Kalla A A, Meyers O L, Chalton D, Heath S, Brown G M, Smith P R, Burger M C
Department of Medicine, University of Cape Town, South Africa.
Br J Rheumatol. 1991 Apr;30(2):91-100. doi: 10.1093/rheumatology/30.2.91.
Osteoporosis in RA is mediated by numerous inflammatory substances. This study was undertaken to see if SAARD could modify the rate of metacarpal bone loss in RA. Combined cortical thickness (CCT) measured at the midshaft of the right second metacarpal was used to calculate bone mass (CA%) using a digitizer. Eighty-one subjects were studied, all of whom had at least three sets of hand X-rays, the last of which was approximately 18 months following initiation of SAARD therapy. There were 12 males and 69 females. The mean age at time of starting therapy was 51 (SD 12) years while the mean duration of disease at the time was 7.6 (SD 8) years. The mean time to referral for SAARD from the general clinic was 2.5 (SD 3) years. The percentage fall in bone mass prior to therapy was 2.51%/day compared to a gain of 0.6%/day after therapy (P less than 0.05). Forty-nine patients were aged over 50 years while 32 were 50 years or younger at the time of study. Comparison showed that in the pretreatment period, the rate of change in CCT and CA% was not significantly dependent age (P less than 0.1). During that therapy, the rate of change in CCT and CA% significantly different in the two age groups. Patients aged over 50 years continued to lose bone, but at a slower rate (P less than 0.05). Patients aged 50 years or less either stopped losing or gained metacarpal bone mass during the study period (P less than 0.005). The time to referral for SAARD and disease duration (comparable in the two age groups) did not have a significant effect on changes in CA% during therapy. Change in bone mass could be predicted by change in disease activity. We conclude that SAARD have a significant sparing effect on metacarpal osteoporosis in RA. This positive effect is masked by the overwhelming influence of age (and menopause) and could be missed. Metacarpal osteoporosis seems a pathophysiologically more useful measure of radiological change in RA than erosions or joint space narrowing.
类风湿关节炎中的骨质疏松由多种炎性物质介导。本研究旨在观察慢作用抗风湿药（SAARD）是否能改变类风湿关节炎患者掌骨骨质流失的速率。使用数字化仪测量右手第二掌骨中段的联合皮质厚度（CCT），以计算骨量（CA%）。研究了81名受试者，他们均至少有三组手部X线片，最后一组X线片是在开始SAARD治疗后约18个月时拍摄的。其中男性12名，女性69名。开始治疗时的平均年龄为51（标准差12）岁，当时的平均病程为7.6（标准差8）年。从普通诊所转诊至使用SAARD的平均时间为2.5（标准差3）年。治疗前骨量下降百分比为2.51%/天，而治疗后增加0.6%/天（P<0.05）。49例患者年龄超过50岁，32例患者在研究时年龄为50岁或以下。比较显示，在治疗前期，CCT和CA%的变化率与年龄无显著相关性（P<0.1）。在治疗期间，两个年龄组的CCT和CA%变化率有显著差异。年龄超过50岁的患者继续骨质流失，但速率较慢（P<0.05）。年龄50岁及以下的患者在研究期间要么停止骨质流失，要么掌骨骨量增加（P<0.005）。转诊至使用SAARD的时间和病程（两个年龄组相当）对治疗期间CA%的变化无显著影响。骨量变化可通过疾病活动度变化来预测。我们得出结论，SAARD对类风湿关节炎患者的掌骨骨质疏松有显著的保护作用。这种积极作用被年龄（和绝经）的压倒性影响所掩盖，可能会被忽视。掌骨骨质疏松在病理生理学上似乎比侵蚀或关节间隙狭窄更能有效衡量类风湿关节炎的放射学变化。
