PubMed · 2012794
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K J Hardy, J Lipton, M O Scase, J H Scarpello, D H Foster. 1991. Diabetes and retinal function.. https://doi.org/10.1136/bjo.75.3.191-a
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
PURPOSE: To investigate whether the method of retinopexy influences the visual recovery rate and the breakdown of the blood-ocular barrier after conventional retinal detachment surgery. METHODS: Forty-eight patients (48 eyes) with primary rhegmatogenous retinal detachment entered into the study. All eyes were phakic, had an attached macula, and were scheduled for conventional scleral buckling surgery. Patients were randomly assigned to have either laser or cryotherapy for retinopexy. All visual acuity and flare measurements were performed by a masked observer. The interventional procedure was cryopexy at the time of scleral buckling surgery or postoperative (4 weeks) laser photocoagulation. Visual acuity testing with ETDRS chart and aqueous flare measurement with laser flare photometry were performed by a masked observer at standard intervals: preoperatively and 1 day, 7 days, 4 weeks, and 10 weeks postoperatively. Analysis of covariance by multiple linear regression was used for statistical evaluation. RESULTS: Postoperative flare values from patients receiving cryotherapy were significantly higher at each measurement point in time (P < or =.001). The visual recovery was slower in the patients receiving cryotherapy (1 week, P =.003; 4 weeks, P =.03; 10 weeks, P =.081). CONCLUSION: Laser flare photometry proved sufficiently sensitive to quantify an increase in aqueous flare after limited external retinal cryotherapy. Postoperative flare, as a measure of blood-ocular barrier breakdown, was significantly higher and visual recovery slower in the cryotherapy group. Visual acuity after 10 weeks was not significantly different between both groups.
Chemokine production at the blood-retina barrier probably plays a critical role in determining the influx of tissue-damaging cells from the circulation into the retina during inflammation. The blood-retina barrier comprises the retinal microvascular endothelium and the retinal pigment epithelium. Chemokine expression and production by human retinal microvascular endothelial cells (REC) have never been reported previously, so we examined the in vitro expression and production of monocyte chemoattractant protein-1 (MCP-1), regulated on activation of normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, interleukin (IL)-8, epithelial cell-derived neutrophil activating protein-78 (ENA-78) and growth related oncogene alpha (GROalpha) in these cells, both unstimulated and stimulated by cytokines likely to be present during the evolution of an inflammatory response. We compared this to expression and production of these chemokines in vitro in human retinal pigment epithelial cells (RPE). MCP-1 was expressed and produced constitutively by REC but all the chemokines were produced in greater amounts upon stimulation with the proinflammatory cytokines IL-1beta and tumour necrosis factor-alpha (TNF-alpha). MCP-1 and IL-8 were produced at much higher levels than the other chemokines tested. MIP-1alpha and MIP-1beta were present only at low levels, even after stimulation with IL-1beta and TNF-alpha. Cytokines with greater anti-inflammatory activity, such as IL-4, IL-10, IL-13, transforming growth factor-beta (TGF-beta) and IL-6, had little effect on chemokine production either by REC alone or after stimulation with IL-1beta and TNF-alpha. RPE, although a very different cell type, showed a similar pattern of expression and production of chemokines, indicating the site-specific nature of chemokine production. Chemokine production by REC and RPE is probably significant in selective leucocyte recruitment during the development of inflammation in the retina.
Macular edema is a common feature of posterior segment diseases. It is an expression of abnormal permeability in either retinal vessels (inner blood-retinal barrier) or in the retinal pigment epithelium (outer blood-retinal barrier). It occurs in either a diffuse pattern where the macula appears generally thickened or, in more severe cases, as cystoid edema with the typical petaloid appearance. Grid laser treatment may be useful to reduce macular edema. Spots of 100-250 micrometers in diameter are applied to the whole posterior pole, one to two groups apart. The foveal avascular zone remains untouched. In patients treated bilaterally, areas temporal and nasal to the macula must be spared to prevent the development of deep scotomas. The mechanism yielding positive results with the grid technique is still debated. Among the most reliable hypotheses are: Proliferation of pigment epithelial cells, followed by and improved efficiency of the outer blood-retinal barrier; proliferation of endothelial cells in retinal capillaries followed by an improved efficiency of the inner blood-retinal barrier; improvement of the retinochoroidal exchanges, and finally, release by coagulative necrosis of a factor able to improve the efficiency of the blood-retinal barriers. Lasers with long wavelengths, such as krypton red and diode, are the most appropriate ones to perform grid treatment.