Concept Library

The all-polymer microfluidic theranostic smart contact lens (AP-TSCL) demonstrated pressure-triggered delivery of timolol or brimonidine above preset thresholds in in vitro (artificial eye model), ex vivo (enucleated bovine eyes), and in vivo (rabbit ocular hypertension) studies.

Organic cation transporter 2 (OCT2) and multidrug and toxin extrusion protein 1 (MATE1) may contribute to the interindividual variability of brimonidine concentrations and effects.

Organic cation transporter 2 (OCT2) and multidrug and toxin extrusion protein 1 (MATE1) may play a role in brimonidine uptake into the human eye.

The uptake of brimonidine by OCT2 and MATE1 was time- and concentration-dependent in HEK293 cells.

Brimonidine, a selective α2-adrenergic agonist, was transported by organic cation transporter 2 (OCT2) and multidrug and toxin extrusion protein 1 (MATE1) but not by OCT1, OCT3, or MATE2K in HEK293 cells.

Topical carbonic anhydrase inhibitor (CAI) use was associated with increased hazards of anxiety disorders (aHR range 1.30-1.48; all P < 0.001) in glaucoma patients aged ≥40 years.

Topical carbonic anhydrase inhibitor (CAI) use was associated with increased hazards of antidepressant initiation (aHR 2.45 at 3 months; 2.03 at 6 months; 1.83 at 1 year) in glaucoma patients aged ≥40 years.

Topical carbonic anhydrase inhibitor (CAI) use was associated with increased hazards of depression (aHR 1.36 at 3 months; 1.28 at 6 months; 1.27 at 1 year) in glaucoma patients aged ≥40 years.

Anxiety disorders occurred more often in topical carbonic anhydrase inhibitor (CAI) users across all time points (all P < 0.001) compared to controls in glaucoma patients aged ≥40 years.

Antidepressant prescriptions were more frequent in topical carbonic anhydrase inhibitor (CAI) users compared to controls at 3 months (3.57% vs. 1.28%), 6 months (5.0% vs. 2.49%), and 1 year (7.7% vs. 4.4%; all P < 0.001) in glaucoma patients aged ≥40 years.

Topical carbonic anhydrase inhibitor (CAI) users had new-onset depression more frequently than controls at 3 months (1.42% vs. 0.77%), 6 months (2.46% vs. 1.41%), and 1 year (4.05% vs. 2.47%; all P < 0.001) in glaucoma patients aged ≥40 years.

Pre-existing use of alpha-2 adrenergic (AA) agonists was identified as a protective factor for developing an intraocular pressure (IOP) spike following micropulse transscleral laser therapy (MPTLT), with an odds ratio of 0.20 (95% CI: 0.42 to 0.91, P =0.038) in 80 eyes from 66 glaucoma participants.

Pre-existing use of alpha-2 adrenergic (AA) agonists was associated with reduced intraocular pressure (IOP) elevation (coefficient -4.31, 95% CI: -7.61 to -1.01, P =0.01) following micropulse transscleral laser therapy (MPTLT) in 80 eyes from 66 glaucoma participants.

In a discrete choice experiment (DCE) completed by 2445 eye drop-treated patients from Danish national registries, 25% had previously discontinued treatment with intraocular pressure-lowering eye drops due to adverse effects.

In a discrete choice experiment (DCE) completed by 2445 eye drop-treated patients from Danish national registries, more females than males reported currently experiencing adverse effects (48% vs. 35%) from intraocular pressure-lowering eye drops.

A discrete choice experiment (DCE) completed by 2445 eye drop-treated patients (24% response rate; 55% male; median age: 67 years) from Danish national registries showed that moderate acute discomfort and non-persistent cosmetic changes were the least important adverse effects of intraocular pressure-lowering eye drops to patients.

A discrete choice experiment (DCE) distributed to 10,000 eye drop-treated patients aged 40-75 years from Danish national registries, with 2445 patients completing the DCE, revealed that severe blurred vision, persistent cosmetic changes, and persistent discomfort were the adverse effects of intraocular pressure-lowering eye drops that exhibited the highest levels of disutility for patients.

In a multicenter, randomized, double-blind, placebo-controlled trial, the venule-to-arteriole (V:A) ratio was consistently lower in the acetazolamide (ACZ) group compared to the placebo group from month 1 (1.20 vs. 1.24, respectively; P = 0.03) to month 6 (1.16 vs. 1.23, P = 0.02) in participants (n = 165) with mild visual loss due to papilledema secondary to idiopathic intracranial hypertension (IIH).

In a multicenter, randomized, double-blind, placebo-controlled trial, acetazolamide (ACZ) significantly reduced venule diameters by -4.59 µm (P = 0.02) at month 1 in participants (n = 165) with mild visual loss due to papilledema secondary to idiopathic intracranial hypertension (IIH), whereas placebo showed no change (+1.21 µm; P = 0.54).

