Ophthalmology最新文献

Purpose: To assess the efficacy of a behavioral intervention using Eye-Use Monitoring technology to delay the onset and progression of myopia in children.

Design: A prospective, cluster-randomized, parallel-groups, examiner-masked, clinical trial (Chinese Clinical Trial Registry, ChiCTR2100052101).

Participants: A total of 413 children from grades 2 to 4 in Shandong, China, from October 2021 to December 2023 were randomized by class into three groups: reminder & feedback (6 classes, 156 children), reminder-only (5 classes, 147 children), and control (3 classes, 110 children). Children with prior myopia control interventions, significant eye conditions, or a history of eye diseases were excluded.

Methods: The reminder-only group received real-time vibration alerts for prolonged near work, close proximity, head tilt, or inadequate lighting. The reminder & feedback group received these alerts plus behavioral feedback, including praise, rewards, and weekly reports. The control group received no intervention. The intervention lasted 49 weeks, followed by a 49-week observation period without intervention.

Main outcome measures: The primary outcome was the mean change in cycloplegic spherical equivalent at 49 weeks. Secondary outcomes included changes in axial length, myopia incidence, rates of rapid myopic shift, participant compliance, and eye-use behaviors.

Results: At 49 weeks, changes in spherical equivalent and axial length were least in the reminder & feedback group (spherical equivalent: -0.52±0.35D vs. -0.59±0.43D vs. -0.73±0.48D, axial length: 0.30±0.14mm vs. 0.33±0.16mm vs. 0.40±0.20mm, in reminder & feedback group, reminder only group, and control group, respectively, both P<0.001). Myopia incidence was lowest in the reminder & feedback group (13.3% vs. 21.6% vs. 27.78%, in reminder & feedback group, reminder only group, and control group, respectively, P<0.05). However, differences diminished by the 98-week follow-up.

Conclusions: This study demonstrated that the combination of Eye-Use Monitoring reminders and feedback on eye-use behaviors can effectively delay the onset and progression of myopia in children. However, sustained intervention may be necessary to maintain long-term benefits.

Purpose: To evaluate the cost-utility of Luminopia (Luminopia, Inc) and CureSight (NovaSight, Ltd) as therapy for amblyopia compared with current common amblyopic treatments such as glasses, atropine drops, and patching.

Design: Cost analysis based on data from published randomized control trials (RCTs).

Subjects: Data from Luminopia, CureSight, and atropine RCTs.

Methods: A cost-utility analysis was performed using patient preference-based time trade-off utility values from previous literature. Costs for eye examinations were calculated using reimbursement data; device costs for duration of treatment were provided by sales representatives of Luminopia and CureSight. All treatments were inclusive of the cost of eyeglasses. Visual acuity (VA) and stereoacuity outcomes were extrapolated from the RCTs for atropine, Luminopia, and CureSight. A quality-adjusted life-year (QALY) was calculated by multiplying utility gain, a value correlated with VA gain, by length of time of benefit.

Main outcome measures: Cost, cost per QALY, and cost per stereoacuity gain.

Results: The cost to treat amblyopia with glasses alone for 12 weeks was $514. The cost of treating with patching for 12 weeks was $540 and with atropine for 16 weeks was $652, whereas the cost of treating with Luminopia or CureSight for 12 weeks was $1951 and $1564 or $1814, respectively. Treatment with glasses alone or patching for 12 weeks resulted in a cost per QALY gained of $427 and $101, respectively. Atropine treatment for 16 weeks resulted in a cost per QALY gained of $151. The cost per QALY for 12-week Luminopia treatment was $618 versus $368 or $427 for 12-week CureSight treatment and $314 or $354 for 16-week CureSight treatment (P < 0.05). Cost per stereoacuity gain for 12-week treatment duration was $6421/log arcsec (glasses), $1801/log arcsec (patching), and $3007/log arcsec or $3488/log arcsec (CureSight).

Conclusions: Treatment of amblyopia with Luminopia or CureSight is cost-effective in comparison with established willingness-to-pay thresholds and can provide a viable treatment option, especially for those who are unable to tolerate patching or atropine penalization. Cost-effectiveness values based on VA gain of Luminopia and CureSight were comparable.

Financial disclosure(s): Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Objective: Extracellular lipoprotein aggregation is a critical event in AMD pathogenesis. In this study, we sought to analyze associations between clinical and genetic-based factors related to lipoprotein metabolism and risk for age-related macular degeneration (AMD) in the All of Us research program.

Design: Cross-sectional retrospective data analysis.

Subjects: 5028 healthy and 2328 AMD patients from All of Us.

Methods: Participants with and without AMD were age, race, and gender-matched in a 1:2 ratio respectively. Smoking status, history of hyperlipidemia, and statin use were extracted in a binary manner. Statin use was further subcategorized into hepatically vs. non-hepatically metabolized statins. Laboratory values for low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides (TG) were also extracted, and outliers were excluded from analysis. The PLINK toolkit was used to extract single-nucleotide polymorphisms (SNPs) associated with LDL and HDL dysregulation, as published in prior work. Odds ratio curves were computed to assess the risk between LDL, TG, and HDL versus AMD. All clinical and genetic variables were input into a multivariable logistic regression model, and odds ratios and p-values were generated.

Main outcome measures: Statistical significance of risk factors for AMD, thresholded at p ≤ 0.05.

Results: On multivariable regression analysis, statin use, and low and high HDL were significantly associated with increased AMD risk (p <0.001, <0.001, 0.004, <0.001 respectively). Additionally, the multivariable regression implicated HDL associated SNPs increased risk for AMD. Lastly, LPA was identified (p =0.007) as a novel SNP associated with increased AMD risk.

Conclusions: There exists a U-shaped relationship between HDL and AMD risk, such that high and low HDL are significantly associated with increased AMD risk. Additionally, SNPs associated with HDL metabolism are associated with AMD risk. This analysis further establishes the role of HDL in AMD pathogenesis.