Estimation of systemic complement C3 activity in age-related macular degeneration

• Published in: Archives of ophthalmology (1960) Vol. 125; no. 4; p. 515
• Main Authors: Sivaprasad, Sobha, Adewoyin, Temi, Bailey, Tracey A, Dandekar, Sam S, Jenkins, Sharon, Webster, Andrew R, Chong, Ngaihang Victor
• Format: Journal Article
• Language: English
• Published: United States 01.04.2007
• Subjects: Choroidal Neovascularization - blood; Choroidal Neovascularization - etiology; Choroidal Neovascularization - genetics; Complement Activation - physiology; Complement C3a - analysis; Complement Factor H - genetics; Enzyme-Linked Immunosorbent Assay; Genotype; Humans; Macular Degeneration - blood; Macular Degeneration - etiology; Macular Degeneration - genetics; Polymorphism, Single Nucleotide
• ISSN: 0003-9950
• 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.