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Tuberous Sclerosis Complex
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Joana Jesus Ribeiro, Filipe Palavra, Flávio Reis
There is a wide range of differential diagnoses of cutaneous lesions, including vitiligo, Alezzandrini syndrome, Vogt−Koyanagi−Harada disease, scleroderma and other autoimmune diseases, Birt−Hogg−Dubé syndrome (BHD), and multiple endocrine neoplasia type 1 (MEN1) [74]. For most TSC patients, no skin biopsy is required; however, it may be appropriate if there is uncertainty regarding the clinical diagnosis, i.e., when angiofibromas are few or later in onset [2,74]. Indeed, multiple facial angiofibromas remain a major feature for diagnosis when their onset occurs in childhood. In the unusual circumstance when angiofibromas have their onset in adulthood, they should be considered as a minor feature and the differential diagnosis expanded to include BHD and MEN1 [2].
Ribavirin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Emily Woolnough, Amanda Wade, Joe Sasadeusz
Vascular ophthalmologic side effects, including subconjunctival hemorrhage and retinopathy, have been noted in patients receiving ribavirin and interferon therapy for HCV infection but are more likely caused by interferon than ribavirin (Andrade et al., 2006). Approximately 35% of 23 HIV–HCV co-infected patients receiving ribavirin and pegylated interferon developed ophthalmologic pathology that was also attributed to the pegylated interferon (Farel et al., 2004). Case reports of Vogt-Koyanagi-Harada disease and unilateral oculomotor nerve palsy while receiving ribavirin and interferon for HCV infection are noted (Nakamura et al., 2005; Papastathopoulos et al., 2006).
Ocular Trauma
Published in Stephen M. Cohn, Matthew O. Dolich, Kenji Inaba, Acute Care Surgery and Trauma, 2016
Jorge A. Montes, Heidi I. Becker, Mark Kelly Green
Sympathetic ophthalmia (SO) is a potentially devastating complication of ocular trauma first described during ancient times and further characterized during the Civil War era. There is the inciting eye, or eye that has been traumatized, and the sympathizing eye. The sympathizing eye is the untraumatized eye that is undergoing an autoimmune inflammatory response by the exposure of ocular antigens by the inciting eye. A bilateral granulomatous panuveitis arises after penetrating injury or surgery to one or both eyes. The majority of cases arise within 3 months of the initial insult with 90% manifesting within 1 year of injury [6]. Modern incidence varies in reports from 0.03/100,000 to 0.2%–0.5% after penetrating injury, a substantial drop from the 16% incidence reported during the Civil War [6]. The decrease in incidence is believed to reflect improved surgical techniques for primary closure of ruptured globes and also is thought to be due to better understanding and recognition of other etiologies of bilateral inflammatory ocular disease such as Vogt–Koyanagi–Harada disease.
Choroidal Detachment following an Intravitreal Injection in a Patient with Vogt-Koyanagi- Harada Disease
Published in Ocular Immunology and Inflammation, 2021
Nitin Kumar, Neeti Rana, Reema Bansal
Vogt-Koyanagi-Harada disease is a T cell-mediated autoimmune response primarily to melanocytes in the choroid. An inflammatory CNVM is a well-known complication of VKH disease and worsens its prognosis. It responds favorably to anti-vascular growth endothelial factor (VEGF) injections. However, recently, an intravitreal injection in a patient with VKH disease and CNVM has been reported to be complicated by rebound inflammation, in a previously quiescent eye.4 The authors postulated that the release of uveal melanocytes into the eye after an intravitreal injection triggered activation of T lymphocytes and induced inflammation.4 Choroid being the primary target of inflammation in VKH disease is vulnerable to a rebound inflammation following an inciting event, such as an intravitreal injection.
Induction of Vogt-Koyanagi-Harada Disease by Interferon-Alpha and Ribavirin Treatment in Patients with Hepatitis C: A Case Report and Review of the Literature
Published in Ocular Immunology and Inflammation, 2019
Jialiang Duan, Yang Wang, Danyan Liu, Jingxue Ma
Interferon-alpha (IFN-α), an antiviral and immunomodulatory agent, has been the mainstay in the treatment of hepatitis C during the past decades. IFN-α treatment can trigger some ocular complications and systemic autoimmune diseases, such as autoimmune thyroid disease, autoimmune hepatitis, and type 1 diabetes.1 The most frequent ocular complication is interferon-associated retinopathy, which is characterized by cotton-wool spots and retinal haemorrhages.2 However, IFN-α-induced autoimmune ocular disease is infrequent. Vogt-Koyanagi-Harada disease (VKH) is a multisystem autoimmune disease associated with ocular, neurological, auditory, and integumentary manifestations.3 Here, a patient presenting with VKH after IFN-α and ribavirin therapy for hepatitis C is described. In addition, a review of the relevant literature for VKH associated with IFN-α treatment is presented.
Unilateral Ocular Manifestations of Vogt–Koyanagi–Harada Disease
Published in Ocular Immunology and Inflammation, 2018
Edmund Tsui, Alexander Bottini, Quraish Ghadiali, Chandrakumar Balaratnasingam, Irene Barbazetto
We present an atypical unilateral clinical variant of VKH disease. Traditional diagnostic criteria have been defined in 2001 at the International Workshop on Vogt–Koyanagi–Harada disease.1 This workshop reported five criteria necessary for complete VKH disease including no history of penetrating ocular trauma, no other evidence of other ocular disease, bilateral ocular involvement, neurological/auditory findings, and integumentary findings. Although bilateral ocular involvement has been deemed necessary for diagnosis by these criteria, unilateral involvement has also been recognized.1 It is important to consider other causes of posterior uveitis, such as sympathetic ophthalmia, posterior scleritis, sarcoidosis, uveal effusion syndrome, syphilitic uveitis, tuberculosis uveitis, and intraocular lymphoma.1 In our case, the ocular and angiographic findings, headache, decreased hearing, and significant improvement with systemic corticosteroids were consistent with VKH disease. Additionally, all other laboratory testing was negative, excluding other potential causes of disease.