The effect of a novel selenium disulphide-containing topical treatment on comfort, comfortable wear time and ocular signs in symptomatic contact lens wearers: An exploratory study

Stapleton, Fiona; Tan, Jacqueline; Jia, Tianni; Gleeson, Marc; Bosworth, Charles F.

doi:10.1016/j.clae.2022.101680

Cited by 2 publications

(2 citation statements)

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“…Novel therapies to restore mucin function have only been evaluated in preclinical and early clinical studies to date [12]. Several promising compounds are currently in late-stage (phase 2 or 3) clinical development for the treatment of DED associated with MGD (Table 1) [160][161][162][163][164].…”

Section: Emerging Pharmacologic Treatmentsmentioning

confidence: 99%

“…Hyperkeratinization may play a role in meibomian duct obstruction in MGD [172]. In a small randomized study (NCT04314362), patients with MGD (n = 22) were randomly assigned to receive AZR-MD-001 1% or vehicle control ointment administered to the lower eyelid margin [163]. Evaluation at 2 weeks showed that AZR-MD-001 significantly decreased the tear evaporation rate and increased TFBUT and the number of meibomian glands yielding liquid secretion relative to the vehicle control group; however, there were no between-group differences observed in lipid layer thickness or DED symptoms (OSDI score) [163].…”

Section: Emerging Pharmacologic Treatmentsmentioning

confidence: 99%

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Dry Eye Disease Associated with Meibomian Gland Dysfunction: Focus on Tear Film Characteristics and the Therapeutic Landscape

Sheppard

Nichols

2023

Ophthalmol Ther

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Meibomian gland dysfunction (MGD) is highly prevalent and is the leading cause of evaporative dry eye disease (DED). MGD is characterized by a reduction in meibum secretion and/or a change in meibum composition that results in the disruption of the tear film lipid layer and an increase in the tear film evaporation rate. Excessive evaporation causes tear film instability, desiccation, tear hyperosmolarity, inflammation, and apoptosis of ocular surface cells, resulting in a continuous cycle of DED. The primary treatment goal for DED associated with MGD is to restore the tear film lipid layer and decrease evaporation, thereby reducing ocular signs and symptoms. The management of MGD includes home care options (eyelid hygiene, warming eye masks, ocular lubricants) and office-based treatments (manual expression, microblepharoexfoliation, thermal pulsation, intense pulsed light, intraductal probing).Topical ophthalmic prescription medications attempt to alter various factors that may contribute to DED (e.g., inflammation, bacterial growth, inadequate tear production). In this review, clinical evidence regarding available treatments and emerging therapies from randomized studies in patients with DED associated with MGD is summarized. Although some treatment modalities have been evaluated specifically for DED patients with MGD, largescale randomized controlled trials are needed to confirm efficacy and safety in this patient population. Currently, there are no approved prescription pharmacologic treatments specifically indicated for DED associated with MGD, and those medications approved for the treatment of DED do not target the key driver of the disease (i.e., excessive evaporation). NOV03 (perfluorohexyloctane; under review with the US Food and Drug Administration) is the most advanced emerging therapy for DED associated with MGD and has demonstrated statistically significant improvements in both signs and symptoms in randomized controlled trials. Development of novel pharmacotherapies will improve therapeutic options and allow for a more individualized approach for patients with DED associated with MGD.

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