Andress D L, Hercz G, Kopp J B, Endres D B, Norris K C, Coburn J W, Sherrard D J
Department of Medicine, Seattle Veterans Administration Medical Center, WA.
J Bone Miner Res. 1987 Dec;2(6):525-31. doi: 10.1002/jbmr.5650020609.
Bone biopsies and plasma parathyroid hormone (PTH) from 27 diabetic dialysis patients were compared to biopsies and PTH levels from matched patients without diabetes to determine if PTH has a role in preserving bone mass in diabetic renal osteodystrophy. Significantly lower values were present in the diabetic group for mineralized bone area (p less than 0.003), osteoblastic osteoid (p less than 0.01), resorptive surface (p less than 0.001), fibrosis (p less than 0.005), bone apposition rate (p less than 0.01), bone formation rate (BMU level) (p less than 0.04), and plasma PTH (p less than 0.05). Bone-surface aluminum was higher in the diabetic group (44 +/- 5% vs. 20 +/- 5%, p less than 0.005). Linear regression analysis revealed significant positive correlations of mineralized bone area with time on dialysis, bone formation rate, bone resorption, and PTH only in the group without diabetes. While both groups had significant positive correlations of PTH with osteoblastic osteoid and bone resorption, only in the nondiabetic group was there a positive correlation of PTH with bone apposition and bone formation rate (BMU level), observations suggesting that the lower bone formation in the diabetic patients may have arisen in part from a failure of PTH to promote bone mineralization. We conclude that relatively low PTH levels and high bone aluminum in diabetic patients with chronic renal failure may be responsible in part for low bone mass when compared to uremic patients without diabetes.
对27名糖尿病透析患者的骨活检和血浆甲状旁腺激素（PTH）水平与匹配的非糖尿病患者的活检及PTH水平进行比较，以确定PTH在糖尿病肾性骨营养不良中对维持骨量是否起作用。糖尿病组的矿化骨面积（p<0.003）、成骨类骨质（p<0.01）、吸收表面（p<0.001）、纤维化（p<0.005）、骨沉积率（p<0.01）、骨形成率（骨多单位水平）（p<0.04）和血浆PTH（p<0.05）的值均显著较低。糖尿病组的骨表面铝含量较高（44±5%对20±5%，p<0.005）。线性回归分析显示，仅在非糖尿病组中，矿化骨面积与透析时间、骨形成率、骨吸收和PTH呈显著正相关。虽然两组的PTH与成骨类骨质和骨吸收均呈显著正相关，但只有在非糖尿病组中，PTH与骨沉积和骨形成率（骨多单位水平）呈正相关，这些观察结果表明，糖尿病患者较低的骨形成可能部分源于PTH促进骨矿化的功能失效。我们得出结论，与非糖尿病的尿毒症患者相比，慢性肾衰竭糖尿病患者相对较低的PTH水平和较高的骨铝含量可能部分导致了骨量较低。
