Decrease of collagen deposition in wound repair in type I diabetes independent of glycemic control
Decrease of collagen deposition in wound repair in type I diabetes independent of glycemic control
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DOI：
10.1001/archsurg.138.1.34
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发表时间：
2003-01-01
影响因子：
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通讯作者：
Gottrup, F
中科院分区：
文献类型：
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作者：
Black, E;Vibe-Petersen, J;Gottrup, F
假设：1 型和 2 型糖尿病和血糖控制影响人类伤口愈合。设计：使用人体伤口愈合模型进行实验研究。设置：多学科伤口愈合部门、医学系和研究实验室之间的合作。患者、对照受试者和方法：34 名 1 型（胰岛素依赖型）糖尿病患者和 25 名 2 型（非胰岛素依赖型）糖尿病患者以及 5 名非糖尿病对照患者受试者与2型糖尿病患者相匹配，伤口愈合能力通过皮下胶原蛋白的积累（以羟脯氨酸测量）来确定。植入两根扩张的聚四氟乙烯管，10天后取出。羟脯氨酸含量采用高效液相色谱法测定；通过使用放射性标记的胶原底物来测定胶原酶活性。研究了患者组中伤口培养的成纤维细胞的增殖情况。结果：与 2 型糖尿病相比，1 型糖尿病患者的羟脯氨酸沉积减少了 40% (P=.03)（中位数为 0.70 vs 1.16 nmol/mg；四分位数范围为 0.48-1.04 vs 0.56-1.63 nmol/mg），与对照组没有显着差异（中位数，1.35 nmol/mg；四分位数范围，0.72-1.88 nmol/mg）。 1 型糖尿病中胶原蛋白沉积的减少并不是由胶原酶活性增加引起的。在任一糖尿病组中，羟脯氨酸的沉积与糖基化血红蛋白水平均不显着相关（r(s) = 0.07；P=.63）。与 2 型糖尿病患者和对照组相比，1 型糖尿病患者的成纤维细胞生长也有所减少。结论：1 型糖尿病患者急性伤口中的胶原蛋白沉积受损，可能是由于成纤维细胞增殖减少所致。在 2 型糖尿病中，胶原蛋白沉积是正常的。血糖控制不会影响 1 型或 2 型糖尿病急性伤口修复中的胶原蛋白沉积。
Hypothesis: Type 1 and type 2 diabetes mellitus and glycemic control influence wound healing in humans.Design: Experimental study using a human wound-healing model.Setting: Collaboration among a multidisciplinary wound-healing department, department of medicine, and research laboratories.Patients, Control Subjects, and Methods: In 34 patients with type 1 (insulin-dependent) and 25 with type 2 (non-insulin-dependent) diabetes and 5 nondiabetic control subjects matched with the type 2 diabetic patients, wound-healing capacity was determined as subcutaneous accumulation of collagen measured as hydroxyproline. Two expanded polytetrafluoroethylene tubes were implanted and removed 10 days later. The hydroxyproline level was determined by means of high-performance liquid chromatography; the collagenase activity, by using a radiolabeled collagen substrate. Proliferation of fibroblasts cultured from the wounds was studied in patient groups.Results: The deposition of hydroxyproline decreased by 40% (P=.03) in type 1 compared with type 2 diabetes (median, 0.70 vs 1.16 nmol/mg; interquartile range, 0.48-1.04 vs 0.56-1.63 nmol/mg), which in turn did not differ significantly from that of controls (median, 1.35 nmol/ mg; interquartile range, 0.72-1.88 nmol/mg). The decreased collagen deposition in type 1 diabetes was not caused by increased collagenase activity. The deposition of hydroxyproline did not correlate significantly (r(s)= 0.07; P=.63) with glycosylated hemoglobin levels in either diabetic group. Fibroblast growth was also decreased in type 1 compared with type 2 diabetic patients and controls.Conclusions: Collagen deposition in acute wounds is impaired in type 1 diabetes, possibly due to a decreased fibroblast proliferation. In type 2 diabetes, collagen deposition is normal. Glycemic control does not influence collagen deposition in acute wound repair in type 1 or in type 2 diabetes mellitus.