Rituximab Therapy for Refractory Scleritis

Suhler, Eric B.; Lim, Lyndell L; Beardsley, Robert S.; Giles, Tracy; Pasadhika, Sirichai; Lee, Shelly T.; Sardos, Alexandre de Saint; Butler, Nicholas J.; Smith, Justine R.; Rosenbaum, James T.

doi:10.1016/j.ophtha.2014.04.044

Cited by 79 publications

(22 citation statements)

References 22 publications

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“…7 The mechanism by which rituximab causes macular edema is unclear, but interestingly, acute exacerbations in scleritis and idiopathic orbital inflammation shortly after rituximab administration have also been reported. 8, 9 …”

Section: Discussionmentioning

confidence: 99%

Waldenström's Macroglobulinemia Masquerading as Birdshot Chorioretinopathy

Kim

Jaworski

Patel‐Donnelly

et al. 2017

RETINAL Cases &Amp; Brief Reports

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Purpose To describe Waldenström’s macroglobulinemia (WM) as a masquerade syndrome. Method Case report. Results A 59-year-old human leukocyte antigen (HLA)-A29-negative Caucasian male presented with a seven-year history of floaters, progressive vision loss, and poor contrast sensitivity along with choroidal lesions suggestive of birdshot chorioretinopathy (BCR). Fluorescein angiography, fundus autofluorescence, and indocyanine green angiography showed multiple areas of hyperfluorescence and hypofluorescence. Electroretinography showed reduced cone and rod responses. Comprehensive work-up for infectious, paraneoplastic, and other causes including sarcoidosis was negative at the time. The patient was treated with multiple immunomodulatory agents without any significant improvement. Two years after initial presentation, the patient developed normocytic anemia and high levels of inflammatory markers. Further work-up yielded a diagnosis of WM. His choroidal lesions were significantly reduced after treatment with rituximab and bendamustine. Conclusion We report a case of WM masquerading as BCR. Other indolent diseases should be considered in the differential diagnosis for HLA-A29-negative patients presenting with birdshot-like lesions, especially if they are clinically unresponsive to multiple systemic immunosuppressive agents.

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Section: Discussionmentioning

confidence: 99%

Waldenström's Macroglobulinemia Masquerading as Birdshot Chorioretinopathy

Kim

Jaworski

Patel‐Donnelly

et al. 2017

RETINAL Cases &Amp; Brief Reports

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“… 47 Preliminary results indicate that rituximab may be an effective treatment for non-infectious refractory scleritis, but conversely there is no case of scleritis induced by this agent. 48 …”

Section: ‘Borderline’ Paesmentioning

confidence: 99%

Paradoxical reactions under TNF-α blocking agents and other biological agents given for chronic immune-mediated diseases: an analytical and comprehensive overview

2016

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Paradoxical adverse events (PAEs) have been reported during biological treatment for chronic immune-mediated diseases. PAEs are defined as the occurrence during biological agent therapy of a pathological condition that usually responds to this class of drug. A wide range of PAEs have been reported including dermatological, intestinal and ophthalmic conditions, mainly with antitumour necrosis factor α (TNF-α) agents. True PAEs include psoriasis, Crohn's disease and hidradenitis suppurativa. Other PAEs may be qualified as borderline and include uveitis, scleritis, sarcoidosis and other granulomatous diseases (granuloma annulare, interstitial granulomatous dermatitis), vasculitis, vitiligo and alopecia areata. Proposed hypotheses to explain these PAEs include an imbalance in cytokine production, the differential immunological properties between the monoclonal antibodies and TNF-α soluble receptor, an unopposed type I interferon production and a shift towards a Th1/Th2 profile. Data from registries suggest that the risk for paradoxical psoriasis is low and non-significant. We discuss management of these PAEs, which depends on the type and severity of the adverse events, pre-existing treated conditions and the possibility of alternative therapeutic options for the underlying disease. Paradoxical adverse events are not restricted to anti-TNF-α agents and close surveillance of new available biological drugs (anti-interleukin-17/23, anti-integrin) is warranted in order to detect the occurrence of new or as yet undescribed events.

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“…Our group reported successful treatment of recalcitrant scleritis with rituximab in 75% of patients; however, partly due to rarity, none of those patients had scleritis secondary to sarcoidosis. 112 In one case report, thalidomide was successfully used to treat cutaneous sarcoidosis and nodular scleritis in a patient who failed azathioprine and corticosteroid therapy. 113 Thalidomide is considered a sedative, hypnotic agent, but also has anti-inflammatory activity.…”

Section: Treatment Of Ocular Sarcoidosismentioning

confidence: 99%

Ocular Sarcoidosis

Pasadhika

Rosenbaum

2015

Clinics in Chest Medicine

Self Cite

215

185

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Sarcoidosis is one of the leading causes of inflammatory eye disease. Ocular sarcoidosis can involve any part of the eye and its adnexal tissues, and may cause uveitis, episcleritis/scleritis, eyelid abnormalities, conjunctival granuloma, optic neuropathy, lacrimal gland enlargement and orbital inflammation. Glaucoma and cataract can be complications from inflammation itself or adverse effects from therapy. Ophthalmic manifestations can be isolated, or associated with other organ involvement. Patients with ocular sarcoidosis can present with a wide range of clinical presentations and severity. Multi-disciplinary approaches are required to achieve the best treatment outcomes for both ocular and systemic manifestations.

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Rituximab Therapy for Refractory Scleritis

Cited by 79 publications

References 22 publications

Waldenström's Macroglobulinemia Masquerading as Birdshot Chorioretinopathy

Waldenström's Macroglobulinemia Masquerading as Birdshot Chorioretinopathy

Paradoxical reactions under TNF-α blocking agents and other biological agents given for chronic immune-mediated diseases: an analytical and comprehensive overview

Ocular Sarcoidosis

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