Bagdade J D, Stewart M, Walters E
Diabetes. 1978 Jun;27(6):677-81. doi: 10.2337/diab.27.6.677.
When the ability of granulocytes from 10 poorly controlled diabetic patients with fasting hyperglycemia and no evidence of ketoacidosis (mean fasting glucose 293 +/- 20 mg. per 100 ml.; mean +/- S.E.M.) to adhere to a nylon fiber column was assessed, the number of adherent granulocytes from whole blood was only 53 +/- 6 per cent of the values observed in controls. After antidiabetic treatment for one to two weeks and lowering of fasting glucose levels (mean 198 +/- 29 mg. per 100 ml.), adherence improved significantly (p less than 0.01) in the diabetics; however, their values were still subnormal (diabetic 74 per cent +/- 8 of control; p less than 0.02). Adherence values before and after treatment correlated with the fasting glucose level (r = 0.88, p less than 0.001). These findings suggest that, in addition to previously reported abnormalities in migration and the ingestion and killing of bacteria, granulocyte adherence may also be impaired in poorly controlled diabetic patients. This functional abnormality correlates directly with the fasting glucose and is reversed by insulin treatment. A defect of this type may compromise the normal inflammatory response in some diabetics and impair their capacity to resist infection.
对10名空腹血糖高且无酮症酸中毒迹象（平均空腹血糖293±20毫克/100毫升；均值±标准误）的血糖控制不佳的糖尿病患者的粒细胞黏附于尼龙纤维柱的能力进行评估时，全血中黏附的粒细胞数量仅为对照组观察值的53±6%。在进行一到两周的抗糖尿病治疗并降低空腹血糖水平（平均198±29毫克/100毫升）后，糖尿病患者的黏附能力显著改善（p<0.01）；然而，其数值仍低于正常水平（糖尿病患者为对照组的74%±8；p<0.02）。治疗前后的黏附值与空腹血糖水平相关（r = 0.88，p<0.001）。这些发现表明，除了先前报道的粒细胞在迁移以及吞噬和杀灭细菌方面的异常外，血糖控制不佳的糖尿病患者的粒细胞黏附能力也可能受损。这种功能异常与空腹血糖直接相关，并可通过胰岛素治疗得到改善。这种类型的缺陷可能会损害一些糖尿病患者的正常炎症反应并削弱其抗感染能力。
