Gough A, Abraha H, Li F, Purewal T S, Foster A V, Watkins P J, Moniz C, Edmonds M E
Diabetic Department, King's College Hospital, London, UK.
Diabet Med. 1997 Jul;14(7):527-31. doi: 10.1002/(SICI)1096-9136(199707)14:7<527::AID-DIA404>3.0.CO;2-Q.
Excess osteoclast activity is believed to be responsible for the early bone changes associated with Charcot neuroarthropathy in diabetes mellitus. Markers of osteoclast and osteoblast activity were measured in four groups of patients: 16 with an acute Charcot foot, 16 with a chronic Charcot foot, 10 diabetic controls, and 10 non-diabetic controls. Serum carboxyterminal telopeptide of type 1 collagen (1CTP), a marker of osteoclastic bone resorption, was significantly raised in the dorsal venous arch of the acute Charcot foot, 6.1 +/- 1.5 microg l(-1) (mean +/- SD) compared with the chronic Charcot foot 4.1 +/- 1.4, diabetic controls 3.3 +/- 1.4, and non-diabetic controls 2.8 +/- 1.4, p < 0.0001. This local increase in 1CTP was also reflected systemically in a study subgroup of 6 patients with acute Charcot neuroarthropathy, in whom peripheral antecubital vein 1CTP was 9.2 +/- 2.6 compared with 9.0 +/- 3.1 in the foot. In 6 chronic Charcot neuroarthropathy patients, foot (3.8 +/- 1.3) and systemic (4.0 +/- 1.5) 1CTP values were similar. Serum procollagen carboxyterminal propeptide (P1CP), an indicator of osteoblastic bone formation, was not significantly different between the feet of patients with acute Charcot neuroarthropathy 112 +/- 1.5 microg l(-1), patients with chronic Charcot neuroarthropathy 109 +/- 1.5 microg l(-1), diabetic controls 93.5 +/- 2.3 microg l(-1), and non-diabetic controls 90.1 +/- 1.5 microg l(-1). These results suggest that the acute Charcot foot demonstrates excess osteoclastic activity without concomitant increase in osteoblastic function. This may be important in its pathogenesis.
破骨细胞活性过高被认为是糖尿病中与夏科氏神经关节病相关的早期骨骼变化的原因。在四组患者中测量了破骨细胞和成骨细胞活性的标志物：16例急性夏科氏足患者、16例慢性夏科氏足患者、10例糖尿病对照者和10例非糖尿病对照者。1型胶原羧基末端肽（1CTP）是破骨细胞骨吸收的标志物，在急性夏科氏足的足背静脉弓中显著升高，为6.1±1.5μg l(-1)（均值±标准差），而慢性夏科氏足为4.1±1.4，糖尿病对照者为3.3±1.4，非糖尿病对照者为2.8±1.4，p<0.0001。在6例急性夏科氏神经关节病患者的研究亚组中，这种1CTP的局部升高在全身也有体现，其中外周肘前静脉1CTP为9.2±2.6，而足部为9.0±3.1。在6例慢性夏科氏神经关节病患者中，足部（3.8±1.3）和全身（4.0±1.5）的1CTP值相似。血清前胶原羧基末端前肽（P1CP）是成骨细胞骨形成的指标，急性夏科氏神经关节病患者足部为112±1.5μg l(-1)，慢性夏科氏神经关节病患者足部为109±1.5μg l(-1)，糖尿病对照者为93.5±2.3μg l(-1)，非糖尿病对照者为90.1±1.5μg l(-1)，各组之间无显著差异。这些结果表明，急性夏科氏足表现出破骨细胞活性过高，而成骨细胞功能没有相应增加。这在其发病机制中可能很重要。
