94 research outputs found
Ruthenium-106 Plaque Therapy for Diffuse Choroidal Hemangioma in Sturge-Weber Syndrome
Diffuse choroidal hemangiomas associated with Sturge-Weber syndrome (SWS) are classically treated with external beam radiotherapy (EBR), but there are a few reports usually of single cases indicating the usefulness of plaque therapy. We present our observations on two cases of diffuse choroidal hemangiomas with exudative retinal detachment associated with SWS treated with Ruthenium-106 plaque therapy. Outcomes included best-corrected visual acuity (BCVA) and regression in tumor thickness measured by ultrasonography. The initial BCVA of the affected eyes was counting fingers at 1 meter and light projection. Pretreatment tumors thickness was 3.5 mm and 4.7 mm. In a follow-up period of 18–24 months, significant reduction in thickness of choroidal hemangiomas up to 1.2 mm and 1.4 mm with prompt resolution of exudative retinal detachment was observed. BCVA achieved 20/200 and 20/400, respectively. The findings in this paper indicate that Ruthenium-106 plaque therapy is effective in treatment of diffuse choroidal hemangiomas associated with SWS
The role of optical coherence tomography in post cataract surgery macular edema in diabetic patients
Autophagy : a new insight into pathogenesis and treatment possibilities in age-related macular degeneration
Zwyrodnienie plamki związane z wiekiem (AMD – age-related macular degeneration) to obecnie istotny problem zdrowotny, bowiem w krajach rozwiniętych jest jedną z najczęstszych przyczyn utraty widzenia centralnego u osób powyżej 50. roku życia. Patogeneza AMD jest wieloczynnikowa i niedokładnie poznana. Wśród czynników odpowiedzialnych za rozwój choroby wymienia się, poza naturalnym procesem starzenia się siatkówki, nasilony stres oksydacyjny, nadmierną aktywację dopełniacza, tlące się przewlekłe zapalenie w przestrzeni podsiatkówkowej, uwarunkowania genetyczne i środowiskowe. W ostatnim czasie zwrócono uwagę na zaburzenia procesów autofagii jako wiodącej przyczyny rozwoju AMD. Autofagia jest mechanizmem komórkowym, polegającym na eliminowaniu zużytych lub uszkodzonych fragmentów i składników komórki, pozwalającym osiągnąć komórce dynamiczną równowagę między syntezą a rozkładem jej komponentów, umożliwia zatem przeżycie komórki w warunkach stresowych. Zaburzenia tych mechanizmów w postaci ich nadmiernej aktywacji lub inhibicji prowadzą do rozwoju wielu patologii. Autofagia pełni zatem podwójną rolę, jest odpowiedzialna zarówno za ochronę, jak i za śmierć komórki.
W pracy przybliżono mechanizmy autofagii oraz jej znaczenie w fizjologicznym procesie starzenia się komórek siatkówki oraz omówiono istotny wpływ jej zaburzeń na rozwój zmian zwyrodnieniowych w plamce jakim jest AMD. Przedstawiono także potencjalny wpływ leczenia doszklistkowymi iniekcjami czynników anty-VEGF na zjawiska autofagii w siatkówce oraz możliwe nowe terapie AMD oparte na modulowaniu zjawiska autofagii.Age-related macular degeneration (AMD) is a significant problem in healthcare, because it is a leading cause of central vision loss in individuals over 50 years old in well-developed countries. Pathogenesis of AMD is multifactorial and still not completely understood. Proven risk factors include the following: natural senescence of retina, oxidative stress, complement activation, chronic subretinal inflammatory reaction, genetic and environmental factors. Data on links between autophagy and AMD development are being raised. Autophagy is a cellular process involving the degradation of long-lived proteins and damaged fragments and components of cells; it is responsible for the maintenance of dynamic intracellular homeostasis and it enables cell survival under stress conditions. Disturbances of autophagy mechanisms, i.e. its activation or inhibition, may lead to the development of many various pathologies. Thus, autophagy plays a dual role, as a mechanism responsible for protecting or killing cells. The paper describes autophagy mechanisms and their role in the natural process of retinal cells senescence and presents the autophagy impairment as a crucial cause of AMD development. We also describe the impact of intravitreal anti-VEGF therapy on retinal autophagy mechanisms and potential new therapeutic modalities for AMD based on autophagy modulation
Hypertensive crisis-a serious problem in medical practice
There has recently been a considerable increase in interest in hypertensive crisis-a life-threatening condition. Recent publications indicate that hypertensive crisis is a problem not only in general medicine but also in ophthalmology. Visual disturbances may be the initial symptoms of severe hypertension and can reflect severe systemic changes. It seems appropriate to conduct further studies on the pathogenesis of vascular hypertensive changes, and particularly any associated inflammatory reactions. It also seems justified to introduce screening for hypertensive changes on the eye fundus photographs in emergency departments
Altered plasma cytokine levels in acute and chronic central serous chorioretinopathy
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-1b, IL-2, IL-4, IL-5, IL-6, IL-10 and IL-12 p70, granulocyte-macrophage
colony-stimulating factor, interferon-c, tumour necrosis factor-a (TNF-a) 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 IL12 p70 and multidirectional IL-10 cytokines were upregulated, while proangiogenic 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-a 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
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