Arkkila P E, Rönnemaa T, Koskinen P J, Kantola I M, Seppänen E, Viikari J S
Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland.
Diabet Med. 2001 Oct;18(10):816-21. doi: 10.1046/j.1464-5491.2001.00576.x.
Connective tissue alterations may contribute to the development of diabetic long-term complications in eyes, kidneys and peripheral nerves. Collagen deposition may be increased in micro- and macrovascular disease in diabetic subjects. We tested whether biochemical markers of type III and I collagen metabolism are associated with retinopathy and neuropathy in Type 1 diabetes.
A total of 28 patients, mean age 43.4 +/- 9.5 (sd) and duration of diabetes 25.2 +/- 9.7 years, were studied. Stereoscopic colour fundus photographs were taken for assessment of retinopathy which was classified as no, background or proliferative. Concentrations of aminoterminal propeptide of type III procollagen (PIIINP), carboxyterminal propeptide of type I procollagen (PICP) and carboxyterminal cross-linked telopeptide of type I collagen (ICTP) in serum and urinary excretion of cross-linked N-telopeptides of type I collagen (NTX) and deoxypyridinoline crosslinks (DPyr) into urine were measured.
Average serum PIIINP was higher in subjects with proliferative (3.2 +/- 1.1 microg/l) than without proliferative retinopathy (2.5 +/- 0.6 microg/l) (P = 0.03). Average serum PICP was higher in subjects without retinopathy (181.7 +/- 19.5 microg/l) than in subjects with background retinopathy (132.1 +/- 42.7 microg/l) (P = 0.02). Concentrations of other collagen markers were not different in subjects with or without retinopathy. No association between collagen markers and neuropathy was found.
The increased synthesis of type III collagen, reflecting deposition of matrix and basement membrane connective tissue, may be involved in the pathogenesis of proliferative retinopathy in Type 1 diabetic subjects. On the other hand, we observed decreased synthesis of Type I collagen, which can result in weakened vascular integrity in subjects with retinopathy.
结缔组织改变可能促使糖尿病患者眼部、肾脏及周围神经出现长期并发症。糖尿病患者的微血管和大血管病变中，胶原蛋白沉积可能增加。我们检测了III型和I型胶原蛋白代谢的生化标志物是否与1型糖尿病患者的视网膜病变和神经病变相关。
共研究了28例患者，平均年龄43.4±9.5（标准差）岁，糖尿病病程25.2±9.7年。拍摄立体彩色眼底照片以评估视网膜病变，将其分为无病变、背景性病变或增殖性病变。检测血清中III型前胶原氨基端前肽（PIIINP）、I型前胶原羧基端前肽（PICP）和I型胶原蛋白羧基端交联末肽（ICTP）的浓度，以及尿中I型胶原蛋白交联N-末肽（NTX）和脱氧吡啶啉交联物（DPyr）的排泄量。
增殖性视网膜病变患者的平均血清PIIINP（3.2±1.1微克/升）高于无增殖性视网膜病变患者（2.5±0.6微克/升）（P = 0.03）。无视网膜病变患者的平均血清PICP（181.7±19.5微克/升）高于背景性视网膜病变患者（132.1±42.7微克/升）（P = 0.02）。有或无视网膜病变患者的其他胶原蛋白标志物浓度无差异。未发现胶原蛋白标志物与神经病变之间存在关联。
反映基质和基底膜结缔组织沉积的III型胶原蛋白合成增加，可能参与1型糖尿病患者增殖性视网膜病变的发病机制。另一方面，我们观察到I型胶原蛋白合成减少，这可能导致视网膜病变患者的血管完整性减弱。
