Interferon-alpha-associated presumed ocular sarcoidosis

Doycheva, Deshka; Deuter, Christoph; Stuebiger, Nicole; Zierhut, Manfred

doi:10.1007/s00417-008-1002-5

Cited by 52 publications

(32 citation statements)

References 42 publications

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“…Azathioprine, methotrexate, tacrolimus and mycophenolate mofetil are used but based mostly on experience rather than on evidence. Caution must be observed with biological agents, such as anti-TNF agents and interferon-alpha, as sarcoidosis has been reported to develop during treatment with these agents or rheumatic disease [24,25]. Etanercept may induce sarcoid intermediate uveitis [26].…”

Section: Therapeutic Strategymentioning

confidence: 99%

Ocular sarcoidosis

et al. 2012

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Sarcoidosis, a chronic multisystem disease, is a common cause of ocular inflammation. Even though clinical features are well-established, diagnosis requires histological confirmation, which remains difficult in patients with uveitis. Thus, the frequency of ocular sarcoidosis is overestimated. A set of criteria has been recently established in order to improve the diagnostic procedure. New imaging tools will enable the ophthalmologist to evaluate the level of ocular inflammation and to monitor its resolution after treatment initiation. Indocyanine green angiography and optical coherence tomography have dramatically improved our understanding of choroidal granulomas and macular edema. Treatment is based on topical and systemic corticosteroids in most of the cases, but immuno-suppressive agents may be necessary. The visual outcome remains favorable but severe complications, including glaucoma, cystoid macular edema and choroidal neovascularization, may need a prompt and aggressive management.

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Section: Therapeutic Strategymentioning

confidence: 99%

Ocular sarcoidosis

et al. 2012

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“…One hypothesis that has garnered considerable attention involves the inverse and interdependent relationship between TNFα and interferon levels (both α and γ), and the role of increased interferon in the development of autoimmune diseases, 31 including both psoriasis 32 and sarcoidosis. 33,34 Similar changes in the cytokine balance in response to TNFα inhibition have been suggested to elicit auto-antibody and immune complex formation, both of which may have broadly inflammatory effects. 35 Others have suggested that TNFα inhibition may directly or indirectly increase the rate of infection by organisms implicated in noncaseating granuloma formation, such as Propionibacterium acnes and nontuberculous Mycobacterium species.…”

mentioning

confidence: 82%

Drug-induced Inflammation in Patients on TNFα Inhibitors

Cunningham

Pasadhika

Suhler

et al. 2012

Ocular Immunology and Inflammation

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“…53 Other medications can also result in either toxic demyelination or inflammation of the chiasm. Ethambutol has been shown to cause demyelination of the optic nerves, tracts, and chiasm, with the initial lesions showing a predilection for the optic chiasm in primates and rats.…”

Section: Medication Related and Mitochondrial Toxicitymentioning

confidence: 99%

“…Noncaseating granulomatous inflammation has been reported in various organ systems of patients undergoing therapy with interferon and ribavirin for hepatitis C. 53 One cases series demonstrated granulomatous panuveitis in 3 patients undergoing interferon-a therapy for hepatitis C. 53 There is also one case report of interferon and ribavirin therapy causing granulomatous adenohypophysitis in the setting of hepatitis C. 54 The association between these medications, particularly interferon-a, and a sarcoidosis-like disorder, has been reported to occur in several organ systems. 53 Other medications can also result in either toxic demyelination or inflammation of the chiasm.…”

Section: Medication Related and Mitochondrial Toxicitymentioning

confidence: 99%

Visual Findings in Chiasmal Syndromes

Foroozan¹

2016

International Ophthalmology Clinics

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The optic chiasm is an important neuroanatomic landmark, in particular as it relates to the pituitary gland and endocrinologic syndromes. Pathology that affects the chiasm helps emphasize key principles of neuroanatomy. The most common visual consequence of pituitary tumors is chiasmal compression, and visual findings remain important indicators of central nervous system pathology in many patients with sellar/suprasellar lesions.In this review, I have illustrated several different clinical syndromes that ensue from pathology involving the optic chiasm and discussed the various etiologies of chiasmal pathology. In addition, I have provided several examples of the neuroimaging findings that highlight the anatomy and pathology involving the optic chiasm.I hoped to provide a logical basis for the practicing ophthalmologist in approaching chiasmal disorders. ' AnatomyThe intracranial optic nerves exit the optic canals and travel at a 30-to 45-degree angle to make up the optic chiasm. The optic chiasm is 12 to 18 mm in diameter and contains the decussation of nasal retinal nerve fibers from each of the optic nerves. 1 Inferior retinal fibers representing the superior visual field cross first, whereas macular fibers cross more posteriorly. The chiasm lies 10 mm above the sella turcica, which contains the pituitary gland (Fig. 1).The space inferior to the chiasm and above the sella is the basal cistern. Anteriorly, the chiasm is exposed to cerebrospinal fluid; posteriorly it abuts the hypothalamus and the anterior portion of the third ventricle. The anatomic position of the chiasm is described as

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Interferon-alpha-associated presumed ocular sarcoidosis

Abstract: Uveitis can be a sign of sarcoidosis induced by interferon alpha. Further studies are required to support the observation that with early diagnosis the prognosis of uveitis seems to be good.

Cited by 52 publications

References 42 publications

Ocular sarcoidosis

Ocular sarcoidosis

Drug-induced Inflammation in Patients on TNFα Inhibitors

Visual Findings in Chiasmal Syndromes

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