Riboflavin and Ultraviolet Light A Therapy as an Adjuvant Treatment for Medically Refractive Acanthamoeba Keratitis

Khan, Yasín A.; Kashiwabuchi, Renata T.; Martins, Suy Anne Rebouças; Castro-Combs, Juan; Kalyani, S; Stanley, Philip M.; Flikier, David; Behrens, Ashley

doi:10.1016/j.ophtha.2010.06.041

Cited by 129 publications

(95 citation statements)

References 42 publications

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“…Recently, photorefractive surgery seems to be a very promising modality and have been used in four cases of early stage Acanthamoeba keratitis, where the patients developed large corneal abscesses in the upper third thickness of stroma [85]. Another relatively new approach is collagen cross-linking which has shown promising results in clinically [48,92,126]. It is presumed that collagen probably prevents further tissue damage and prevents reproduction of amoebae and hence the patients showed rapid reduction in ocular symptoms and ulcer size.…”

Section: Treatmentmentioning

confidence: 99%

Pathogenesis of microbial keratitis

Lakhundi

Siddiqui

Khan

2017

Microbial Pathogenesis

167

121

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Microbial keratitis is a sight-threatening ocular infection caused by bacteria, fungi, and protist pathogens. Epithelial defects and injuries are key predisposing factors making the eye susceptible to corneal pathogens. Among bacterial pathogens, the most common agents responsible for keratitis include Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus pneumonia and Serratia species. Fungal agents of corneal infections include both filamentous as well as yeast, including Fusarium, Aspergillus, Phaeohyphomycetes, Curvularia, Paecilomyces, Scedosporium and Candida species, while in protists, Acanthamoeba spp. are responsible for causing ocular disease. Clinical features include redness, pain, tearing, blur vision and inflammation but symptoms vary depending on the causative agent. The underlying molecular mechanisms associated with microbial pathogenesis include virulence factors as well as the host factors that aid in the progression of keratitis, resulting in damage to the ocular tissue. The treatment therefore should focus not only on the elimination of the culprit but also on the neutralization of virulence factors to minimize the damage, in addition to repairing the damaged tissue. A complete understanding of the pathogenesis of microbial keratitis will lead to the rational development of therapeutic interventions. This is a timely review of our current understanding of the advances made in this field in a comprehensible manner. Coupled with the recently available genome sequence information and high throughput genomics technology, and the availability of innovative approaches, this will stimulate interest in this field.

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Section: Treatmentmentioning

confidence: 99%

Pathogenesis of microbial keratitis

Lakhundi

Siddiqui

Khan

2017

Microbial Pathogenesis

167

121

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“…Recently, scientists have examined treatment with riboflavin and ultraviolet A light (UVA) in cases of severe infectious keratitis [140,[148][149][150][151]. The mechanism by which this process is thought to work is via collagen crosslinking.…”

Section: Infectious Keratitismentioning

confidence: 99%

“…All of the eyes responded to the photochemical treatment with improvement of symptoms and reduced signs of inflammation; epithelial healing was achieved in all cases and only two required antibiotic administration, one requiring an amniotic membrane transplant [152]. The adjunctive use of UVA and B2 therapy seems to be a possible alternative for medication-resistant Acanthamoeba keratitis (AK) [151]. Treatment of AK is noticeably challenging and is faced with difficulties such as long and intensive regimens, resistance to medication, adverse effects from the medications, and reinfection after surgical management.…”

Section: Infectious Keratitismentioning

confidence: 99%

The Role of Ultraviolet Radiation in the Ocular System of Mammals

et al. 2014

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Abstract:With decreasing levels of ozone in the atmosphere, we are being exposed to higher levels of ultraviolet radiation (UVR) than ever before. UVR carries higher energy than visible light, and its effects on tissues include DNA damage, gene mutations, immunosuppression, oxidative stress and inflammatory responses. In the eye, UVR is strongly associated with the development of basal and squamous cell carcinoma of the eyelid, pterygium, photokeratitis, climatic droplet keratopathy, ocular surface squamous neoplasia, cataracts, and uveal melanoma, and is weakly associated with age-related macular degeneration. Despite overwhelming evidence regarding the deleterious effects on UVR, public health measures to encourage UV protection of the eyes is generally lacking. Options for photoprotection include sunglasses, wide brim hats, windshields, plastic films for side windows in cars, UV blocking contact lenses, and following the UV Index report daily. The American National Standards Institute currently has regulations regarding properties of UV blocking sunglasses; however, compliance in the US is not mandatory. On the other hand, UVR does have therapeutic applications in the eye, particularly, riboflavin activated by ultraviolet A light (UVA) radiation is used clinically to slow the progression of keratoconus, post-LASIK keratectasia, and bullous keratopathy by crosslinking corneal collagen fibers. OPEN ACCESSPhotonics 2014, 1 348 Additionally, riboflavin activated by UVA has been shown to have antibacterial, antiviral, and antiparasitic effects. This is clinically relevant in the treatment of infectious keratitis. Finally, exposure to low levels of light in the UV spectrum has been found to regulate the growth of the eye and lack of adequate exposure may increase the risk of development and progression of myopia.

