Rush Eric T, Goodwin Jennifer L, Braverman Nancy E, Rizzo William B
Department of Pediatrics, University of Nebraska Medical Center, Omaha, NE, USA; Departments of Internal Medicine and Orthopaedic Surgery, University of Nebraska Medical Center, Omaha, NE, USA; Children's Hospital and Medical Center, Omaha, NE, USA.
Department of Pediatrics, University of Nebraska Medical Center, Omaha, NE, USA.
Mol Genet Metab. 2016 Jan;117(1):33-7. doi: 10.1016/j.ymgme.2015.11.009. Epub 2015 Nov 24.
Patients with Zellweger Spectrum Disorders (ZSDs) have impaired peroxisome biogenesis and severe, multisystem disease. Although the neurologic symptoms of ZSD tend to be the most prominent, patients also have hepatic, renal and adrenal impairment. Little is known about bone health in patients with ZSD, particularly those with mild or moderate presentation. We investigated 13 ZSD patients who had strikingly abnormal bone mineral density for age. DXA scans showed mean lumbar and femoral neck Z-scores of -3.2. There were no major differences between ambulatory and nonambulatory patients, and no biochemical abnormalities consistent with rickets or vitamin D deficiency were seen. Cyclic bisphosphonate therapy in one ZSD patient was successfully used to increase in bone mineral density. Although the etiology of bone disease in this condition is unknown, we speculate that altered signaling through the PPARγ pathway or deficient plasmalogens in patients with ZSD disrupts osteogenesis, resulting in poor bone formation and poor mineralization. Further investigation into the pathogenic mechanisms of bone disease in ZSD and the role of peroxisomal metabolism in osteogenesis may yield insights into the pathology of bone disease and suggest novel treatment options.
泽尔韦格谱系障碍(ZSD)患者的过氧化物酶体生物合成受损,患有严重的多系统疾病。尽管ZSD的神经系统症状往往最为突出,但患者还存在肝脏、肾脏和肾上腺功能损害。对于ZSD患者的骨骼健康,尤其是那些表现为轻度或中度的患者,人们了解甚少。我们调查了13名年龄相关骨矿物质密度显著异常的ZSD患者。双能X线吸收法扫描显示腰椎和股骨颈的平均Z值为-3.2。能走动的患者和不能走动的患者之间没有重大差异,也未发现与佝偻病或维生素D缺乏相符的生化异常。一名ZSD患者接受了周期性双膦酸盐治疗,成功提高了骨矿物质密度。尽管这种情况下骨病的病因尚不清楚,但我们推测,ZSD患者通过PPARγ途径的信号改变或缩醛磷脂缺乏会破坏骨生成,导致骨形成不良和矿化不良。对ZSD骨病的致病机制以及过氧化物酶体代谢在骨生成中的作用进行进一步研究,可能会深入了解骨病的病理,并提出新的治疗选择。