METHODS: Data was collected from the web-based MOH CSR. All consecutive cataract surgery patients from 1st June 2008 to 31st December 2014 were identified. Exclusion criteria were traumatic cataract or previous ocular surgery. Demographic data, ocular co-morbidities, intraoperative details and postoperative visual acuity (VA) at final ophthalmological follow-up were noted. All eyes were taken for analysis. Subjects with POE were compared against subjects with no POE for risk factor assessment using multiple logistic regressions.
RESULTS: A total of 163 503 subjects were screened. The incidence of POE was 0.08% (131/163 503). Demographic POE risk factors included male gender (OR: 2.121, 95%CI: 1.464-3.015) and renal disease (OR: 2.867, 95%CI: 1.503-5.467). POE risk increased with secondary causes of cataract (OR: 3.562, 95%CI: 1.740-7.288), uveitis (OR: 11.663, 95%CI: 4.292-31.693) and diabetic retinopathy (OR: 1.720, 95%CI: 1.078-2.744). Intraoperative factors reducing POE were shorter surgical time (OR: 2.114, 95%CI: 1.473-3.032), topical or intracameral anaesthesia (OR: 1.823, 95%CI: 1.278-2.602), posterior chamber intraocular lens (PCIOL; OR: 4.992, 95%CI: 2.689-9.266) and foldable IOL (OR: 2.276, 95%CI: 1.498-3.457). POE risk increased with posterior capsule rupture (OR: 3.773, 95%CI: 1.915-7.432) and vitreous loss (OR: 3.907, 95%CI: 1.720-8.873). Postoperative VA of 6/12 or better was achieved in 15.27% (20/131) subjects with POE.
CONCLUSION: This study concurs with other studies regarding POE risk factors. Further strengthening of MOH CSR data collection process will enable deeper analysis and optimization of POE treatment.
METHODS: The inhibitory effect of chrysin, kaempferol, morin, silibinin, quercetin, diosmin and hesperidin upon nitric oxide (NO), prostaglandin E(2) (PGE(2)) and tumour necrosis factor-alpha (TNF-alpha) secretion from the LPS-induced RAW 264.7 monocytic macrophage was assessed and IC(50) values obtained. Flavonoids that showed reasonable inhibitory effects in at least two out of the three assays were combined in a series of fixed IC(50) ratios and reassessed for inhibition of NO, PGE(2) and TNF-alpha. Dose-response curves were generated and interactions were analysed using isobolographic analysis.
RESULTS: The experiments showed that only chrysin, kaempferol, morin, and silibinin were potent enough to produce dose-response effects upon at least two out of the three mediators assayed. Combinations of these four flavonoids showed that several combinations afforded highly significant synergistic effects.
CONCLUSIONS: Some flavonoids are synergistic in their anti-inflammatory effects when combined. In particular chrysin and kaempferol significantly synergised in their inhibitory effect upon NO, PGE(2) and TNF-alpha secretion. These findings open further avenues of research into combinatorial therapeutics of inflammatory-related diseases and the pharmacology of flavonoid synergy.