Toxic Epidermal Necrolysis Induced by the Topical Carbonic Anhydrase Inhibitors Brinzolamide and Dorzolamide

Chun, Ji Sun; Yun, Sook Jung; Lee, Jee Bum; Kim, Seong‐Jin; Won, Young Ho; Lee, Seung−Chul

doi:10.5021/ad.2008.20.4.260

Cited by 14 publications

(12 citation statements)

References 7 publications

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“…6 Drug notoriety was determined using different reviews that assessed medication risk of inducing SJS or TEN and case reports. 2,3,[7][8][9][10][11][12][13] Amoxicillin (aminopenicillin) and diclofenac gel (acetic acid NSAID) are both considered to have a definite but lower risk of causing epidermal necrolysis. 7 Brinzolamidetimolol drops, ibuprofen and naproxen (propionic acid NSAIDs), and pregabalin (gabapentinoid) have been loosely associated to severe cutaneous adverse reactions in case reports.…”

Section: Discussionmentioning

confidence: 99%

“…7 Brinzolamidetimolol drops, ibuprofen and naproxen (propionic acid NSAIDs), and pregabalin (gabapentinoid) have been loosely associated to severe cutaneous adverse reactions in case reports. 2,3,[7][8][9][10][11][12][13] All of these medications were stopped before resolution of the TEN. The patient had received ibuprofen previously without any reaction demonstrating a negative prechallenge.…”

Section: Discussionmentioning

confidence: 99%

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Identification of Possible Causative Agents in a Polymedicated Patient Presenting With Toxic Epidermal Necrolysis

Khazaka

Laverdière

Bouchard

et al. 2020

Journal of Pharmacy Practice

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Purpose: To present the pharmacological evaluation process in a case of a polymedicated patient presenting with toxic epidermal necrolysis (TEN). Summary: A 75-year-old Caucasian polymedicated woman had been treated for hip pain with nonsteroidal anti-inflammatory drugs and pregabalin in the months preceding the apparition of an expanding papulo-erythematous rash. She had also started using new medicated eye drops for glaucoma. She presented to the emergency department of a regional hospital where all of her medications were stopped. The patient was transferred and admitted to a tertiary-care teaching hospital’s specialized burn unit for significant cutaneous detachment. It was estimated that 70% to 80% of the body surface area was affected. Skin biopsy showed keratinocyte necrosis with a partial detachment of the epidermis leading to a diagnosis of TEN. The reaction ceased to progress 2 days after the discontinuation of her medications. A complete reepithelialization was objectified after 10 days. A series of steps were followed by the hospital pharmacist to determine which drugs were the most probable culprits. A complete pharmacological history was obtained and a timeline for medication use in the 3 months preceding rash apparition was established. A review of the literature was done to determine the drugs’ relationships to Steven-Johnson syndrome or TEN. Using the algorithm of drug causality for epidermal necrolysis (ALDEN) score, it was determined that naproxen, pregabalin, and brinzolamide–timolol drops were all possible culprits. Conclusion: A systematic method for pharmacological evaluation of a polymedicated patient with TEN is presented. Naproxen, pregabalin, and brinzolamide–timolol drops were all retained as possible culprits.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Identification of Possible Causative Agents in a Polymedicated Patient Presenting With Toxic Epidermal Necrolysis

Khazaka

Laverdière

Bouchard

et al. 2020

Journal of Pharmacy Practice

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“…Other CAIs, such as acetazolamide, and even topical agents, such as brinzolamide and dorzolamide, have also been reported to cause SJS/TEN [22][23][24][25] . Although B59 was also detected in one acetazolamide-induced SJS case, HLA-typing was not performed in most of these cases.…”

Section: Discussionmentioning

confidence: 99%

HLA-B5901* is Strongly Associated with Methazolamide-Induced Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis

Kim

Lee

et al. 2010

Pharmacogenomics

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“…Surprisingly, both topical and oral formulations of CAIs, such as acetazolamide, methazolamide, and dorzolamide, can induce SJS/TEN ( 6 , 26 ). HLA-B*5901 genotype, which occurs in 2.1% of the Korean population, has been suggested as a genetic marker for CAIs-induced SJS/TEN ( 27 , 28 ).…”

Section: Overview Of Causative Drugs and Genetic Predisposition In Komentioning

confidence: 99%

Clinical Aspects of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis With Severe Ocular Complications in South Korea

Kim

Yoon

et al. 2021

Front. Med.

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This review describes the current knowledge regarding genetic susceptibilities and treatment strategies for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), with ocular complications, in Korea. In a case-control study, the gene frequencies of both HLA-A*0206 (20.0%) and HLA-Cw*0304 (15.0%) increased but the gene frequency of HLA-Cw*0303 (1.3%) decreased with cold medicine (CM)-SJS/TEN with severe ocular complications (SOCs). In a case-series, positive genotyping of HLA-B*5801 was 80.0% in allopurinol-induced SJS/TEN without SOCs. In a genome-wide association study, HLA-A*0206 was substantially related to CM-SJS/TEN with SOCs. Both HLA-A*0206 and prostaglandin-E receptor 3 (PTGER3) single nucleotide polymorphism (SNP) rs1327464 exert a synergistic effect on SOCs in CM-SJS/TEN. In the acute stage, conventional procedures, amniotic membrane transplantation or suture-less amniotic contact lenses are applied. Applications of intravenous Immunoglobulin (IVIG) or mega-dose steroids are attempted in patients with high acute ocular and systemic involvement scores. In the chronic stage, keratolimbal transplantation and penetrating keratoplasty are the standard procedures. Either autologous nasal or oral mucosal grafts, or biomaterial-free cultured oral mucosal epithelial cell sheets are transplanted as alternative therapies. Deep anterior lamellar keratoplasty is attempted. Combined photodynamic therapy with intrastromal bevacizumab injection or intense pulse laser are used to resolve chronic ocular complication. Corneoscleral contact lenses are available for a visual rehabilitation. As a last resort, Seoul-type keratoprosthesis had been transplanted. There are unmet needs to standardize nationwide ocular grading system and to correct tarsal scarring using mucosal grafting. This review provides a perspective on the current practices to treat ocular complications in SJS/TEN.

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Toxic Epidermal Necrolysis Induced by the Topical Carbonic Anhydrase Inhibitors Brinzolamide and Dorzolamide

Cited by 14 publications

References 7 publications

Identification of Possible Causative Agents in a Polymedicated Patient Presenting With Toxic Epidermal Necrolysis

Identification of Possible Causative Agents in a Polymedicated Patient Presenting With Toxic Epidermal Necrolysis

HLA-B5901* is Strongly Associated with Methazolamide-Induced Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis

Clinical Aspects of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis With Severe Ocular Complications in South Korea

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Toxic Epidermal Necrolysis Induced by the Topical Carbonic Anhydrase Inhibitors Brinzolamide and Dorzolamide

Cited by 14 publications

References 7 publications

Identification of Possible Causative Agents in a Polymedicated Patient Presenting With Toxic Epidermal Necrolysis

Identification of Possible Causative Agents in a Polymedicated Patient Presenting With Toxic Epidermal Necrolysis

HLA-B*5901 is Strongly Associated with Methazolamide-Induced Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis

Clinical Aspects of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis With Severe Ocular Complications in South Korea

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Product

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HLA-B5901* is Strongly Associated with Methazolamide-Induced Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis