Clofazimine-induced premaculopathy in a vitiliginous patient

Kasturi, Nirupama; Srinivasan, Renuka

doi:10.4103/0976-500x.189685

Cited by 8 publications

(7 citation statements)

References 4 publications

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“…Increasing melanisation of melanocytes eventually results in cellular disruption of these pigment-bearing cells. 9 The possible pathophysiological mechanism of RPE-photoreceptor degeneration in our case could also be the methoxsaleninduced melanisation of RPE followed by cellular rupture. The presentation in previously reported case could be an earlier stage of methoxsalen-induced RPE toxicity, representing the pre-disruptive stage.…”

Section: Discussionmentioning

confidence: 65%

Methoxsalen-induced advanced bull’s eye maculopathy

Ranjan

Manayath

Salian

et al. 2020

European Journal of Ophthalmology

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A number of systemic medications are known to cause macular toxicity, and bull’s eye maculopathy is caused by some of them like hydroxychloroquine and clofazimine. A 55-year-old female, known case of vitiligo with history of undergoing methoxsalen–ultraviolet A therapy, presented with painless defective vision in both eyes. Fundus examination and autofluorescence showed macular degeneration with bull’s eye configuration. Optical coherence tomography showed perifoveal loss of photoreceptors and outer retinal thinning with foveal sparing appearing as ‘flying saucer’. Multifocal electroretinogram showed pan-macular suppression of waveforms. Patient was diagnosed as case of methoxsalen-induced advanced macular toxicity. This is the first reported case of methoxsalen-induced advanced bull’s eye maculopathy.

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Section: Discussionmentioning

confidence: 65%

Methoxsalen-induced advanced bull’s eye maculopathy

Ranjan

Manayath

Salian

et al. 2020

European Journal of Ophthalmology

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“…Çoklu ilaca dirençli tüberküloz ve lepramatöz lepra tedavisinde, Mycobacterium avium kompleksi(MAC) ile enfekte olmuş edinsel immün yetmezlik sendromu (AİDS) gibi mikrobiyal hastalıklarda ve diskoid lupus eritematozus gibi çeşitli kutanöz hastalıkların tedavisinde kullanılmaktadır. [1,2,3,4] Klofaziminin antimikobakteriyel etkinliği esasen iki farklı mekanizmayla ilişkilendirilmiştir. Birincisi reaktif oksijen türevlerinin üretilmesini sağlayan hücre içi redoks döngüsü üzerinden gerçekleşirken ikincisi mikobakterilerin membran yapısını bozarak çeşitli iyonların taşınmasını ve bakteri tarafından ATP üretiminin engellenmesidir.…”

Section: Klofaziminunclassified

“…Bu etkisi sayesinde vitiligo, diskoid lupus gibi pigmenter bozukluklarla seyreden hastalıkların tedavisinde kullanılmaktadır. [3] Klofazimin asıl dapson duyarlı/dirençli lepra tedavisi için endikasyon almıştır ve kullanım dozu; erişkinde başlangıçta 100 mg/ gün dozunda 2-3 yıl diğer ilaçlarla kombine olarak kullanılıp yine aynı dozda monoterapi idame şeklindedir. Aynı endikasyon için önerilen pediatrik doz 1 mg/kg/gün (max 100 mg) şeklindedir.…”

Section: Klofaziminunclassified

“…Tedavinin kesilmesinden 3 ay sonra ise bulgularda iyileşme görülmüştür. [3] Nadir de olsa klofazimin kullanımı fotoreseptör ve RPE hasarı yaparak makulopatiye sebep olabilmektedir. Oftalmologlar bu durumu akılda tutmalıdır ve ilgili birimle iletişime geçerek mevcut tedavinin kesilmesi ve alternatif tedaviye geçilmesi ile olası yan etkilerin ilerlemesi engellenebilir.…”

Section: Klofaziminunclassified

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Medications Damaging Retinal Pigment Epithelium and Photoreceptor Complex-3: Pathogenesis, Diagnosis and Treatment (Clofazimine, Deferoxamine, Vitamin A Deficiency and Celiac Disease, Digoxin)

2023

Güncel Retina (Current Retina)

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Toxic retinopathies are a variety of conditions resulting from retinal damage caused by systemically administered drugs. Although relatively rare, these conditions should be considered, especially when features of unusual retinopathy or maculopathy such as bilateral pigmentary disorder or retinal crystal deposition are present. It has been observed that some drugs damage the RPE and photoreceptor layer. Of these drugs, clofazimine; can be used in the treatment of tuberculosis, leprosy, and various cutaneous diseases, but it can cause color vision defects and bulls-eye maculopathy in a dose-dependent manner. Lesions detectable by various imaging methods have been described as associated with the use of deferoxamine mesylate, which is used as an iron-chelating agent. In vitamin A deficiency characterized by xerophthalmia symptoms, drusenoid deposits have been observed in the photoreceptor outer segment, in which rod function defects are prominent. In the use of digoxin, which has a very narrow therapeutic range, photoreceptor dysfunctions, which are manifested by deterioration in color perception, may develop. Most ocular side effects associated with systemic drug use are reversible after discontinuation of therapy if detected early. However, toxic effects can progress if undetected and cause retinal dysfunction associated with potentially irreversible vision loss.

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“…Often, ocular manifestations of patients on drug therapies may be confusing due to other comorbidities in the patient, which may lead the ophthalmologist to suspect infections and inflammatory pathologies leading to UME and maculopathy rather than toxicity due to the drug. 73,74 Various drugs including antimalarial chloroquine and hydroxychloroquine, 75 topiramate, 76 tacrolimus, 77 antiviral agents such as ritonavir, 78 tamoxifen, 79 clofazimine, 80 sertraline, 81 deferoxamine, 82 clomiphene, 83 paclitaxel, 84 BRAF inhibitors such as Vemurafenib (used in melanomas), 85,86 and recently, antibiotics such as linezolid 74 have been implicated in the development of maculopathy. Maculopathies due to these agents can present with intraretinal cystoid spaces or SRF accumulation (except chloroquine, hydroxychloroquine, and ritonavir).…”

Section: Drug-induced Maculopathiesmentioning

confidence: 99%

Disease of the Year: Differential Diagnosis of Uveitic Macular Edema

Agarwal

Pichi

Invernizzi

et al. 2018

Ocular Immunology and Inflammation

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Uveitic cystoid macular edema (UME) is an important cause of visual morbidity among patients with both infectious and non-infectious uveitis. UME may be associated in more than 30% cases of active uveitis. However, even patients with minimal features of intraocular inflammation may develop recurrent or chronic UME. Therefore, the evaluation and management of UME in patients with uveitis may be challenging. A number of vitreoretinal pathologies may result in UME and accumulation of fluid in the intra-or subretinal space. These need to be carefully distinguished from each other so that appropriate management can be initiated. All types of uveitis, including anterior uveitis (where the primary site of inflammation is not in the posterior segment) can present with UME. Other conditions such as diabetes, and surgery, can present with macular edema. This index review highlights various differential diagnoses of UME and provides illustrative case examples with multimodal imaging evaluation.

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Clofazimine-induced premaculopathy in a vitiliginous patient

Cited by 8 publications

References 4 publications

Methoxsalen-induced advanced bull’s eye maculopathy

Methoxsalen-induced advanced bull’s eye maculopathy

Medications Damaging Retinal Pigment Epithelium and Photoreceptor Complex-3: Pathogenesis, Diagnosis and Treatment (Clofazimine, Deferoxamine, Vitamin A Deficiency and Celiac Disease, Digoxin)

Disease of the Year: Differential Diagnosis of Uveitic Macular Edema

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