PRIMARNI VITREORETINALNI LIMFOM: STAV OFTALMOLOGA O DIJAGNOZI I LIJEČENJU

Primary vitreoretinal lymphoma (PVRL) is a rare subset of central nervous system lymphoma occurring primarily in the vitreous and retina. Often presenting as a masquerade syndrome mimicking infectious or non-infectious uveitis, PVRL presents a diagnostic and therapeutic challenge. A vitreal or retinal biopsy is essential for diagnosis. This paper reviews recent advances and updates in the diagnosis and treatment of PVRL with a focus on intravitreal chemotherapy. Current diagnostic techniques for PVRL are demanding and detailed clinical history, examination, ocular and central nervous system imaging with immunohistochemistry, fl ow cytometry, molecular and genetic analysis are needed. In the last few years, local intravitreal treatment in cases with isolated PVRL is the topic of many published papers, however, the number of patients involved is small and treatment recommendations are not standardized and unique.Primarni vitreoretinalni limfom (PVRL) rijetka je podskupina limfoma središnjega živčanog sustava (SŽS) koja se javlja ponajprije u staklastom tijelu i retini. Često se predstavlja kao maskirani sindrom koji oponaša infektivni ili neinfektivni uveitis pa je dijagnostički i terapijski izazov. Biopsija vitreusa ili retine bitna je za dijagnozu. Ovaj rad prikazuje nedavna dostignuća i ažuriranja u dijagnostici i liječenju PVRL s naglaskom na intravitrealnu kemoterapiju. Suvremene dijagnostičke tehnike za PVRL su zahtjevne. Potrebna je detaljna klinička anamneza, pregled, očna i SŽS slika s imunohistokemijom, protočna citometrija, molekularna i genetska analiza. Posljednjih nekoliko godina lokalno intravitrealno liječenje u slučajevima s izoliranim PVRL tema je brojnih objavljenih radova. Međutim, broj uključenih pacijenata je malen, a preporuke za liječenje- nisu standardizirane i jedinstvene

Functional and Molecular Characterization of Ex Vivo Cultured Epiretinal Membrane Cells from Human Proliferative Diabetic Retinopathy

Characterization of the cell surface marker phenotype of ex vivo cultured cells growing out of human fibrovascular epiretinal membranes (fvERMs) from proliferative diabetic retinopathy (PDR) can give insight into their function in immunity, angiogenesis, and retinal detachment. FvERMs from uneventful vitrectomies due to PDR were cultured adherently ex vivo. Surface marker analysis, release of immunity- and angiogenesis-pathway-related factors upon TNFα activation and measurement of the intracellular calcium dynamics upon mechano-stimulation using fluorescent dye Fura-2 were all performed. FvERMs formed proliferating cell monolayers when cultured ex vivo, which were negative for endothelial cell markers (CD31, VEGFR2), partially positive for hematopoietic- (CD34, CD47) and mesenchymal stem cell markers (CD73, CD90/Thy-1, and PDGFRβ), and negative for CD105. CD146/MCAM and CD166/ALCAM, previously unreported in cells from fvERMs, were also expressed. Secretion of 11 angiogenesis-related factors (DPPIV/CD26, EG-VEGF/PK1, ET-1, IGFBP-2 and 3, IL-8/CXCL8, MCP-1/CCL2, MMP-9, PTX3/TSG-14, Serpin E1/PAI-1, Serpin F1/PEDF, TIMP-1, and TSP-1) were detected upon TNFα activation of fvERM cells. Mechano-stimulation of these cells induced intracellular calcium propagation representing functional viability and role of these cells in tractional retinal detachment, thus serving as a model for studying tractional forces present in fvERMs in PDR ex vivo

Changes in plasma VEGF and PEDF levels in patients with central serous chorioretinopathy

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