Adamiec Joanna, Oficjalska-Młyńczak Jolanta
Katedra i Klinika Okulistyki Akademii Medycznej im. Piastów Slaskich, Wrocław.
Przegl Lek. 2007;64(6):389-92.
Proliferative diabetic retinopathy (PDR) is caused by structural and functional disorders of the retinal vessels. Complex pathobiological mechanisms of this process have not been clearly explained so far.
To prove the role of immunological-inflammatory process in the development of the proliferative diabetic retinopathy.
Forty six patients, aged 63.97+/-9 were enrolled in the study, treated for diabetes type 2 for 12.56+/-6,87 years. In 19 patients (12 women and 7 men aged 64.63+/-8.38, treated for diabetes for 12.47+/-6.75 years) a parallel analysis of given parameters was performed in both serum and vitreous body samples. Vitrectomy, in course of which the vitreous body samples were obtained, was performed in these patients because of vitreous haemorrhage, causing traction retinal detachment in some patients. The control group consisted of 15 patients (9 women and 6 men), aged 63.00+/-14.58, who underwent the vitrectomy procedure because of reasons other than diabetic retinopathy. The concentration values of the soluble forms of ICAM-1, VCAM-1, IL-6 and TNF-alpha were estimated both in the serum and vitreous body samples on the basis of the ELISA method. The biochemical tests were performed routinely in the clinical laboratory.
Mean concentrations of the investigated parameters were significantly higher in the group of patients suffering from PDR, both in the serum and in the vitreous body samples, in comparison with the values observed in the control group. In the presence of HbAlc at the level of 9.21+/-2.17% a directly proportional correlation between the TNF-alpha either in serum or in the vitreous body samples and VCAM-1 in the vitroeus body samples was found. It is worth mentioning that the increase of the TNF-alpha concentration in the vitreous body was significantly related to the rise of the VCAM-1.
The above mention of findings prove the remarkable role of the immunological and inflammatory response in the pathogenesis of this specific vascular complication of diabetes. The research was a source of evidence which highlighted the necessity of optimal metabolic control of the disease in the prevention of vascular complications of diabetes.
增殖性糖尿病视网膜病变(PDR)由视网膜血管的结构和功能紊乱引起。该过程复杂的病理生物学机制迄今尚未得到明确解释。
证明免疫炎症过程在增殖性糖尿病视网膜病变发展中的作用。
46例年龄为63.97±9岁的患者纳入研究,患2型糖尿病12.56±6.87年。19例患者(12名女性和7名男性,年龄64.63±8.38岁,患糖尿病12.47±6.75年)的血清和玻璃体样本进行了给定参数的平行分析。这些患者因玻璃体出血(部分患者导致牵拉性视网膜脱离)接受了玻璃体切除术,术中获取了玻璃体样本。对照组由15例患者(9名女性和6名男性)组成,年龄63.00±14.58岁,因非糖尿病视网膜病变原因接受了玻璃体切除手术。基于酶联免疫吸附测定(ELISA)法评估血清和玻璃体样本中可溶性细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的浓度值。生化检测在临床实验室常规进行。
与对照组观察值相比,PDR患者组血清和玻璃体样本中所研究参数的平均浓度显著更高。当糖化血红蛋白(HbAlc)水平为9.21±2.17%时,发现血清或玻璃体样本中的TNF-α与玻璃体样本中的VCAM-1之间存在直接比例关系。值得一提的是,玻璃体中TNF-α浓度的增加与VCAM-1的升高显著相关。
上述研究结果证明了免疫和炎症反应在糖尿病这种特定血管并发症发病机制中的显著作用。该研究为强调在预防糖尿病血管并发症中对疾病进行最佳代谢控制的必要性提供了证据来源。