Abstract
PurposeA clear link between several variants in genes involved in the complement system and chronic central serous chorioretinopathy (CSC) has been described. In age-related macular degeneration, a disease that shows clinical features that overlap with CSC, both genetic risk factors and systemic activation of the complement system have previously been found. In this case-control study, we assessed whether there is evidence of either systemic activation or inhibition of the complement system in patients with chronic CSC.MethodsA prospective case-control study of 76 typical chronic CSC patients and 29 controls without ophthalmological history was conducted. Complement activity assays (classical, alternative, and mannose-binding lectin pathway), complement factors 3, 4, 4A, 4B, B, D, H, I, and P, activation products C3d, C5a, and sC5b-C9, and the C3d/C3 ratio were analysed in either serum or plasma. A correction for possible effects of gender, age, body mass index, and smoking status was performed.ResultsIn this study, none of the tested variables, including regulation and activation products, proved to be significantly different between the groups. Moreover, no associations with either CSC disease activity or possible CSC related steroid use were observed.ConclusionDespite the available literature regarding a possible relationship between chronic CSC and variants in genes involved in the complement system, we did not find evidence of an association of chronic CSC with either systemic complement activation or inhibition.
Highlights
Central serous chorioretinopathy (CSC) mainly occurs in middle-aged male patients, and may cause irreversible vision loss.[1]
Despite the available literature regarding a possible relationship between chronic CSC and variants in genes involved in the complement system, we did not find evidence of an association of chronic CSC with either systemic complement activation or inhibition
Since information regarding all covariates was available for 76 patients, only the assessments of these chronic CSC patients could be taken into account
Summary
Central serous chorioretinopathy (CSC) mainly occurs in middle-aged male patients, and may cause irreversible vision loss.[1] CSC originates from dysfunction of the choroid, which shows an increase in permeability and thickness. These choroidal abnormalities and retinal pigment epithelium (RPE) damage lead to breakdown of the outer blood-retinal barrier, with subsequent serous subretinal fluid (SRF) leakage and neuroretinal detachment, often in the macula. Earlier reports on the familial occurrence of CSC have been published and associations between CSC and genetic variants in the complement factor H (CFH) gene, part of the innate immune system, have been found in several chronic CSC cohorts of diverse ethnic origins.[4, 14,15,16,17,18] Factor H, produced by both the choroidal and RPE cells, and critical in controlling local intraocular inflammation, is responsible for downregulation of the activation of the complement alternative pathway.[19,20,21] In the CFH gene, the single nucleotide polymorphisms (SNPs) have been observed to be either protective or risk conferring.[14,15,16] A recent study, demonstrating a possible involvement of the complement system in CSC, reported the absence of complement component 4B (C4B) gene copies to be associated with an increase in the risk of developing CSC, whereas the presence of 3 C4B copies is reported to be protective for CSC.[22]
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