American Journal of Ophthalmology最新文献

Purpose: To evaluate the intraocular pressure (IOP)-lowering effect and safety of up to two bimatoprost implant administrations versus selective laser trabeculoplasty (SLT).

Design: Phase 3 (Stage 2), randomized, 24-month, multicenter, patient- and efficacy evaluator-masked, paired-eye clinical trial (NCT02507687).

Participants: Patients (n=183) with open-angle glaucoma or ocular hypertension inadequately managed with topical IOP-lowering medication for reasons other than efficacy.

Intervention: Patients received a single 360° SLT procedure in one eye and 10-µg bimatoprost implant administration in the contralateral eye. Initially, implant-treated eyes received a second implant at week 16 if safety criteria were met. After a protocol amendment, implant-treated eyes were retreated with flexible scheduling if IOP was >17 mm Hg and safety criteria were met.

Main outcome measures: The primary efficacy variable was IOP change from baseline, with primary timepoints at weeks 4, 12, and 24. Safety measures included treatment-emergent adverse events (TEAEs) and ocular safety measures.

Results: Mean (±SE) baseline IOP (mm Hg) was 25.2±0.22 and 25.1±0.22 in implant- and SLT-treated eyes, respectively. Least-squares mean (±SE) IOP reduction from baseline (mm Hg) for eyes treated with up to two implants versus SLT was 6.8±0.28 versus 6.2±0.28 at week 4, 6.9±0.30 versus 6.4±0.30 at week 12, and 6.9±0.27 versus 6.5±0.28 at week 24. The probability of not having required nonstudy (rescue) IOP-lowering treatment at days 360 and 720, respectively, was 67.5% and 50.2% for implant-treated eyes versus 68.7% and 60.6% for SLT-treated eyes. The most common ocular TEAE in both implant- and SLT-treated eyes was increased IOP attributed to wearing off of efficacy. Mean (±SE) percentage change in corneal endothelial cell density from baseline at month 24 was -6.2±1.13% in implant-treated eyes (-7.9±2.04% with fixed readministration; -5.2±1.35% with flexible readministration) versus -3.1±0.43% in SLT-treated eyes.

Conclusions: The bimatoprost implant demonstrated statistical and clinical noninferiority to SLT in IOP reduction from baseline at weeks 4, 12, and 24. In subgroup analysis, patients with flexible implant readministration met the same criteria. Both the implant and SLT demonstrated sustained (2-year) IOP lowering in many eyes. A flexible administration schedule improved the safety profile of the implant over the fixed administration schedule.

Purpose: Treatment of myopia has been informed by more than 3 decades of clinical trials and other observations. However, controversies regarding myopia control remain, such as when to stop treatment and what is the long-term efficacy of treatment. This perspective aims to describe clinically relevant and current controversies regarding myopia treatment.

Design: Perspective.

Methods: We reviewed clinical trial data and other studies regarding myopia control therapies.

Results: Controversies in myopia treatment are related to the efficacy of low dose atropine eyedrops and new lens design spectacles to substantially reduce progression of myopia. In addition to efficacy, safety of therapies including soft contact lenses, orthokeratology and low-level red light remains a concern. The therapeutic role of outdoor time in reducing myopia progression also requires further investigation. More research is necessary to confirm treatment effectiveness, duration of required treatment, tapering schedules and when to begin and stop treatment.

Conclusions: Myopia management is evolving and maintaining competency in the multiple approaches poses a challenge. Key challenges include identifying high-risk children who would benefit most from treatment, limited evidence supporting the effectiveness of myopia progression control treatments in certain populations, and concerns regarding availability and cost of treatment, which may create socioeconomic barriers to access. The limitations of current methods to slow or stop myopia progression highlight the need for continuing rigorous investigation of new and improved strategies to reduce the burden of myopia.

Purpose: To investigate the incidence, clinical spectrum and pathophysiology of microcystoid macular edema (MME) in two cohorts of patients with epiretinal membrane (ERM) and idiopathic full thickness macular hole (FTMH).

Design: Single-center, Retrospective, interventional, cohort study.

Methods: Review of clinical charts, structural and en-face optical coherence tomographty (OCT) and fluorescein angiography (FA) imaging of ERM and FTMH eyes which underwent surgery with pars plana vitrectomy and internal limiting membrane (ILM) peel, with a minimum follow-up of 6 months. Histopathology analysis of three specimens: two human retinas, and one human ILM.