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“…Egy korábbi tanulmányban Khan szintén a szaruhártyahám hiány gyógyulásáról számolt be crosslinking kezelést követően, terápiarezisztens Acanthamoebakeratitisben [24]. Al-Sabai a szaruhártya beolvadásában tapasztalta a gyulladásos jelek megszűnését és a szaruhártya behámo sodását [25], valamint Tóth és mtsai Boston keratoproté zis körüli szaruhártyabeolvadás sikeres crosslinking ke zeléséről számoltak be [26].…”

Section: Megbeszélésunclassified

Crosslinking kezelés hatása a szaruhártya hámosodására

et al. 2017

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Bevezetés és célkitűzés:A crosslinking kezelés szaruhártyahámosodásra gyakorolt hatásának vizsgálata. Betegek és mód-szer: Vizsgálatunkba 39 keratoconusos beteget vontunk be crosslinking kezelés után, és 11 pácienst fotorefraktív keratectomiát követően (kontroll) crosslinking kezelést követően 21, 45 és 69 órával. A festődő szaruhártyahámhi ány területét a fotorefraktív keratectomiát követően 16, 37 és 61 órával meghatároztuk. A fotorefraktív keratectomia kezelések utáni kontrollok időpontja nem egyezett a crosslinking kezelést követő kontrollidőpontokkal, így a fotoref raktív keratectomiás csoportnál a hámhiány feltehető méretét a crosslinking kezelési csoport mérési időpontjaira számítottuk, és χ 2 teszt segítségével hasonlítottuk össze a két csoportban a hámhiány méretét. Eredmények: A cornea crosslinking kezelést követően a szaruhártya hámjának záródása a kezeléstől számított három napon belül, fotorefrak tív keratectomiát követően négy napon belül következett be. 45 és 69 óra elteltével a két csoport között szignifikáns különbség igazolódott a hámhiány méretében (p = 0,005 és p<0,001). Következtetés: A crosslinking kezelést követő en a szaruhártya hámosodása gyorsabb, mint fotorefraktív keratectomiát követően. Vizsgálatunk a crosslinking keze lés hámgyógyulásra kifejtett kedvező hatását igazolta. Orv. Hetil., 2017, 158(10), 376-379. Kulcsszavak: crosslinking, fotorefraktív keratectomia, hámgyógyulás Impact of crosslinking on corneal epithelial healingIntroduction and aim: To analyse the effect of crosslinking (CXL) on corneal epithelial healing. Patients and method: 39 keratoconus patients following CXL and 11 patients following PRK were enrolled in this study. 21, 45 and 69 hours after CXL and 16, 37 and 61 hours following PRK slitlamp photographs were taken using fluorescein staining and the size of the epithelial defect and the time of epithelial closure was determined. As the observation timepoints differed in both groups, the size of the epithelial defect following PRK was calculated for the time points used for analysis of CXL patients. These data were compared using chiquadrat test. Results: Following crosslinking, epithe lial closure occured within 3, following PRK within 4 days. In the area of epithelial erosion 45 and 69 hours after CXL or PRK treatment statistically significant difference (p = 0.005 and p<0.001) was verified. Conclusion: Our re sults show beneficial effect of crosslinking on corneal epithelial healing.

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Riboflavin and Ultraviolet Light A Therapy as an Adjuvant Treatment for Medically Refractive Acanthamoeba Keratitis

Cited by 129 publications

References 42 publications

Pathogenesis of microbial keratitis

Pathogenesis of microbial keratitis

The Role of Ultraviolet Radiation in the Ocular System of Mammals

Crosslinking kezelés hatása a szaruhártya hámosodására

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