Necrosis epidérmica tóxica por colirio de dorzolamida

Asensio-Sánchez, V.M.

doi:10.4321/s0212-71992008000100015

Cited by 4 publications

(5 citation statements)

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“…Regarding carbonic anhydrase inhibitor eye drops, the reported psoriasis and lichenoid eruption cases appear chronologically relevant, with positive rechallenge, but the mechanism is unknown, and only one case involving systemic acetazolamide has been reported in the literature 134 . However, it is worth noting that among the few generalized eruptions reported in association with anti‐glaucoma eye drops, two cases of erythema multiforme 122,123 and two cases of toxic epidermal necrolysis 120,121 had dorzolamide eye drops in common. Although scarce, these data invite us to consider nonsystemic drugs in severe cutaneous adverse reactions.…”

Section: Discussionmentioning

confidence: 99%

Section: Distant Cutaneous Aes Secondary To Anti‐glaucoma Eye Dropsmentioning

confidence: 99%

“…Toxic epidermal necrolysis possibly induced by anti‐glaucoma eye drops was reported in two cases 120,121 . Both patients recovered after eye drop discontinuation 120,121 Moreover, Shelley et al . described the case of a male who experienced alopecia and erythroderma three years after timolol eye drop initiation.…”

Section: Distant Cutaneous Aes Secondary To Anti‐glaucoma Eye Dropsmentioning

confidence: 99%

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Dermatological adverse effects of anti‐glaucoma eye drops: a review

Patchinsky

Petitpain²,

Gillet

et al. 2022

Acad Dermatol Venereol

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Many patients are treated for glaucoma. Like other drugs, anti-glaucoma eye drops may induce dermatological adverse effects. We aim to review the dermatological adverse effects secondary to the active agents in anti-glaucoma eye drops through a literature review. In January 2020, we queried PubMed using the following MeSH terms: glaucoma/drug therapy or glaucoma, open angle/drug therapy cross-referenced with parasympathomimetics/adverse effects or adrenergic agonists/adverse effects or carbonic anhydrase inhibitors/adverse effects or prostaglandins F, synthetic/adverse effects or adrenergic beta antagonists/adverse effects or ophthalmic solutions/adverse effects. The initial search identified 1128 studies, of which 49 were excluded for being in a foreign language, 15 for not involving eye drops, 968 for not focusing on adverse dermatological effects, and 11 for insufficient documentation or redundancy. After adding 38 linked studies, we finally analyzed 123 studies. The ocular and periocular dermatological adverse effects of eye drops are contact dermatitis, hyperpigmentation, prostaglandin analog periorbitopathy, mucous membrane pemphigoid, eyelash depigmentation, skin hypertrichosis, and rare cases of melanoma and skin depigmentation. The reported distant dermatological adverse effects are psoriasis, excessive sweating, lichen planus, alopecia, toxic epidermal necrolysis, erythema multiforme, erythroderma, subacute cutaneous lupus erythematosus, nail pigmentation, and bullous pemphigoid. Most of the cutaneous adverse effects of anti-glaucoma eye drops are ocular and periocular and induced by prostaglandin analogs.Distant adverse effects are rare and sometimes questionable but should be kept in mind, especially mucous membrane pemphigoid, which could lead to blindness. The role of preservatives, such as benzalkonium chloride, should also be considered.

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Section: Discussionmentioning

confidence: 99%

Section: Distant Cutaneous Aes Secondary To Anti‐glaucoma Eye Dropsmentioning

confidence: 99%

Section: Distant Cutaneous Aes Secondary To Anti‐glaucoma Eye Dropsmentioning

confidence: 99%

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Dermatological adverse effects of anti‐glaucoma eye drops: a review

Patchinsky

Petitpain²,

Gillet

et al. 2022

Acad Dermatol Venereol

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“…In principle, the severity of SJS and TEN does not allow re-challenge and intradermal testing with the culprit drugs due to the feared risk of re-inducing a second episode of SJS/TEN, although two case reports describe intradermal testing without triggering of a second episode of TEN [102,103]. Induction of SJS/TEN has, however, been documented following local eye treatment [104,105]. …”