Non-prostaglandin F2α analog (PGFA)-based triple combinations, specifically α2-adrenergic agonists (AAA) plus β-adrenergic blockers (BAB) plus carbonic anhydrase inhibitors (CAI), achieved an intraocular pressure reduction of -7.22 mmHg (-9.04 to -5.40 mmHg), which was similar to the top-ranking PGFA-based combinations.

Synergy was observed with prostaglandin F2α analog (PGFA) plus carbonic anhydrase inhibitors (CAI) (-2.05 mmHg) in intraocular pressure reduction, suggesting a promising avenue for new combinations.

Prostaglandin F2α analog (PGFA)-based combinations demonstrated the greatest intraocular pressure (IOP) reduction, ranging from -7.41 to -5.81 mmHg, with PGFAs plus carbonic anhydrase inhibitors (CAIs) ranking highest among these combinations.

Among monotherapies, nitric oxide-donating prostaglandin analogs (NO-PGA) were the most effective in reducing intraocular pressure (IOP) with a reduction of -5.15 mmHg (95% confidence interval: -6.18 to -4.11 mmHg), followed by prostaglandin F2α analogs (PGFAs) with -4.75 mmHg (-5.19 to -4.31 mmHg) and E-prostanoid receptor 2 (EP2) agonists with -3.50 mmHg (-4.27 to -2.73 mmHg).

A secondary analysis of 7 patients with idiopathic intracranial hypertension (IIH) receiving combined therapy with acetazolamide and glucagon-like peptide 1 (GLP-1) agonists (liraglutide or semaglutide) for a full year of follow-up suggested possible acetazolamide dose reduction following GLP-1 initiation without changing the clinical outcome.

A secondary analysis of 7 patients with idiopathic intracranial hypertension (IIH) receiving combined therapy with acetazolamide and glucagon-like peptide 1 (GLP-1) agonists (liraglutide or semaglutide) for a full year of follow-up revealed a trend of BMI reduction following GLP-1 initiation.

In a retrospective cohort study of 79 patients with idiopathic intracranial hypertension (IIH), glucagon-like peptide 1 (GLP-1) agonists (liraglutide or semaglutide) combined with acetazolamide did not show significant differences in papilledema grade, best corrected visual acuity (BCVA), visual field (VF), or OCT RNFL thickness improvements over a 12-month period compared to acetazolamide monotherapy.

The mean 24-hour interquartile range (IQR) of intraocular pressure (IOP) with fixed combination of beta-blockers and prostaglandin analogues (BB-PGA) (2.3±0.4 mm Hg) was significantly less than that with both beta-blockers (BB) alone (3.8±0.4 mm Hg) and fixed combination of beta-blockers and carbonic anhydrase inhibitors (BB-CAI) (3.2±0.4 mm Hg) in 22 patients with primary open-angle glaucoma implanted with an ocular telemetry sensor.

The mean 24-hour standard deviation (SD) of intraocular pressure (IOP) with fixed combination of beta-blockers and prostaglandin analogues (BB-PGA) (1.9±0.2 mm Hg) and fixed combination of beta-blockers and carbonic anhydrase inhibitors (BB-CAI) (2.0±0.2 mm Hg) were significantly (p<0.05) less than that with beta-blockers (BB) alone (2.4±0.2 mm Hg) in 22 patients with primary open-angle glaucoma implanted with an ocular telemetry sensor.

The mean 24-hour intraocular pressure (IOP) with fixed combination of beta-blockers and prostaglandin analogues (BB-PGA) (17.3±1.1 mm Hg) was significantly (p<0.001) less than that with beta-blockers (BB) alone (18.8±1.1 mm Hg) in 22 patients with primary open-angle glaucoma implanted with an ocular telemetry sensor.

Providers without glaucoma training were more likely to avoid topical carbonic anhydrase inhibitors (CAI) in hypothetical patients with prior sulfonamide antibiotic (SA) rash and/or urticaria (p = 0.004) and anaphylaxis (p = 0.01) than glaucoma-trained providers.

Respondents affiliated with non-glaucoma organizations were more likely to avoid oral carbonic anhydrase inhibitors (CAI) in hypothetical patients with prior sulfonamide antibiotic (SA) rash and/or urticaria than those affiliated with glaucoma organizations (p = 0.03).

Respondents with more than 10 years in practice were more likely to avoid oral carbonic anhydrase inhibitors (CAI) in hypothetical patients with prior sulfonamide antibiotic (SA) rash and/or urticaria than those with 10 years or less in practice (OR 2.27, p = 0.002).

