Procollagen type I carboxy‐terminal extension peptide in serum as a marker of collagen biosynthesis in bone. Correlation with iliac bone formation rates and comparison with total alkaline phosphatase
Procollagen type I carboxy‐terminal extension peptide in serum as a marker of collagen biosynthesis in bone. Correlation with iliac bone formation rates and comparison with total alkaline phosphatase
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DOI：
10.1002/jbmr.5650020510
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发表时间：
1987-10
影响因子：
6.2
通讯作者：
A. Parfitt;L. Simon;A. Villanueva;S. Krane
中科院分区：
文献类型：
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作者：
A. Parfitt;L. Simon;A. Villanueva;S. Krane
我们测量了双四环素标记后所有表面的髂骨形成率，血清1型前胶原羧基末端延伸肽（pColl‐I‐C）水平，以及4名正常受试者和44名各种形式代谢性骨病患者的血清总碱性磷酸酶活性（TAP）水平。在3例有肝脏疾病酶法证据的患者中，两种生化血清标志物均不成比例地升高。在一名特发性轴状骨硬化患者中，血清pColl - I - C选择性地增加了10倍以上。在其余44名受试者中，pColl‐I‐C和TAP水平相互之间存在显著相关性（r = 0.70），并且两者都表现出相同的方向性变化，与以不同方式表达的髂骨形成率的相关性大致相似。总的来说，pColl - I - C水平与松质骨形成率和TAP水平与皮质骨形成率的相关性更好。使用这两种标记物的多重回归预测骨形成率有适度的改善。在15例典型的无并发症的绝经后骨质疏松患者中，生化指标单独或联合与骨形成率的表达均无显著相关性。使用pColl‐I‐C作为标记物的缺点包括：除骨以外的组织中1型胶原生物合成对血清水平的显著贡献，以及（可能）可变的代谢清除率。对于这两种生化标志物，发现与整个活检核体积的总骨形成率具有最一致的高相关性（r = 0.77-0.79），这是活体组织骨器官水平的骨形成率的最佳估计。将骨芯体积作为参考，还可以比较皮质、皮质内和松质表面形成的骨量。血清pColl - I - C水平作为一种无创骨代谢指标值得进一步研究。正常和异常受试者在多种生化指标和多种组织学指标之间关系的差异，有可能为了解骨质疏松症的发病机制提供线索。
We measured iliac bone formation rates on all surfaces after double tetracycline labeling, serum levels of type 1 procollagen carboxy‐terminal extension peptide (pColl‐I‐C), and serum levels of total alkaline phosphatase activity (TAP) in four normal subjects and in 44 patients with various forms of metabolic bone disease. In three patients with enzymatic evidence of liver disease both biochemical serum markers were disproportionately raised. In a patient with idiopathic axial osteosclerosis serum pColl‐I‐C was selectively increased by more than ten‐fold. In the remaining 44 subjects pColl‐I‐C and TAP levels correlated significantly with each other (r = 0.70) and both showed the same directional changes and broadly similar correlations with iliac bone formation rate expressed in different ways. In general, pColl‐I‐C levels correlated better with cancellous bone formation rates and TAP levels with cortical bone formation rates. There was a modest improvement in prediction of bone formation rate with multiple regression using both markers. In 15 patients with typical uncomplicated postmenopausal osteoporosis, neither biochemical marker, singly or jointly, correlated significantly with any expression of bone formation rate. Disadvantages to the use of pColl‐I‐C as a marker include a significant contribution to the serum level from type 1 collagen biosynthesis in tissues other than bone, and (probably) variable metabolic clearance. For both biochemical markers the most consistently high correlations (r = 0.77–0.79) were found with total bone formation rate for the entire biopsy core volume, which is the best estimate available from a biopsy of formation rate at the bone organ level of organization in vivo. The core volume as a referent also allows the amount of bone formed on cortical, endocortical, and cancellous surfaces to be compared. Measurement of serum pColl‐I‐C levels merits further study as a noninvasive index of bone metabolism. Differences between normal and abnormal subjects in the relationships between a variety of biochemical markers and a variety of histologic indices have the potential for providing insight into the pathogenesis of osteoporosis.