Dolan A L, Moniz C, Dasgupta B, Li F, Mackintosh C, Todd P, Corrigall V, Panayi G S
Greenwich District Hospital, London, UK.
Arthritis Rheum. 1997 Nov;40(11):2022-9. doi: 10.1002/art.1780401115.
Polymyalgia rheumatica (PMR) has an abrupt onset of inflammatory symptoms, making it a useful model for studying the effects of inflammation in bone. PMR requires corticosteroid treatment, which may itself have a detrimental effect on bone. This study used serially measured biochemical markers of bone turnover and bone density to address the relative contributions of systemic inflammation and corticosteroid therapy to bone loss.
Fifty untreated patients with PMR were randomized to receive oral prednisolone or intramuscular methylprednisolone. Biochemical bone markers (pyridinoline [PYR], deoxypyridinoline [DPYR], procollagen type I carboxy-terminal peptide [PICP]) and bone mineral density (BMD) were measured at baseline and at 6, 12, and 24 months.
The median disease duration at presentation was 12 weeks (range 5-32 weeks). Levels of urinary crosslinks were increased in patients with untreated PMR compared with controls (PYR 74.9 +/- 30.0 nmoles/mmole creatinine, DPYR 14.6 +/- 6.4 nmoles/mmole creatinine [mean +/- SD]; P = 0.0001); the PICP level was normal (115.0 +/- 39.0 microg/liter). With treatment, the crosslinks levels fell and PICP levels rose within 6 months (P = 0.01). Bone resorption (PYR) correlated with untreated disease activity (erythrocyte sedimentation rate [ESR]) (r = 0.5, P = 0.003) and with interleukin-6 levels (r = 0.48, P = 0.05). There was a significant reduction in BMD of both the hip and the spine after 12 months of treatment (P = 0.0002), with no difference between treatment groups. As the steroid dosage was reduced, bone mass improved. Initial ESR influenced the percent change in BMD at 1 year (r = 0.35, P = 0.05), while cumulative steroid dose, mean ESR, and type of steroid used did not.
Inflammation in PMR increases bone resorption and appears to have a more detrimental effect on bone than does low-dose corticosteroid. If corticosteroids can be tapered and discontinued, bone loss in PMR can be a transient phenomenon.
风湿性多肌痛（PMR）起病急骤，伴有炎症症状，是研究炎症对骨骼影响的有用模型。PMR需要皮质类固醇治疗，而这种治疗本身可能对骨骼有不良影响。本研究使用连续测量的骨转换生化标志物和骨密度，以探讨全身炎症和皮质类固醇治疗对骨质流失的相对影响。
50例未经治疗的PMR患者被随机分为口服泼尼松龙组或肌内注射甲泼尼龙组。在基线以及6、12和24个月时测量骨生化标志物（吡啶啉[PYR]、脱氧吡啶啉[DPYR]、I型前胶原羧基末端肽[PICP]）和骨矿物质密度（BMD）。
就诊时疾病持续时间的中位数为12周（范围5 - 32周）。与对照组相比，未经治疗的PMR患者尿交联物水平升高（PYR 74.9±30.0纳摩尔/毫摩尔肌酐，DPYR 14.6±6.4纳摩尔/毫摩尔肌酐[均值±标准差]；P = 0.0001）；PICP水平正常（115.0±39.0微克/升）。治疗后，交联物水平在6个月内下降，PICP水平上升（P = 0.01）。骨吸收（PYR）与未经治疗的疾病活动度（红细胞沉降率[ESR]）相关（r = 0.5，P = 0.003），与白细胞介素-6水平相关（r = 0.48，P = 0.05）。治疗12个月后，髋部和脊柱的BMD均显著降低（P = 0.0002），治疗组之间无差异。随着类固醇剂量的减少，骨量有所改善。初始ESR影响1年时BMD的变化百分比（r = 0.35，P = 0.05），而累积类固醇剂量、平均ESR和所用类固醇类型则无此影响。
PMR中的炎症会增加骨吸收，且似乎对骨骼的不良影响比低剂量皮质类固醇更大。如果能够逐渐减少并停用皮质类固醇，PMR中的骨质流失可能是一种短暂现象。
