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Sobha Sivaprasad, FRCS; Temi Adewoyin, MRCOphth; Tracey A. Bailey, PhD; Sam S. Dandekar, FRCOphth; Sharon Jenkins, MSc; Andrew R. Webster, FRCOphth; Ngaihang Victor Chong, FRCOphth

Arch Ophthalmol. 2007;125(4):515-519.

Objectives  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.

Methods  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.

Results  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).

Conclusion  Systemic activation of the complement system may contribute to the pathogenesis of age-related macular degeneration independent of CFH polymorphism.

Clinical Relevance  The results of this study may be relevant to aiming new treatment strategies toward reducing systemic low-grade inflammation.

Author Affiliations: Laser and Retinal Research Unit, King's College Hospital, King's College London (Drs Sivaprasad, Adewoyin, and Chong), Moorfields Eye Hospital (Drs Sivaprasad, Dandekar, and Webster, and Ms Jenkins), and Institute of Ophthalmology, University College London (Drs Dandekar, Webster, and Chong and Ms Jenkins), London, England; and Cranfield BioMedical Centre, Cranfield University at Silsoe, Bedfordshire, England (Drs Sivaprasad and Bailey).

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