Purpose: To evaluate plasma levels of selected cytokines and investigate their correlation with choroidal thickness (CT) in patients with acute and chronic central serous chorioretinopathy (CSC).Methods: We enrolled 30 patients with acute CSC, 30 patients with chronic CSC and 20 controls. Plasma concentrations of 12 cytokines, interleukins IL‐8, IL‐1β, IL‐2, IL‐4, IL‐5, IL‐6, IL‐10 and IL‐12 p70, granulocyte‐macrophage colony‐stimulating factor, interferon‐γ, tumour necrosis factor‐α (TNF‐α) and vascular endothelial growth factor (VEGF), were measured using multiplex immunoassays. Differences in cytokine levels between groups were assessed. We also investigated correlations between cytokine levels and CT using swept‐source optical coherence tomography, as well as an association between plasma cytokine profile and systemic hypertension.Results: We noted differences in IL‐6 (p = 0.005), IL‐10 (p = 0.03), IL‐12 p70 (p = 0.028) and VEGF (p = 0.029) levels between groups. Pro‐inflammatory IL‐12 p70 and multidirectional IL‐10 cytokines were upregulated, while pro‐angiogenic VEGF was downregulated in chronic CSC as compared with controls (p = 0.005, p = 0.025 and p = 0.027, respectively). Interleukin‐6 (IL‐6) was upregulated in acute and chronic CSC (p = 0.030 and p = 0.005, respectively). Interleukin‐5 (IL‐5), IL‐6 and IL‐12 levels correlated with mean CT in acute CSC (p = 0.008, p = 0.003 and p = 0.044, respectively), while IL‐8, IL‐6 and TNF‐α plasma levels correlated with hypertension in chronic CSC (p = 0.005, p = 0.033 and p = 0.001, respectively).Conclusion: We provided new evidence for the possible role of plasma cytokines in the pathogenesis of CSC. Our results suggest that IL‐6 may be important in the pathophysiology of acute and chronic CSC. The association between inflammatory response and hypertension in patients with CSC was also confirmed.

Background: The pathogenesis of central serous chorioretinopathy (CSC) remains a subject of intensive research. We aimed to determine correlations between plasma levels of selected angiogenic factors and different forms of CSC. Methods: Eighty patients were enrolled in the study including 30 with a chronic form of CSC, 30 with acute CSC, and 20 controls. Presence of active CSC was determined by fluorescein angiography (FA), indocyanine green angiography (ICGA), and swept-source optical coherence tomography (SS-OCT). Plasma concentrations of angiopoietin-1, endostatin, fibroblast growth factor, placental growth factor (PlGF), platelet-derived growth factor (PDGF-AA), thrombospondin-2, vascular endothelial growth factor (VEGF), VEGF-D, and pigment epithelium–derived factor were measured, and the results were compared between groups. Additionally, mean choroidal thickness (CT) was measured in all patients. Results: Levels of angiopoietin-1 (p = 0.008), PlGF (p = 0.045), and PDGF-AA (p = 0.033) differed significantly between the three groups. Compared with the controls, VEGF (p = 0.024), PlGF (p = 0.013), and PDGF-AA (p = 0.012) were downregulated in the whole CSC group, specifically PDGF-AA (p = 0.002) in acute CSC and angiopoietin-1 (p = 0.007) in chronic CSC. An inverse correlation between mean CT and VEGF levels was noted in CSC patients (rho = −0.27, p = 0.044). Conclusions: Downregulated angiopoietin-1, VEGF, PDGF-AA, and PlGF levels may highlight the previously unknown role of the imbalanced levels of proangiogenic and antiangiogenic factors in the pathogenesis of CSC. Moreover, downregulated VEGF levels may suggest that choroidal neovascularization in CSC is associated with arteriogenesis rather than angiogenesis.

Recent reports have demonstrated that endothelial injury is critical in the pathogenesis of systemic sclerosis (SSc) and is associated with increased levels of circulating inflammatory biomarkers. This study aims to analyze the serum concentrations of selected cytokines and evaluate their relationship with SSc clinics and the long-term course of the disease. This study included 43 SSc patients and 24 matched healthy controls. In both groups, we measured serum levels of inflammatory cytokines related to the inflammatory response, such as tumor necrosis factor (TNF)α, interferon (IFN)γ, interleukin (IL)-4, IL-6, IL-10, and IL-17, and fibroblast activation protein (FAP). Additionally, in SSc patients, we evaluated the presence of four single nucleotide polymorphisms (SNPs) located in the promotor region of the TNFA gene, namely rs361525, rs1800629, rs1799964, and rs1799724, which might be related to increased TNFα concentrations. The main aim consisted of associating inflammatory cytokines with (1) clinical disease characteristics and (2) longitudinal observation of survival and cancer prevalence. SSc patients were characterized by a 17% increase in serum TNFα. There was no other difference in serum cytokines between the studied groups and diffuse vs. limited SSc patients. As expected, evaluated serum cytokines correlated with inflammatory biomarkers (e.g., IL-6 and C-reactive protein). Interestingly, patients with higher IL-17 had decreased left ventricle ejection fraction. During the median 5-year follow-up, we recorded four cases of neoplastic diseases (lung cancer in two cases, squamous cell carcinoma of unknown origin, and breast cancer with concomitant multiple myeloma) and nine deaths. The causes of death included lung cancer (n = 2), renal crisis (n = 1), multiple-organ failure (n = 1), and unknown reasons in five cases. Surprisingly, higher TNFα was associated with an increased cancer prevalence, while elevated IL-17 with death risk in the follow-up. Furthermore, the AG rs361525 genotype referred to higher TNFα levels than GG carriers. Both AG rs361525 and CT rs1799964 genotypes were associated with increased cancer risk. Higher serum concentrations of TNFα characterize the SSc patients, with the highest values associated with cancer. On the other hand, increased IL-17 in peripheral blood might predict poor SSc prognosis. Further research is needed to validate these findings.

