Increase in sICAM-1 and sVCAM-1 levels, as well as their correlation with high vitreous IL-6 and TNF-alpha concentrations in patients with PDR, seem to confirm the inflammatory-immune nature of this process. In diabetes, inadequate metabolic control remains an important risk factor in the development of PDR.

No abstract

Age-related macular degeneration (AMD) is a disease that causes varying degrees of blindness, which afflicts millions of adults in their later years. Preliminary changes occur during normal aging, but in some individuals the pathology leads to the development of AMD. The pathology seems to be a mixture of biochemical, cellular, and molecular events. Lipofuscinogenesis and early drusen genesis are in the early stages of AMD and their inhibition or reversal would dramatically increase the quality of vision in elderly people. The disease is characterized by abnormal extracellular deposits, known as drusen, which accumulate along the basal surface of the retinal pigmented epithelium RPE. Widespread drusen deposition is associated with retinal pigmented epithelial cell dysfunction and degeneration of the photoreceptors. Recent studies have shown that drusen contain a variety of immunomodulatory molecules, suggesting that the process of drusen formation involves local inflammatory events, including activation of the complement cascade. Molecular pathways involved in the etiology of this disease and the potential prospects of its treatment will be presented on the basis of the results of the current studies.

No abstract

Diabetic retinopathy constitutes the most frequent cause of vision loss in professionally active individuals. Progressive impairment of visual acuity results from massive fibrovascular proliferation involving the fundus of the eye, as well as from the apoptosis of the neuronal structures of the retina. The results of many clinical studies, both on experimental models and on human material, confirmed evident enhancement of this process in the course of diabetes. The programmed cell death of retinal ganglion cells predominantly occurs secondarily to caspase--dependent intracellular processes. This paper presents evidence for the considerable involvement of the caspase--dependent mechanism of apoptosis of retinal ganglion cells in the early stages of retinal changes associated with progressive impairment of visual acuity. The authors emphasize the necessity of comprehensive understanding of mechanisms that underlie the programmed death of neural cells in the eyes of patients with diabetes. This clinical problem becomes of vital importance in view of the constantly increasing incidence of diabetes and severe impairment associated with the disorders of carbohydrate metabolism. Identification of a key component involved in this process would enable attempts oriented at pharmacological blockade of apoptosis in the retinal ganglion cells of patients with diabetes (Adv Clin Exp Med 2015, 24, 3, 531-535).

Vitreoretinal interface pathologies, such as vitreomacular traction syndrome, epiretinal membranes and macular holes are sight-threatening conditions and one of the important causes of vision defects and vision loss. To this date, vigilance with observation of how the vitreomacular traction resolves, or vitreoretinal surgery in more severe cases, were the only treatment options. Recent rapid progress in ophthalmology, especially in diagnostic and visualization techniques, provided better insight into the mechanisms taking place on the vitreoretinal surface, which enabled a more accurate selection of treatment options. Development of ophthalmic pharmacological procedures, such as treatment of vitreomacular traction syndrome with ocriplasmin, constitutes an innovative breakthrough in ophthalmology. The enzyme is a genetically engineered form of human plasmin, a component of blood coagulation cascade that has been envisioned for human therapy since 1950s. It has never been used for vitreolysis in ophthalmology before. The aim of this review is to analyze and compare therapeutic options for symptomatic vitreomacular adhesion and vitreoretinal traction, with particular emphasis on microplasmin. We reviewed the results of recent studies comparing ocriplasmin to other widespread treatment options, such as pars plana vitrectomy.

Purpose: To report 12-month outcomes of a Polish National Treatment Program using aflibercept and ranibizumab in eyes with wet, age-related macular degeneration in routine clinical practice. Material and Methods: This was a non-randomized, retrospective, observational multicenter study. Anonymous data contained in the electronic Therapeutic Program Monitoring System were utilized in this study. Results: The study population consisted of 2828 eyes from 2718 patients. The median age was 76.0 [70.0, 81.0] years; 61.7% were female. Best corrected visual acuity increased from 58.86 [50.05, 69.95] letters to 65.1 [50.1, 73.9] letters (p < 0.001). The median change in best corrected visual acuity was 0.0 [−4.0, 12.2] letters: 2.9 [−2.9, 15.1] letters for treatment-naïve eyes and 0.0 [−4.0, 8.8] letters for those continuing treatment (p < 0.001). The median central retinal thickness was significantly reduced from 341.0 [281.0, 422.0] to 275.0 [221.0, 344.0] μm (p < 0.001). The median number of visits was 9.0 [8.0, 9.0]. The median number of injections was 7.0 [6.0, 8.0]: 8.0 [7.0, 8.0] for treatment-naïve eyes and 6.0 [5.0, 7.0] for those continuing treatment (p < 0.001). Conclusion: Eyes treated as part of the Polish therapeutic program gained functional stability and morphological improvement. Treatment-naïve eyes showed the greatest functional benefit.

Glucocorticoid receptor (GR) activity plays a significant role in the etiology of obesity and is essential for glucose homeostasis, the development of hyperinsulinaemia and subsequent increased fat deposition. Several polymorphisms in the GR gene have been described, and at least three of them seem to be associated with altered glucocorticoid sensitivity and changes in glucose homeostasis, and other metabolic parameters. The N363S polymorphism has been associated with increased sensitivity to glucocorticoides, increased insulin response to dexamethasone and increased plasma glucose level. BclI polymorphism is associated with increased abdominal obesity, hyperinsulinaemia and increased insulin resistance. Another polymorphism, ER22/23EK, in contrast to the others, is associated with relative resistance to glucocoricides actions and more beneficial metabolic profile-lower insulin resistance level, decreased lower cardiovascular risk and subseuent prolongation of life time. More research is still needed to understand the mechanisms behind these associations at the molecular level.