Barrettstanton4036
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Combined average visual field index is a simple, novel tool for binocular visual field which agrees with the existing binocular integrated visual field model, as well as patient reported activity limitation in glaucoma.
To determine the correlation between novel models of binocular visual field with the existing integrated visual field (IVF) and glaucoma activity limitation.
Integrated visual fields were calculated from the monocular visual fields of 58 patients with primary glaucoma and the novel binocular visual field models termed binocular summation visual field index (BiSumVFI) and combined average visual field index (CaVFI) were derived from the visual field indices (VFI) of both fields. Glaucoma activity limitation (GAL-9) questionnaire was administered to the patients. The relationship between IVF and the two newer models of binocular fields were determined and the correlation of IVF, BiSumVFI and CaVFI with GAL-9 was estimated.
A very strong correlation was seen between IVF and BiSumVFI (r=-0ts' perception of activity limitation in glaucoma.
No significant difference was found between the intraocular pressure (IOP) lowering of omidenepag isopropyl 0.002% once daily (QD) and twice daily (BID). However, adverse events (AEs) were higher in the BID arm; thus, QD dosing is the preferred dosing frequency for further investigation.
This phase 2, randomized, double-masked, parallel-arm, multicenter study (NCT03858894) was conducted in the United States to examine whether the efficacy and safety of omidenepag isopropyl 0.002% BID dosing was superior to QD dosing in subjects with primary open-angle glaucoma or ocular hypertension.
Randomized subjects (11) received omidenepag isopropyl 0.002% QD (n=50) or BID (n=48) for 6 weeks (after a ≤4-week washout period). IOP was measured at 800 am, 1200 pm, and 400 pm at baseline and weeks 2 and 6. The primary efficacy endpoint was IOP at each timepoint at weeks 2 and 6. DNA Repair inhibitor AEs were evaluated.
Baseline mean diurnal IOP (±SD) post washout was 25.4±2.9 mm Hg (BID) and 24.6±1.9 mm Hg (QD). At weeks 2 and 6, clinically significant IOP reductions from baseline were observed for omidenepag isopropyl BID and QD treatments. Least-squares mean (±SE) IOP differences (BID versus QD) were not statistically significant (week 2 0.44±0.68 to 1.08±0.65 mm Hg; week 6 0.36±0.63 to 0.68±0.68 mm Hg) at any timepoint (all P > 0.05). AEs were 3-fold greater in the BID arm (41.7%; QD 14.0%); the most frequently reported AE was conjunctival/ocular hyperemia (BID 22.9%; QD 2.0%). Five subjects discontinued omidenepag isopropyl prematurely, 4 of 5 owing to AEs (BID 4; QD 0).
In this study, the benefit-risk profile of omidenepag isopropyl 0.002% QD was more favorable than the benefit-risk profile of BID. This difference was driven by a higher incidence of local tolerability issues in the BID arm.
In this study, the benefit-risk profile of omidenepag isopropyl 0.002% QD was more favorable than the benefit-risk profile of BID. This difference was driven by a higher incidence of local tolerability issues in the BID arm.
XEN implant was associated with low endothelial cell density (ECD) reduction. In fact, when combined with phacoemulsification, the reduction in ECD was similar to that expected after phacoemulsification alone.
The purpose of this study was to assess the impact of XEN implant, either alone or in combination with phacoemulsification, on ECD.
Multicenter, prospective, observational study conducted on consecutive open-angle glaucoma patients, who were enrolled in the Italian XEN Glaucoma Treatment Registry and have complete endothelial cell count data at baseline and at 6 months after implantation. The primary endpoint was the mean percentage change in ECD between baseline and month 6.
The study included 108 open-angle glaucoma eyes (68 in the XEN-solo and 40 eyes in the XEN+phaco groups) and 60 control eyes (phaco-solo group). As compared with baseline, mean (95% confidence interval, CI) ECD reduction was -5.6% (-7.0% to -4.9%), -11.3% (-13.8% to -10.9%), and -13.0% (14.8% to -11.8%) in the XEN-solo, XEN+phaco, and phaco-solo groups, respectively (P=0.0004, <0.0001, and <0.0001, respectively). As compared with the XEN-solo group, the ECD reduction was significantly greater in the XEN+phaco group (mean difference=5.7%; 95% CI 4.1%-7.3%, P<0.0001) and in the phaco-solo group (mean difference=7.4%; 95% CI 5.7%-9.1%, P<0.0001). ECD reduction was similar in XEN+phaco and phaco-solo groups (P=0.9). In absolute terms, ECD reduction was significantly greater in the XEN+phaco (mean difference=169±306, P=0.021) and in the phaco-solo (mean difference=192±302, P=0.0022) groups than in the XEN-solo group.
The mean ECD reduction 6 months after XEN implantation was low. The ECD reduction in the XEN+phaco group was larger than in the XEN-solo group but was similar to that observed in the phaco-solo group.
The mean ECD reduction 6 months after XEN implantation was low. The ECD reduction in the XEN+phaco group was larger than in the XEN-solo group but was similar to that observed in the phaco-solo group.
The lack of available biomarkers for diagnosing and predicting different stages of liver disease with a noninvasive strategy is currently one of the main challenges that clinicians are facing. Recent evidence indicates that the plasma levels of specific microRNAs (miRNAs) may be significantly altered in patients with liver injury, including those with HIV type 1 (HIV-1) infections.
Large-scale deep sequencing analysis of small RNA expression was performed on plasma samples from 46 patients with HIV-1/hepatitis C virus (HCV) coinfections that did not exhibit liver fibrosis at the time of sampling.
A total of 1065 different miRNAs were identified. After a mean of 10.3 years, 26 out of the 46 patients developed liver fibrosis (stage F2-4) and 20 remained without signs of liver fibrosis (stage F0-1). We identified a signature of seven miRNAs 100-5p, 192-5p, 99a-5p, 122-5p, 125b-2-3p, 1246 and 194-5p, which were highly correlated with progression to liver fibrosis. These seven miRNAs detected liver fibrosis progression with an area under the curve (AUC) of 0.