、周围关节和附着点表现。