The significance of pigment epithelial detachment in central serous chorioretinopathy.

PURPOSE: To investigate the significance of the presence and form of pigment epithelial detachment in the course of central serous chorioretinopathy as well as corticosteroid use as a risk in our patient cohort. MATERIAL AND METHODS: Retrospective, single center study of central serous chorioretinopathy patients between January 2013 and January 2019 recording corticosteroid use prior to onset and presence and type of pigment epithelial detachment (flat-irregular, dome-shaped, none) in relationship to disease course. RESULTS: We analyzed 53 eyes of 53 consecutive central serous chorioretinopathy patients treated in our department. Mean patient age was 53 ± 13 years. A flat-irregular pigment epithelial detachment was associated with either chronic or recurrent central serous chorioretinopathy, whereas the absence of a pigment epithelial detachment correlated positively with acute central serous chorioretinopathy (chi-square test, p < 0.05). Of the 53 patients, 10 reported corticosteroid use, 40 denied steroid use, and 3 patients failed to make a clear statement. Corticosteroid use was not correlated with the onset of central serous chorioretinopathy (Student's t-test, p = 0.0001, chi-square test, p < 0.005). CONCLUSION: A small, flat-irregular pigment epithelial detachment could be a marker for chronic or recurrent central serous chorioretinopathy, whereas the absence of pigment epithelial detachment could favor acute central serous chorioretinopathy. Advanced imaging studies may provide more information on the exact characteristics and nature of pigment epithelial detachments. Corticosteroid use as possible disease trigger was not confirmed in this study.

The immunomodulatory sphingosine 1-phosphate analog FTY720 reduces lesion size and improves neurological outcome in a mouse model of cerebral ischemia.

Cerebral ischemia is accompanied by fulminant cellular and humoral inflammatory changes in the brain which contribute to lesion development after stroke. A tight interplay between the brain and the peripheral immune system leads to a biphasic immune response to stroke consisting of an early activation of peripheral immune cells with massive production of proinflammatory cytokines followed by a systemic immunosuppression within days of cerebral ischemia that is characterized by massive immune cell loss in spleen and thymus. Recent work has documented the importance of T lymphocytes in the early exacerbation of ischemic injury. The lipid signaling mediator sphingosine 1-phosphate-derived stable analog FTY720 (fingolimod) acts as an immunosuppressant and induces lymphopenia by preventing the egress of lymphocytes, especially T cells, from lymph nodes. We found that treatment with FTY720 (1mg/kg) reduced lesion size and improved neurological function after experimental stroke in mice, decreased the numbers of infiltrating neutrophils, activated microglia/macrophages in the ischemic lesion and reduced immunohistochemical features of apoptotic cell death in the lesion.