Differences in anti-endothelial and anti-retinal antibody titers: implications for the pathohysiology of acute and chronic central serous chorioretinopathy.

The aim of the study was to evaluate the prevalence of serum anti-retinal (ARAs) and anti-endothelial cell antibodies (ACEAs) in patients with acute and chronic central serous chorioretinopathy (CSC). We enrolled 28 patients with acute CSC, 42 patients with chronic CSC, and 40 healthy controls. The presence of ARAs was determined by indirect immunofluorescence using monkey retina as an antigen substrate, while the presence of AECAs was determined using cultivated human umbilical vein endothelial cells (HUVECs) and primate skeletal muscle according to the manufacturer's instructions (Euroimmun AG). There were no differences in the prevalence of antibodies against rods, cones, cytoplasmic components of retinal nuclear layer cells, and retinal vessels between the acute and chronic CSC groups and the control group (P = 0.27, P = 0.16, P = 0.71, and P = 0.06, respectively). However, AECAs reactive with HUVECs were observed in 46% of patients with acute CSC, 45% of those with chronic CSC, and 22% of controls, whereas AECAs reactive with the skeletal muscle were present in 46%, 45%, and 15%, respectively (difference between groups: P = 0.045 for HUVECs and P = 0.005 for the skeletal muscle). Furthermore, AECA titers were higher in CSC patients than in controls (P = 0.004). This study provides evidence for the possible involvement of an autoimmune process directed against vessel antigens in the pathogenesis of CSC. AECAs may be more important than ARAs in this disease and may be involved in endothelial damage in the choroidal vessels and choriocapillaris, leading to hyperpermeability, which is central to the pathophysiology of CSC.

Autoimmune thyroiditis and central serous chorioretinopathy may have a relation.

Autoimmune thyroiditis (AT) is an important cause of hypothyroidism, and central serous chorioretinopathy (CSCR) is an independent disease of the choroid and retina that leads to accumulation of fluid beneath the retina. While AT has been associated with multiple antibodies, CSCR is still regarded as idiopathic despite extensive research. We hypothesize a causative association between these 2 conditions on the basis of our experience of a case where both CSCR and AT presented simultaneously and depicted a parallel course. CSCR was documented with retinal imaging while AT was documented with serum antibody titers. Further, we discuss the possible mechanisms that may be involved in this intriguing association.

Antiretinal antibodies in central serous chorioretinopathy: prevalence and clinical implications.

PURPOSE: To investigate the possible role of autoimmune reactions directed against retinal tissue in central serous chorioretinopathy (CSC), by analysing the presence of serum antiretinal antibodies (ARAs) and establishing their clinical relevance. METHODS: Sixty-three patients with CSC were included, and clinical characteristics were collected. Serum samples of all patients with CSC, 101 uveitis patients and 60 healthy donors were analysed for the presence of ARAs by indirect immunofluorescence. Furthermore, all CSC serum samples were analysed on Western blot. Correlations between laboratory findings and clinical features of CSC were determined by logistic regression. RESULTS: Antiretinal antibodies (ARAs) were present in 54% of the patients with CSC, in 46% of uveitis patients (p = 0.153) and in 17% of healthy controls (p < 0.001). The majority of ARAs in CSC were directed against photoreceptors (27%), which occurred significantly more often compared to uveitis patients (15%, p = 0.039) and to healthy controls (5%, p = 0.003). No associations between clinical CSC characteristics and the presence of ARAs were found. CONCLUSION: Serum ARAs are present in more than half of the patients with CSC, and especially, ARAs directed against photoreceptors were detected more frequently compared to both healthy controls and uveitis patients. Further research is warranted to unravel the role of ARAs in the pathogenesis of CSC.

Systemic complement activation in central serous chorioretinopathy.

PURPOSE: A 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. METHODS: A 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. RESULTS: In 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. CONCLUSION: 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.