维生素D缺乏继发甲状旁腺功能亢进症患者的临床特点

Clinical characteristics of patients with secondary hyperparathyroidism induced by vitamin D deficiency

目的分析3例严重维生素D缺乏继发甲状旁腺功能亢进症患者的临床特点及治疗策略。方法收集确诊为维生素D缺乏继发甲状旁腺功能亢进患者3例,对其进行详细的病史采集和体格检查,生物化学指标测定及影像学检查。结果患者1、2起病隐匿,临床症状不典型;患者3有长期双下肢乏力,全身疼痛,进行性加重的活动障碍及身高变矮。实验室检查结果:血25羟维生素D (25 hydroxyvitamin D,25OHD)低于检测值下限(<8. 0μg/L),甲状旁腺素(parathyroid hormone,PTH)水平升高,碱性磷酸酶(alkaline phosohatase,ALP)及Ⅰ型胶原C端肽(C-terminal telopeptide of type 1 collagen,β-CTX)升高。双能X线吸收检测仪(dual energy X-ray absorptiometry,DXA)检测骨密度,提示骨密度显著降低。给予维生素D联合钙剂治疗3个月后,患者临床症状好转,随着25OHD水平升高,血PTH及骨转换标志物水平均下降,骨密度检查可见骨量增加。结论维生素D缺乏在人群中普遍存在,由于早期缺乏临床症状易被忽视,但当其引起继发性甲状旁腺功能亢进时,会对骨骼产生严重影响,导致骨转换增加,骨量流失加快,摔倒及骨折风险增加等。因此,应重视维生素D缺乏的早期防治,避免发生继发性甲状旁腺功能亢进。

Objective To analyze the clinical features and treatment strategies of three patients with secondary hyperparathyroidism induced by severe vitamin D deficiency. Methods The clinical data of three patients were collected, including clinical manifestation, biochemical parameters, and radiographic characteristics. Results Patient 1 and 2 lack typical clinical symptoms, while patient 3 had a long-lasting lower limb weakness, generalized pain,, shortened height and progressively declining life quality. Laboratory examinations showed that levels of 25 hydroxyvitamin D （25OHD） were lower （ 〈8.0 μg/L） than the minimum of detection while parathyroid hormone and bone turnover markers such as bone formation marker blood alkaline phosphatase （ALP） and bone resorption marker C-termimal telopeptide of type 1 collagen （β-CTX） were increased. Dual energy X-ray absorptiometry （DXA） suggested low bone mineral density. After treatment with vitamin D combined with calcium for 3 months, patients＇ clinical symptoms were improved. With the increasing of 250HD, the levels of serum PTH and bone turnover markers decreased. Increased bone mineral density were also observed. Conclusions Vitamin D deficiency is an important clinical problem all over the world. At early stage, due to the absence of clinical symptoms, it is easily overlooked. However, when severe vitamin D deficiency causes secondary hyperparathyroidism, it will have a serious impact on the bone, leading to increased bone turnover and accelerated bone loss, causing an increasing risk of fractures and fall. Therefore, we should pay attention to prevention and treatment of vitamin D deficiency to avoid secondary hyperparathyroidism.