Sivaprasad Sobha, Adewoyin Temi, Bailey Tracey A, Dandekar Sam S, Jenkins Sharon, Webster Andrew R, Chong Ngaihang Victor
Laser and Retinal Research Unit, King's College Hospital, King's College London, England.
Arch Ophthalmol. 2007 Apr;125(4):515-9. doi: 10.1001/archopht.125.4.515.
To determine the role of systemic complement activation in the pathogenesis of age-related macular degeneration and to examine whether serum C3a des Arg reflects systemic complement activation, independent of individual complement component levels.
Plasma complement C3a des Arg levels and a single nucleotide polymorphism at position 402 of the complement factor H gene (CFH) were determined in 3 groups of subjects: 42 subjects with early age-related maculopathy, 42 subjects with neovascular (wet) age-related macular degeneration, and a control group of 38 subjects with no clinical evidence of age-related changes at the macula.
The median (range) of plasma complement C3a des Arg levels in the age-related maculopathy and neovascular age-related macular degeneration groups were 52.6 (2.8-198.1) ng/mL and 60.9 (3.1-173.1) ng/mL, respectively. The levels were significantly raised compared with the control group (n = 38), which had a median (range) plasma complement C3a des Arg level of 40.3 (6.1-81.7) ng/mL (analysis of variance, P = .02). The concentration of plasma C3a des Arg did not differ significantly between those with different CFH genotypes (P = .07).
Systemic activation of the complement system may contribute to the pathogenesis of age-related macular degeneration independent of CFH polymorphism.
The results of this study may be relevant to aiming new treatment strategies toward reducing systemic low-grade inflammation.
确定全身补体激活在年龄相关性黄斑变性发病机制中的作用,并研究血清C3a去精氨酸是否反映全身补体激活,而不受单个补体成分水平的影响。
测定3组受试者的血浆补体C3a去精氨酸水平和补体因子H基因(CFH)第402位的单核苷酸多态性:42例早期年龄相关性黄斑病变患者、42例新生血管性(湿性)年龄相关性黄斑变性患者,以及38例黄斑无年龄相关性变化临床证据的对照组。
年龄相关性黄斑病变组和新生血管性年龄相关性黄斑变性组血浆补体C3a去精氨酸水平的中位数(范围)分别为52.6(2.8 - 198.1)ng/mL和60.9(3.1 - 173.1)ng/mL。与对照组(n = 38)相比,这些水平显著升高,对照组血浆补体C3a去精氨酸水平的中位数(范围)为40.3(6.1 - 81.7)ng/mL(方差分析,P = .02)。不同CFH基因型患者的血浆C3a去精氨酸浓度无显著差异(P = .07)。
补体系统的全身激活可能独立于CFH多态性而参与年龄相关性黄斑变性的发病机制。
本研究结果可能与旨在减少全身低度炎症的新治疗策略相关。