Purpose: We report here a unique case of a sudden loss of vision as the first symptom of an advanced chronic nephropathy. Methods and Results: A 25-year-old man was referred to the Department of Ophthalmology with sudden visual deterioration presumptively diagnosed as bilateral retinitis. The patient had never been under any medical care before and had never had any clinical signs of any chronic disease. He underwent an ophthalmic examination with optical coherence tomography (OCT). Based on the clinical features, OCT scans and systemic blood pressure (BP) assessment (225/145 mm Hg), the patient was definitely diagnosed with hypertensive retinopathy and choroidopathy due to hypertensive crisis. After urgent diagnostic procedures, the patient was diagnosed with a chronic kidney disease at stage 5 in the course of chronic glomerulonephritis. Immediately, a renal replacement therapy was started and the patient was qualified for renal transplantation. Conclusion: Adolescents with an unclear picture of retinal lesions, who have neither a history nor clinical signs of a systemic disease, should undergo careful systemic screening with BP assessment. A sudden deterioration of vision may be the first symptom of a previously undiagnosed severe systemic disease (very rare chronic) that requires immediate treatment.

Background and Objectives: Retinal pigment epitheliopathy and hyperpermeability of choroidal vessels were postulated to be involved in the pathogenesis of central serous chorioretinopathy (CSC). Imbalanced levels of vascular endothelial growth factor (VEGF) and pigment-epithelium–derived factor (PEDF) were previously implicated in the development of chorioretinal diseases characterized by increased vascular permeability. We aimed to compare the plasma levels of proangiogenic VEGF and antiangiogenic PEDF for 26 patients with acute CSC, 26 patients with chronic CSC, and 19 controls. Materials and Methods: VEGF and PEDF levels were measured using a multiplex immunoassay or enzyme-linked immunosorbent assay. Correlations with disease duration were assessed. Results: VEGF levels differed between groups (p = 0.001). They were lower in patients with acute CSC (p = 0.042) and chronic CSC (p = 0.018) than in controls. PEDF levels were similar in all groups. The VEGF-to-PEDF ratio was lower in CSC patients than in controls (p = 0.04). A negative correlation with disease duration was noted only for PEDF levels in the group with chronic CSC (rho = −0.46, p = 0.017). Discussion: Our study confirmed that patients with CSC have imbalanced levels of VEGF and PEDF. This finding may have important implications for the pathogenesis of CSC. VEGF-independent arteriogenesis rather than angiogenesis may underlie vascular abnormalities in these patients.

Inflammation plays a key role in the induction of choroidal neovascularization (CNV). Inflammatory choroidal neovascularization (iCNV) is a severe but uncommon complication of both infectious and non-infectious uveitides. It is hypothesized that its pathogenesis is similar to that of wet age-related macular degeneration (AMD), and involves hypoxia as well as the release of vascular endothelial growth factor, stromal cell-derived factor 1-alpha, and other mediators. Inflammatory CNV develops when inflammation or infection directly involves the retinal pigment epithelium (RPE)–Bruch’s membrane complex. Inflammation itself can compromise perfusion, generating a gradient of retinal–choroidal hypoxia that additionally promotes the formation of choroidal neovascularization in the course of uveitis. The development of choroidal neovascularization may be a complication, especially in conditions such as punctate inner choroidopathy, multifocal choroiditis, serpiginous choroiditis, and presumed ocular histoplasmosis syndrome. Although the majority of iCNV cases are well defined and appear as the “classic” type (type 2 lesion) on fluorescein angiography, the diagnosis of iCNV is challenging due to difficulties in differentiating between inflammatory choroiditis lesions and choroidal neovascularization. Modern multimodal imaging, particularly the recently introduced technology of optical coherence tomography (OCT) and OCT angiography (noninvasive and rapid imaging modalities), can reveal additional features that aid the diagnosis of iCNV. However, more studies are needed to establish their role in the diagnosis and evaluation of iCNV activity.