Rethinking the Drop with iDose TR: Patient Access

I. Paul Singh, MD; Deborah Ristvedt, DO; and Kevin Talbot, MD

Eyetube

In this special podcast episode, I. Paul Singh, MD, speaks with Deborah Ristvedt, DO, and Kevin Talbot, MD, regarding the use of iDose TR (Glaukos), a procedural pharmaceutical, as an interventional glaucoma approach. They outline who the optimal patients are for this procedure, how to educate patients about drug delivery technology, and share pearls on reimbursement.

Examining Meibomian Gland Structure and Function in Patients With Demodex Blepharitis

Findings from a retrospective analysis highlight the association between Demodex blepharitis and meibomian gland structure and function.

Cecelia Koetting, OD, FAAO, DipABO and Elizabeth Yeu, MD

Cataract and Refractive Surgery Today

Meibomian gland disease (MGD) is defined as dysfunction of meibomian glands (e.g. obstruction, atrophy, or poor-quality meibum) that leads to tear film disruption, visual disturbance, and ocular discomfort.1 Inflammation from Demodex mites may cause serious consequences, like Demodex blepharitis and MGD. When discussing MGD, it’s important to include consideration of concurrent Demodex blepharitis. According to a study published in 2022, 58% of US patients (n = 595/1032) who visited an eye care clinic and underwent a slit-lamp examination, regardless of chief complaint, had Demodex blepharitis, including consultations for cataract or refractive surgery.2 A retrospective study by Cheng et al reported a positive rate of Demodex infestation in MGD patients (89%; n = 103 eyes of 52 patients) compared to control (43%; n = 62 eyes of 31 non-MGD patients).3 In a separate single-center study, Bhandari et al concluded that the incidence of Demodex infestation was 60% for patients with MGD (n = 60) and 18% for control (n = 50).4 Finally, Lim Bon Siong et al reported that the overall incidence of Demodex blepharitis was 85% for MGD patients (n = 65) and 34% for control patients (n = 50).5 Although Demodex blepharitis may be asymptomatic in a small proportion of patients (≤1% in one prospective observational study of 515 patients; n = 4), most patients (98.3%) reported two or more symptoms.6 Symptoms can stem from Demodex mites triggering inflammation leading to swollen eyelid margins, reduced gland openings, and compromised meibum flow.7,8 Additionally, Demodex infestation may be an important contributor to inflammatory MGD and can lead to structural and functional changes in the meibomian glands.8 Symptoms from Demodex blepharitis and MGD can impact tear film stability and ocular surface integrity, and may also lead to altered biometry and abnormal corneal topography measurements, which can potentially affect cataract or refractive surgery planning and increase the risk of postoperative dissatisfaction.9-12 Therefore, evaluation for Demodex blepharitis should be considered when managing MGD, particularly in patients undergoing such procedures. Study Rationale and Design In early 2025, we published a study in the Journal of Cataract and Refractive Surgery to answer one primary question: How do structural and functional measures of MGD compare in eyes with moderate-to-severe Demodex blepharitis (collarette grades 2–4) versus those with collarette grade 0? For this retrospective, single-center, observational study, we examined case records of 438 patients ≥18 years with available data for collarettes and MGD signs (e.g., telangiectasia, meibum expressibility, meibum quality, meibography).8 Collarettes were graded per eyelid on a 0 to 4 scale: Grade 0: 0 to 2 lashes/eyelid with collarettes. Grade 1: 3 to 10 lashes/eyelid with collarettes. Grade 2: >10 to <1/3 (~50) lashes/eyelid with collarettes. Grade 3: ≥1/3 to <2/3 (~100) lashes/eyelid with collarettes. Grade 4: ≥2/3 (~150) lashes/eyelid with collarettes.

Novel MOAs in Wet AMD

The pipeline is full of therapies that hold promise for extending treatment efficacy.

Lejla Vajzovic, MD, FASRS; Robert L. Avery, MD; Carl D. Regillo, MD; and Durga S. Borkar, MD, MMCi

Retina Today

KEY TAKEAWAYS Novel drug delivery approaches hold promise for extending treatment efficacy for patients with wet AMD, including gene therapy and tyrosine kinase inhibition. Extending treatment durability should also decrease visit burden for patients with wet AMD, maybe with the help of new imaging tools such as home OCT. Several hurdles remain, including the risk of inflammation, the potential for the denaturization and aggregation of macromolecules, and cost. Other novel approaches include tweaking the VEGF-A and angiopoietin-2 blockades, interleukin-6, WNT agonism, and direct Tie2 agonism. The advent of anti-VEGF agents, coupled with OCT imaging, transformed the care of our patients with wet AMD. We now have amazingly effective therapies to preserve and even restore vision for these patients (Figure), with second-generation agents providing even more durability. Now, clinicians and researchers are working to extend efficacy to reduce treatment burden with novel sustained delivery platforms, gene therapies, and various mechanisms of action.