Impact of systemic steroids combined with immunosuppressive treatment on glaucomatous features in patients with systemic lupus erythematosus.

AIM: To evaluate the incidence of increased intraocular pressure (IOP) and glaucomatous changes in systemic lupus erythematosus (SLE) patients in comparison with systemic steroids and immunosuppressive treatment. METHODS: Sixty-two women with SLE were divided into two groups: treated (n=47, 94 eyes) and not treated (n=15, 30 eyes) with systemic glucocorticosteroids (GC; GC-free). Twenty-one individuals in GC group were treated with immunosuppressive agents (immunomodulating and biologic). The visual acuity and IOP with ocular pulsatile amplitude (OPA) measurements, as well as scanning laser polarimetry (GDx) with nerve fiber index (NFI) measurement, spectral domain optical coherence tomography (SD-OCT) of the optic disk with retinal nerve fiber layer (RNFL) analysis and the macular region with ganglion cell analysis (GCA) were performed. RESULTS: Mean IOP values in group with combined GC and immunosuppressive therapy was 15.8±2.56 mm Hg and was significantly lower than in individuals with exclusive GC treatment (17.63±4.38 mm Hg, P=0.043). Contrary, no differences in mean IOP values between GC-free group and individuals treated with combined GC and immunosuppressive therapy were detected (P=0.563). Similarly, mean IOP in GC was 17.14±3.94 mm Hg and in GC-free patients was equal to 16.67±3.45 mm Hg (P=0.671). According to treatment regimen no statistical differences in optic disk SD-OCT for RNFL thickness, RNFL symmetry, cupping volume and the C/D ratio were observed. Similarly, no statistical differences for the mean and minimal ganglion cell layer (GCL) thickness measured in macular SD-OCT or NFI in GDx were detected. CONCLUSION: Combined immunosuppressive and systemic GC therapy in SLE patients may lower the risk of iatrogenic ocular hypertension. No relationship between treatment regimen and glaucomatous damage of optic nerve fibers in analyzed groups with SLE is detected.

Serum selenium levels are associated with age-related cataract.

OBJECTIVE: The aim of the study is to analyse correlations between age-related cataract (ARC), serum selenium levels and glutathione peroxidase gene 1 and 4 (GPX-1 and GPX-4). MATERIAL AND METHODS: A total sample of 275 participants were enrolled into the study: group A, 94 subjects elligible for ARC surgery, and group B, 181 volunteers without ocular symptoms, gender-, age-, and smoking- status and volume-matched at 1:2 with subjects in group A. All participants (n=275) were divided according to the Lens Opacities Classification System III (LOCS III) into: 1) study group (subjects with clinically significant cataract; N≥3 or C≥3 or P≥2), 2) control group (controls with clinically non-significant cataract; N<3 and C<3 and P<2). The single nucleotide polymorphisms of GPX-1 and GPX-4 were assessed using Real Time PCR. Serum selenium levels were assayed using Inductively Coupled Plasma Mass Spectrometry. RESULTS: Low selenium levels significantly predicted any age-related cataract (OR 7.969; p<.01), nuclear cataract (OR 12.823; p<.01) and cortical cataract (OR 3.31; p<.01). There was no significant effect of gender, age, SNP GPX-1 and SNP GPX-4 on the prevalence of age-related nuclear, cortical and posterior sub-capsular cataract. Serum selenium levels of 75-85 µg/L were associated with the lowest prevalence of ARC. CONCLUSIONS: Due to a confirmed association between serum selenium levels and age-related cataract, low serum selenium levels may constitute a potential risk factor of age-related cataract.

Stem Cells are mobilized from the bone marrow into the peripheral circulation in response to retinal pigment epithelium damage--a pathophysiological attempt to induce endogenous regeneration.

PURPOSE: Stem cell regeneration of damaged tissue has recently been reported in many different organs. Here, we investigated the mobilization of different stem/progenitor cell (SPC) populations into the peripheral blood (PB), their subsequent homing to the injured retina (IR) and contribution to its regeneration in a retinal pigment epithelium (RPE) damage model induced by sodium iodate (NaIO(3)). METHODS: Mobilization of SPCs was evaluated by flow cytometry. SPCs distribution in IR was assessed using bone marrow (BM)-derived GFP(+)Lin(-) cells transplanted intravenously into NaIO(3)-treated C57Bl/6 mice. The quantity of the chemokine SDF-1 in PB and IR was measured by ELISA and qRT-PCR, respectively. Apoptosis (TUNEL assay), cell proliferation (PCNA analysis) as well as functional retinal activity (electroretinogram) were examined at several time points after NaIO(3) administration. RESULTS: Mobilization of SPCs along with the highest cell proliferation and massive apoptosis within IR were observed on the third day after NaIO(3) administration. Similarly, donor GFP(+)Lin(-) cells were detected in the retina as soon as day 4 after NaIO(3) injection. Plasma levels of SDF-1 did not differ significantly in mice exposed to NaIO(3) compared to healthy controls, however mRNA for SDF-1 was overexpressed locally in IR. Functional retinal recovery was not achieved. CONCLUSION: Our study provides evidence that BM SPCs egress into PB and home to the injured retina, but are not capable of restoring its function. These results indicate that if the range of retinal destruction is profound, endogenous regeneration is ineffective and may ultimately require adjuvant therapeutic transplantation of specific SPCs subpopulations.