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D.M. Miller, J.M. Legra, S.R. Dubovy, I.J. Suner, R.D. Dix, D.D. Sedmak, S.W. Cousins; The Association of Exudative Age-Related Macular Degeneration With Prior Infection . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1747.
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Purpose: The development of choroidal neovascularization (CNV) in age-related macular degeneration (ARMD) is the leading cause of blindness in the elderly. We have previously demonstrated that high activity macrophages are present in the blood of some patients, and may be important in the development of CNV. We hypothesize that infection may contribute to macrophage activation. An emerging paradigm in vascular pathobiology is the role of chronic infection in pathologic vascular responses. Specifically, cytomegalovirus (CMV), Chlamydia pneumoniae (CPN), and Helicobacter pylori (HPY) have been implicated in the pathobiology of atherogenesis, transplant vascular sclerosis, systemic sclerosis, and vasculitis. Herein, we test the hypothesis that prior infection with either CMV, CPN, or HPY is associated with CNV in ARMD and that higher titers of pathogen specific antibodies correlate with progression from dry to wet ARMD. Methods: Serum was collected from patients with dry ARMD (n=22), wet ARMD (n=34), and age-matched controls (n=47) without a maculopathy. Standard commercial ELISAs were performed to detect CMV-, CPN-, and HPY-, specific IgG antibodies in the serum samples. The results were divided into low, intermediate, and high titer groups. Results: An increase in the prevalence of high titer antibody was observed in patients with wet ARMD versus dry ARMD for HPY (26% wet vs. 14% dry), CPN (35% wet vs. 13% dry), and CMV (33% wet vs. 23% dry). In addition, the prevalence of high titer antibody in the wet ARMD group was higher than the prevalence of high titer antibody in age-matched controls without ARMD. Conclusions: This serologic data supports the hypothesis that prior infection with HPY, CPN, or CMV may be associated with the progression from dry to wet ARMD. We postulate that high antibody titers might identify a subgroup of patients with persistent subclinical infection or recent reactivation of these pathogens. In these patients, infection may stimulate macrophage activation and contribute to progression of ARMD.
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