Abstract
To assess whether the serum levels of mannose-binding lectin of the lectin complement pathway are associated with age-related macular degeneration. Patients with age-related macular degeneration and age-matched controls underwent full ophthalmologic examination and optical coherence tomography. Using a time-resolved immunofluorometric assay, blood samples were evaluated to determine the serum mannose-binding lectin levels. A total of 136 individuals were evaluated, including 68 patients with age-related macular degeneration (34 exudative and 34 nonexudative) and 68 age-matched controls. The median mannose-binding lectin level was 608 ng/mL (range, 30-3,415 ng/mL) in patients with age-related macular degeneration and 739 ng/mL (range, 30-6,039 ng/mL) in controls, with no difference between the groups. Additionally, the median mannose-binding lectin level was 476 ng/mL (range, 30-3,415 ng/mL) in exudative cases and 692 ng/mL (range, 30-2,587 ng/mL) in nonexudative cases. Serum mannose-binding lectin levels were not associated with age-related macular degeneration or with the exudative and nonexudative forms of the disease.
Highlights
Age-related macular degeneration (AMD) is a multi factorial disease with an increasing prevalence worldwide and significant morbidity
We investigated the role of mannose-binding lectin (MBL) in AMD, which is a key element in the activation of lectin pathway (LP)
Deregulation in complement system activation may be related to the development or aggravation of several diseases, including AMD[12,13]
Summary
Age-related macular degeneration (AMD) is a multi factorial disease with an increasing prevalence worldwide and significant morbidity. Initial studies in the early 1980s indicated the significant burden that AMD would have in the following years. That inflammation plays a fundamental role in the development of AMD, with the complement system playing a central underlying role in the physiopathological process in addition to the vascular endothelial growth factor (VEGF)(3,4). Serum levels of both VEGF and complement proteins have been found to be increased in AMD. MBL may offer protection against invading microorganisms; high MBL levels may cause biological disadvantages in other situations through the aggravation of local and systemic inflammation involving complement activation and modulation of proinflammatory cytokine production[10]. Diabetic retinopathy was associated with high MBL levels in a Chinese population[11]
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