Byersrytter4550

When categorized by disease severity, CDVA improved in less severe eyes (stage 1) and more severe eyes (stage 2 or 3; P=0.049 and P=0.00009, respectively). Selleck mTOR inhibitor Total OIS was not significantly different between baseline and last follow-up (P=0.754); however the epithelial defect score was significantly less (P=0.034). Twenty-four of 31 eyes (77.4%) continued wearing the PROSE device, with a mean daily wearing time of 10.0±4.6 hrs. CONCLUSIONS In patients with LSCD, vision improved and the OIS remained stable with PROSE, suggesting that the device could be considered for visual rehabilitation in this population.OBJECTIVES Many contact lens (CL) users permanently discontinue wear because of ocular dryness and discomfort. This study aimed to determine whether refitting symptomatic soft CL wearers in to orthokeratology could improve ocular symptoms and signs. METHODS This was a prospective, 3-month, open-label study of symptomatic (Contact Lens Dry Eye Questionnaire [CLDEQ-8] ≥12) soft CL wearers who were between the ages of 18 and 45 years. All subjects were refit into orthokeratology CLs (Emerald, Euclid Systems). The following tests were completed CL history, Standardized Patient Evaluation of Eye Dryness (SPEED) questionnaire, CLDEQ-8, CLDEQ-4, logarithm of the minimum angle of resolution visual acuity, pupil size, refractive error, slit-lamp biomicroscopy, noninvasive tear break-up time, tear meniscus height, phenol red thread, conjunctival staining, corneal aesthesiometry, and corneal topography. RESULTS Twenty-nine of 40 qualifying subjects (age=24.43±4.62 years) completed the study. No significant differences were detected between completed and noncomplete subjects. Completed subjects had significantly better CLDEQ-8, CLDEQ-4, and SPEED scores at 3 months compared with baseline. Completed subjects had significantly better conjunctival staining scores and flatter keratometry values at 1 month compared with baseline. CONCLUSIONS Although not all symptomatic soft CL wearers were able to be refit into orthokeratology, subjects who were wearing orthokeratology at 3 months had a significant and clinically meaningful improvement in ocular symptoms. Additional work is needed to determine the mechanism leading to improved comfort because few clinical signs were changed after switching to orthokeratology.PURPOSE Omega-3 (n-3) fatty acid supplementation is used to treat systemic inflammatory diseases, but the role of n-3 in the pathophysiology and therapy of dry eye disease (DED) is not definitive. We evaluated the relationship of systemic n-3 levels with signs and symptoms at baseline in the Dry Eye Assessment and Management (DREAM) Study. METHODS Blood samples from participants at baseline were analyzed for n-3 and n-6, measured as relative percentage by weight among all fatty acids in erythrocytes. Symptoms were evaluated using the Ocular Surface Disease Index. Signs including conjunctival staining, corneal staining, tear breakup time (TBUT), and Schirmer's test with anesthesia were also evaluated. RESULTS There was no correlation between the systemic n-3 levels and DED symptoms. When the associations with signs of DED were assessed, lower DHA levels were associated with higher conjunctival staining, with mean scores of 3.31, 2.96, and 2.82 for low, medium, and high levels of DHA, respectively (linear trend P=0.007). None of the other signs were associated with DHA or the other measures of n-3. CONCLUSION Previous studies have found varying results on the role of n-3 supplementation with the signs and symptoms of DED. Among patients with DED enrolled in the DREAM Study, lower systemic n-3 levels were not associated with worse symptoms and most signs of DED.OBJECTIVES To evaluate the changes of corneal sub-basal nerve (SBN) and dendritic cell (DC) in contact lens (CL) wearers with mild dry eye and their potential relationship. METHODS Twenty mild dry eye volunteers who had never worn CLs were recruited for long-term CL wearing. Each subject underwent ocular surface evaluations at baseline and at 1, 4, 12, and 24 weeks, including Ocular Surface Disease Index (OSDI) questionnaire, tear film break-up time (TBUT), and Schirmer I test. In vivo confocal microscopy was used to examine the density, area, number of dendrites, total dendritic length of DC, and SBN densities in central and peripheral corneas. Only right eyes were included. RESULTS The DCs were activated and peaked at week 4 after wearing CLs. The peripheral DC density increased beginning the first week, whereas the central ones increased by week 4. After 4 weeks, both began to decrease, but still higher than baseline at week 24. The central and peripheral SBN densities decreased. However, the peripheral SBN tended to increase beginning at week 12. In early period, SBN was negatively correlated with DC parameters. After 4 weeks, the correlation changed to be positive. The OSDI increased, whereas the Schirmer I test and TBUT showed no significant change. CONCLUSIONS After wearing CLs, corneal DC were activated and increased, indicating ocular surface inflammation and decreased after week 4. In the early period, increases in DC may lead to decreases in SBN. Upon decrease of DC, the SBN may regenerate.PURPOSE OF REVIEW With the exception of familial hypercholesterolaemia, the value of genetic testing for managing dyslipidaemias is not established. We review the genetics of major dyslipidaemias in context of clinical practice. RECENT FINDINGS Genetic testing for familial hypercholesterolaemia is valuable to enhance diagnostic precision, cascade testing, risk prediction and the use of new medications. Hypertriglyceridaemia may be caused by rare recessive monogenic, or by polygenic, gene variants; genetic testing may be useful in the former, for which antisense therapy targeting apoC-III has been approved. Familial high-density lipoprotein deficiency is caused by specific genetic mutations, but there is no effective therapy. Familial combined hyperlipidaemia (FCHL) is caused by polygenic variants for which there is no specific gene testing panel. Familial dysbetalipoproteinaemia is less frequent and commonly caused by APOE ε2ε2 homozygosity; as with FCHL, it is responsive to lifestyle modifications and statins or/and fibrates.