Bromfenac-induced neurotrophic keratitis in a corneal graft

Raj, Nimmy; Panigrahi, Arnav; Alam, Mahboob; Gupta, Vivek

doi:10.1136/bcr-2022-249400

Cited by 6 publications

(4 citation statements)

References 18 publications

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“…In addition, topical therapy with steroidal and non-steroidal anti-inflammatory drugs produces the phenomenon of corneal melting, favoured by corneal anaesthesia or hypoesthesia [ 3 - 6 ]. The literature reports patients with neurotrophic keratitis induced by topical treatment with steroidal or non-steroidal anti-inflammatory drugs [ 6 , 7 ].…”

Section: Discussionmentioning

confidence: 99%

Corneal perforation after corneal foreign body - Case Report

Macarie

Vlad

Macarie³

2023

rjo

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Section: Discussionmentioning

confidence: 99%

Corneal perforation after corneal foreign body - Case Report

Macarie

Vlad

Macarie³

2023

rjo

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“…Therefore, NSAIDs may be combined with other treatments, such as corticosteroids or anti-VEGF agents [44]. Nevertheless, NSAIDs should be used with caution as they can cause corneal ulceration and melting [45] and neurotrophic keratitis [46]. Bromfenac sodium (0.09%) ophthalmic solution is a clinically useful topical NSAID.…”

Section: Nsaidsmentioning

confidence: 99%

Available Therapeutic Options for Corneal Neovascularization: A Review

Drzyzga,

Śpiewak,

Dorecka

et al. 2024

IJMS

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Corneal neovascularization can impair vision and result in a poor quality of life. The pathogenesis involves a complex interplay of angiogenic factors, notably vascular endothelial growth factor (VEGF). This review provides a comprehensive overview of potential therapies for corneal neovascularization, covering tissue inhibitors of metalloproteinases (TIMPs), transforming growth factor beta (TGF-β) inhibitors, interleukin-1L receptor antagonist (IL-1 Ra), nitric oxide synthase (NOS) isoforms, galectin-3 inhibitors, retinal pigment epithelium-derived factor (PEDF), platelet-derived growth factor (PDGF) receptor inhibitors, and surgical treatments. Conventional treatments include anti-VEGF therapy and laser interventions, while emerging therapies such as immunosuppressive drugs (cyclosporine and rapamycin) have been explored. Losartan and decorin are potential antifibrotic agents that mitigate TGF-β-induced fibrosis. Ocular nanosystems are innovative drug-delivery platforms that facilitate the targeted release of therapeutic agents. Gene therapies, such as small interfering RNA and antisense oligonucleotides, are promising approaches for selectively inhibiting angiogenesis-related gene expression. Aganirsen is efficacious in reducing the corneal neovascularization area without significant adverse effects. These multifaceted approaches underscore the corneal neovascularization management complexity and highlight ideas for enhancing therapeutic outcomes. Furthermore, the importance of combination therapies and the need for further research to develop specific inhibitors while considering their therapeutic efficacy and potential adverse effects are discussed.

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“…However, the effectiveness of NSAIDs in treating corneal neovascularization can vary, and their use does not always lead to complete regression of abnormal blood vessels. Non-steroidal anti-inflammatory drugs (NSAIDs) should be used with caution, as they can cause corneal ulceration and melting [18] and neurotrophic keratitis [19].…”

Section: Nonsteroidal Anti-inflammatory Drugs (Nsaids)mentioning

confidence: 99%

Update on Therapeutic Approaches to Corneal Neovascularisation

Drzyzga,

Śpiewak,

Wyględowska-Promieńska

2023

Preprint

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A healthy cornea is a nonvascularized, transparent tissue. It is nourished by diffusion through the tear film, aqueous fluid and neurotrophins supplied by the corneal innervation. The cornea is devoid of both blood and lymphatic vessels, which makes it an immunologi-cally privileged tissue. Corneal neovascularization develops due to an imbalance between angiogenic and anti-angiogenic factors and can lead to a significant decrease in visual acui-ty. It may cause scarring, lipid keratopathy, and corneal edema. The resulting pathological vascularization of the cornea reduces its immune privilege and significantly worsens the prognosis after subsequent penetrating keratoplasty, increasing the risk of rejection of the transplanted flap. Neovascularization is favored by many disease processes, including auto-immune diseases, viral inflammations, mainly herpes and varicella-zoster, and blepharitis [1]. There are several options to treat corneal neovascularization, both pharmacological and surgical. Angiostatic treatment involves inhibiting the growth of new vessels by suppressing inflammatory responses. VEGF inhibitors, steroids, cyclosporine A, and amniotic membrane grafts secured to the cornea work this way. VEGF inhibitors are the agents with the direct and most potent angiostatic effect. Angioregressive treatment, on the other hand, results in the regression of already existing pathological vessels. This therapy is also based on VEGF inhibitors, which, however, have the most potent effect on newly formed and small vessels but are less effective in reducing large-caliber and mature vessels. A more effective method for such vessels is ablation, which involves surgical closure. The most commonly used an-gio-occlusive method is needle diathermy and argon or yellow laser therapy. In advanced corneal neovascularization, corneal transplant surgery may be necessary. It is best performed after pretreatment with anti-VEGF preparations, often continued after corneal transplanta-tion to reduce the risk of transplant rejection [2]. This paper discusses the pathogenesis of corneal neovascularization and the current and future trends in its treatment.

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Bromfenac-induced neurotrophic keratitis in a corneal graft

Cited by 6 publications

References 18 publications

Corneal perforation after corneal foreign body - Case Report

Corneal perforation after corneal foreign body - Case Report

Available Therapeutic Options for Corneal Neovascularization: A Review

Update on Therapeutic Approaches to Corneal Neovascularisation

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