Section: Management and Therapymentioning

confidence: 99%

Toxic epidermal necrolysis and Stevens-Johnson syndrome

Harr

French

2010

Orphanet J Rare Dis

512

556

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Toxic epidermal necrolysis (TEN) and Stevens Johnson Syndrome (SJS) are severe adverse cutaneous drug reactions that predominantly involve the skin and mucous membranes. Both are rare, with TEN and SJS affecting approximately 1or 2/1,000,000 annually, and are considered medical emergencies as they are potentially fatal. They are characterized by mucocutaneous tenderness and typically hemorrhagic erosions, erythema and more or less severe epidermal detachment presenting as blisters and areas of denuded skin. Currently, TEN and SJS are considered to be two ends of a spectrum of severe epidermolytic adverse cutaneous drug reactions, differing only by their extent of skin detachment. Drugs are assumed or identified as the main cause of SJS/TEN in most cases, but Mycoplasma pneumoniae and Herpes simplex virus infections are well documented causes alongside rare cases in which the aetiology remains unknown. Several drugs are at "high" risk of inducing TEN/SJS including: Allopurinol, Trimethoprim-sulfamethoxazole and other sulfonamide-antibiotics, aminopenicillins, cephalosporins, quinolones, carbamazepine, phenytoin, phenobarbital and NSAID's of the oxicam-type. Genetic susceptibility to SJS and TEN is likely as exemplified by the strong association observed in Han Chinese between a genetic marker, the human leukocyte antigen HLA-B*1502, and SJS induced by carbamazepine. Diagnosis relies mainly on clinical signs together with the histological analysis of a skin biopsy showing typical full-thickness epidermal necrolysis due to extensive keratinocyte apoptosis. Differential diagnosis includes linear IgA dermatosis and paraneoplastic pemphigus, pemphigus vulgaris and bullous pemphigoid, acute generalized exanthematous pustulosis (AGEP), disseminated fixed bullous drug eruption and staphyloccocal scalded skin syndrome (SSSS). Due to the high risk of mortality, management of patients with SJS/TEN requires rapid diagnosis, evaluation of the prognosis using SCORTEN, identification and interruption of the culprit drug, specialized supportive care ideally in an intensive care unit, and consideration of immunomodulating agents such as high-dose intravenous immunoglobulin therapy. SJS and TEN are severe and life-threatening. The average reported mortality rate of SJS is 1-5%, and of TEN is 25-35%; it can be even higher in elderly patients and those with a large surface area of epidermal detachment. More than 50% of patients surviving TEN suffer from long-term sequelae of the disease.

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“…The intensity of SJS and TEN forbids rechallenge and subcutaneous screening with the offending medications because of the perceived danger of doing so, despite the fact that two case reports have recorded intradermal testing without causing a second episode of TEN [89]. However, after local ocular therapy, induction of SJS/TEN has been described [90]. Patch-testing is an experimental approach; however, it is not currently a common diagnostic method.…”

Section: Allergological Testingmentioning

confidence: 99%

Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis- An Overview

Garg¹

2022

Preprint

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Both Stevens Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN) are main injurious cutaneous medication reactions that mostly affect the epidermis and mucus membranes. TEN and SJS affecting nearly 1 or 2/1,000,000 people per year, and can recognized as medical crises since they may be deadly. Mucocutaneous discomfort, hemorrhagic erosions, erythema, and more or less severe epidermal separation that appear as ulcer and patches of dermic loss are their defining characteristics. The sole difference between TEN and SJS at this time is the degree of skin detachment, making them two extremes of a spectrum of severe cutaneous adverse drug reactions (cADRs). In the majority of cases, drugs are considered as the principal reason of SJS/TEN, but herpes simplex virus and Mycoplasma pneumoniae infections are also recognized causes, along with lesser number of cases in which the cause is still unknown. Among the drugs with a "high" likelihood of producing TEN/SJS are carbamazepine (CBZ), trimethoprim-sulfamethoxazole, phenytoin, aminopenicillins, allopurinol, cephalosporins, other sulfonamide antibiotics, quinolones, phenobarbital, and NSAIDs of the oxicam variety. There is strong genetic evidence for SJS and TEN in Han Chinese due to the substantial association between the human leukocyte antigen (HLA-B*1502) and SJS brought on by CBZ. The diagnosis is made mostly based on clinical symptoms and the histological study of a dermal biopsy. Pemphigus vulgaris, bullous pemphigoid, linear IgA dermatosis, paraneoplastic pemphigus, disseminated fixed bullous drug eruption, acute generalized exanthematous pustulosis (AGEP), and staphylococcal scalded skin syndrome (SSSS) are among the differential diagnoses. The management of patients with SJS/TEN is complicated by the high risk of mortality, necessitating early diagnosis, estimation of the SCORTEN prognosis, identification and discontinuation of the causative drug, specialized supportive care, and high-dose injectable Ig therapeutic interventions. The reported fatality rates for SJS are 1-5% on average and 25-35% for TEN; it can be even higher in patients who are elderly or who have a significant amount of epidermal detachment on their skin. More than 50% of TEN patients who survive the disease experience long-term consequences.

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Necrosis epidérmica tóxica por colirio de dorzolamida

Cited by 4 publications

References 0 publications

Dermatological adverse effects of anti‐glaucoma eye drops: a review

Dermatological adverse effects of anti‐glaucoma eye drops: a review

Toxic epidermal necrolysis and Stevens-Johnson syndrome

Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis- An Overview

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