Scleritis: Immunopathogenesis and molecular basis for therapy

Wakefield, Denis; Girolamo, Nick Di; Thurau, Stephan; Wildner, Gerhild; McCluskey, Peter

doi:10.1016/j.preteyeres.2013.02.004

Cited by 73 publications

(73 citation statements)

References 168 publications

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“…Increased use of combination immunosuppressive therapy and biological agents in patients with severe and refractory ocular inflammatory disease has contributed to modifications in the prognosis of these conditions 1 . Scleral necrosis and melting may occur after pterygium surgery due to the use of adjunctive irradiation (6) and mitomycin C (7) , although the use of these gents reportedly contributes to prolonged inhibition of wound healing.…”

Section: Discussionmentioning

confidence: 99%

“…Scleritis is currently recognized as a heterogeneous group of diseases characterized by inflammation of the sclera, which may be caused by a local or systemic infection, an immune-mediated di sease, or a primary manifestation of an acquired connective tissue disorder or vasculitic disease, often signaling a life-threatening situation (1,2) . Surgically induced necrotizing scleritis (SINS) occurs after ocular surgeries for cataract extraction, trabeculectomy, strabismus, and pterygium retinal detachment (3) .…”

Section: Introductionmentioning

confidence: 99%

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Management of necrotizing scleritis after pterygium surgery with rituximab

Fidelix

Vieira

Trevisani

2016

Arquivos Brasileiros De Oftalmologia

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The authors present a case of necrotizing scleritis after pterygium excision successfully treated with rituximab after attempts with high doses of corticosteroids and immunosuppressive drugs. A literature review revealed case reports and a phase I/II dose-ranging randomized clinical trial using rituximab for necrotizing scleritis with or without association with autoimmune disease. This is the only case report on rituximab treatment for necrotizing scleritis after pterygium surgery. In cases with refractoriness to immunosuppressive drugs, a CD20 antibody can be used.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Management of necrotizing scleritis after pterygium surgery with rituximab

Fidelix

Vieira

Trevisani

2016

Arquivos Brasileiros De Oftalmologia

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“…The genetic constitution may affect the course of the condition; for instance, patients having the HLA-DRB1 phenotype are more likely to develop this complication. 6 The reason why the sclera is possibly more susceptible to an inflammatory reaction than other tissues is that the vascular circulations around the sclera are unique in that both the superficial and deep choroidal arteries are end arteries. Although there are major anastamoses that guarantee a continuous circulation to the front of the eye, the anastamoses superficially are between arteries and hence the arterial circulation is sluggish or even oscillating, leaving time for immune reactions to take place.…”

Section: Discussionmentioning

confidence: 99%

“…2 p 155, Figures 7.2, 7.3, 7.5). 6 What has not been clear is what is triggering the inflammatory response, what is the immune response driven against, and what causes the inflammation to persist. In addition, it has not been certain why, once the immune response has been triggered, the manifestations of the disease are so different in each individual.…”

Section: Immunohistological Changesmentioning

confidence: 99%

“…The presentation, investigation, and treatment of most severe forms of scleral inflammation have been extremely well covered in recently revised texts by Watson et al, 2 Sainz de la Maza et al, 3 the recent review articles by Wieringa et al, 4 by Watson and Young, 5 and the very extensive and thorough review of Wakefield et al, 6 and hence this information will not be reiterated here.…”

Section: Introductionmentioning

confidence: 99%

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The impact of new methods of investigation and treatment on the understanding of the pathology of scleral inflammation

Watson

Romanò

2014

Eye

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Recent advances in the understanding of the initiation and perpetuation of the immune response strongly suggest that all forms of noninfective immunologically induced scleral inflammation have a common origin. Analysis of the progress of patients with scleritis corroborates the current clinical classification that, together with studies of the immunohistology fluoresceine/ICG angiography, 3D proteoglycan, and keratan sulphate electron microscopy of scleritis, strongly suggests that from the initiation of the inflammatory process, necrotizing scleritis and diffuse and nodular scleritis not only pursue a different course but also have a different pathogenesis; nonnecrotizing scleritis being the consequence of an auto immune response, whereas necrotizing scleritis being the complication of an already present (if not always manifest), systemic immune-mediated systemic disease and its associated vasculitis. The increasing imaging capacity of anterior segment ocular coherence tomography (OCT) and en face OCT enables the changes occurring in the sclera during the course of the disease to be observed for the first time. These observations suggest that the inflammatory changes involve the potential suprachoroidal space between choroid and sclera, an observation supported by the presence of subscleral granulomas on histopathology. New imaging techniques have also been able to explain the changes seen in the cornea as a complication of scleritis. These findings have implications for investigation and the treatment of these conditions.

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