Results: A hundred and seventy-two patients with ERM (123) and FTMH (49) were included in the study and followed up a mean of 9.1 ± 4.7 and of 8.2 ± 3.6 months, respectively. Preoperatively, MME was present in 27 out of 123 eyes with ERM (21.9%), and in none of 49 eyes with FTMH (p<0.001). MME was significantly associated with advanced ERM stages (p<0.001). MME was typically located below continuous ERM-ILM adherence areas. FA in 46 ERM eyes showed capillary leakage in 36.4% of eyes without MME or cystoid macular edema (CME), in 39% of eyes with MME, and increased hyper-fluorescence in CME. Postoperatively, new-onset MME appeared in 13 out of 84 ERM eyes (15.5%) and in 1 FTMH eye (2%, p=0.014). MME resolved in 7 out of 40 ERM eyes with either preoperative or postoperative MME (17.9%) by 2.8 ± 1.5 months post-surgery. MME showed variable evolution postoperatively. The association between MME and postoperative best corrected visual acuity was significant only in univariate analysis (p=0.037). Histopathology analysis showed anatomical continuity between Müller cells and ERM, suggesting a higher risk of iatrogenic damage in ERM eyes during peeling maneuvers.

Conclusions: Postoperative MME was a frequent finding in ERM and a rare occurrence in FTMH, suggesting that ILM peeling alone may not be sufficient to cause MME. The morphology and clinical characteristics of ERM-related MME are unlikely related to neurodegenerative processes and rather attributable to Müller cell disruption and iatrogenic damage. The characteristics of MME and CME may overlap, blurring the differences between the two entities.

Introduction: Botulinum toxin is an alternative to conventional strabismus surgery for treatment for acute, acquired, comitant esotropia (AACE). Previous studies suggest that the two treatment approaches may be equally effective for 6 months. The purpose of our study was to determine whether botulinum toxin remains as effective as strabismus surgery for 36 months after treatment.

Methods: Design: Multicenter, retrospective, nonrandomized, comparative, clinical, non-inferiority study.

Setting: Two tertiary care pediatric hospitals.

Study population: 76 children with AACE followed for at least 36 months after treatment.

Intervention: Treatment with either botulinum toxin ('BTX group') or strabismus surgery ('surgery group').

Main outcome measure: Success rate at 36 months (horizontal deviation of 10 prism diopters or less and evidence of binocular vision).

Results: There were 44 patients in the BTX group and 32 patients in the surgery group with a median deviation of 35 PD in both groups (range 10-55). The duration of general anesthesia (6 vs 71 min, P<0.0001) and time in the post-anesthesia care unit (40 vs 95 min, P<0.0001) were significantly shorter in the BTX group. At 36 months, the success rate was 72% in the BTX group and 56% in the surgery group with a similar median deviation and median stereoacuity. BTX was non-inferior to surgery at 36 months (95%CI for difference in success rate (BTX minus surgery) was -5% to +38%). At 36 months, the median time from esotropia onset to any intervention was 6.5 months without treatment success and 4 months in those with treatment success (P<0.05).

Conclusions/relevance: Botulinum toxin was non-inferior to strabismus surgery in the treatment of AACE at 36 months while reducing the duration of general anesthesia. Longer delay from esotropia onset to treatment was an independent risk factor for worse sensorimotor outcomes irresepctive of the type of treatment.

Purpose: To summarize and categorize postulated mechanisms of immune checkpoint inhibitor (ICI)-mediated retinal and choroidal inflammation and discuss resulting implications for evaluation and management of these adverse reactions.

Design: Targeted literature review with interpretation and perspective Methods: We performed a review of selected literature describing immune-mediated retinal and choroidal adverse reactions associated with ICI therapy, synthesizing and categorizing the likely underlying pathogenic mechanisms. Based on these mechanistic categories, we provide perspective on a rational approach to the evaluation of patients with ICI-associated inflammatory disorders of the retina and choroid.

Results: ICI-induced posterior segment adverse reactions can be categorized into three major mechanisms of unintended, targeted inflammation that share similarities to immunotherapy-related adverse events (irAEs) seen in other organ systems. In Type 1 reactions, T cell activation by ICIs can result in cross-reactivity of anti-tumor T cells with ocular tissues (Type 1a) or expansion of eye-specific T cells in predisposed individuals (Type 1b), leading to ocular inflammation that mimics known uveitic conditions. In Type 2 reactions, non-specific ocular or systemic inflammation exacerbated by ICI use can cause retinal vasculitis through a "bystander" mechanism, potentially resulting in vision-threatening vascular occlusions. Finally, in Type 3 reactions, ICI use can prompt autoantibody-mediated inflammation and/or exacerbation of paraneoplastic processes likely related to T cell driven expansion of B cell populations.

Conclusions: Although relatively uncommon, posterior segment inflammatory disorders associated with systemic ICI therapy may be vision-threatening if not identified and treated appropriately. We propose that the pathogenic mechanisms underlying these chorioretinopathies falls into three major categories involving inadvertent T cell mediated inflammation. Visual prognosis with appropriate treatment is generally favorable, but some reactions, such as longstanding exudative retinal detachments and ICI-induced occlusive retinal vasculitis, can result in permanent visual defects.