Over 90% of 250 respondents would avoid oral carbonic anhydrase inhibitors (CAI) in hypothetical patients with prior severe sulfonamide antibiotic (SA) hypersensitivity.

27% of 250 respondents would avoid topical carbonic anhydrase inhibitors (CAI) and 52% would avoid oral CAI in hypothetical patients with prior sulfonamide antibiotic (SA) rash and/or urticaria.

Dunn's test showed that aflibercept levels in the aqueous humor were significantly higher in cases using inflow drugs (e.g., carbonic anhydrase inhibitor, beta-blockers, and alpha-2 agonists) compared to both controls (P = 0.0085) and cases using outflow drugs (e.g., prostaglandin analog) (P = 0.044) at 1 month after the first intravitreal aflibercept (IVA) injection.

Mean aflibercept levels in the aqueous humor (AH) in cases using inflow drugs (e.g., carbonic anhydrase inhibitor, beta-blockers, and alpha-2 agonists) were 15.95 µg/mL (interquartile range: 7.20-22.57) at 1 month after the first intravitreal aflibercept (IVA) injection.

Omidenepag (OMD) bound to EP2 receptors, but neither OMD nor omidenepag isopropyl (OMDI) bound to α2A, β1, and β2 adrenergic receptors or inhibited enzymatic activities of CA1 and CA2.

Brimonidine and unoprostone isopropyl had SUCRA scores below 4.0%, indicating modest but limited efficacy for long-term intraocular pressure control in normal tension glaucoma patients.

In a nationwide population-based cohort study utilizing insurance claims data from Taiwan's National Health Insurance Research Database between 2008 and 2019, glaucoma patients on topical alpha-2 adrenergic agonist monotherapy exhibited a significantly higher Alzheimer's disease (AD) risk (aHR 1.15, 95% CI = 1.01-1.31) compared to those on beta-blockers.

Three months post-Descemet-stripping endothelial keratoplasty (DSEK) in the left eye of a 62-year-old woman, uncontrolled intraocular pressure (IOP) ranged from the mid-20s to mid-30s despite maximum tolerated medical therapy consisting of acetazolamide 250 mg by mouth 2 times a day, brimonidine 2 times a day, dorzolamide 2 times a day, and timolol 2 times a day.

Among perioperative intraocular pressure (IOP) lowering medications, prostaglandin analogues, alpha-agonists, and topical carbonic anhydrase inhibitors (CAIs) showed the smallest effect in reducing postoperative IOP following uncomplicated phacoemulsification.

Among perioperative intraocular pressure (IOP) lowering medications, intracameral cholinergics or fixed-combination carbonic anhydrase inhibitor-beta-blocker (FCCB) formulations showed the largest effect in reducing postoperative IOP at both 2-8 hours and 12-24 hours following uncomplicated phacoemulsification.

A systematic review and meta-analyses investigating potential differences in efficacy and safety between benzalkonium chloride (BAK)-preserved and BAK-free anti-glaucomatous eye drops found no significant differences in efficacy (IOP-lowering effect) between BAK-preserved and BAK-free eye drops.

The addition of acetazolamide lowered the pressure to 19 mm Hg in both eyes of a 62-year-old woman with glaucoma, but she tolerated it poorly; methazolamide was also attempted with similar side effects.

A 62-year-old woman with glaucoma was successively trialed on fixed combination brimonidine-timolol, dorzolamide, and netarsudil, in addition to latanoprost, but her IOP remained in the mid- to upper 20s in both eyes.

Topical carbonic anhydrase inhibitors (CAIs) may be associated with higher risks of metabolic acidosis in patients with primary open-angle glaucoma (POAG) and pre-dialysis advanced chronic kidney disease (CKD), with hospital admissions due to metabolic acidosis being higher in CAI users (incidence = 21.54 events per 100 patient-years) compared with non-users (incidence = 11.87 events per 100 patient-years; adjusted hazard ratio = 1.89, 95% CI = 1.07-3.36).

Topical carbonic anhydrase inhibitors (CAIs) may be associated with higher risks of long-term dialysis in patients with primary open-angle glaucoma (POAG) and pre-dialysis advanced chronic kidney disease (CKD), with an incidence of 1,216.85 events per 100 patient-years for CAI users versus 764.17 events per 100 patient-years for non-users (adjusted hazard ratio = 1.17, 95% CI = 1.01-1.37).

The ripasudil-brimonidine fixed-dose combination (RBFC, K-232) demonstrated a superior intraocular pressure (IOP)-lowering effect compared to brimonidine 0.1% ophthalmic solution, with a difference of -1.8 mm Hg (95% CI = -2.3 to -1.4 mm Hg; P < .001) in patients with primary open-angle glaucoma or ocular hypertension.