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Sulfiram
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
A 47-year-old woman developed an exanthema with diffuse and considerable dermal edema affecting all of her body, though initially it was less severe on the face and neck. On her admission the red areas were rapidly becoming covered by large numbers of small pustules which were coalescing to form lakes of subcorneal pus. The horny layer now started to disintegrate and to be shed in vast sheets- the one below her right knee like a stocking in one piece. The pustules were distributed diffusely, and not in groups or in rings. Mucous membranes were unaffected. She had a fever and was severely ill. A cytological smear from the pustules showed a great quantity of polymorph neutrophils but no bacteria. No organisms were cultured. This exanthema was diagnosed as toxic epidermal necrolysis. It had evolved from a rash starting 3 hours after the application of a 25% alcoholic solution of sulfiram diluted with 3 parts of water for the treatment of scabies. Previously, she had become sensitized to the related rubber compound tetramethylthiuram disulfide from her work in a munition factory. Patch tests were positive to tetramethylthiuram disulfide and sulfiram 14% water (or the 25% alcoholic solution diluted with six parts of water?), the latter inducing a very severe eczematous reaction within three hours of application (2). It should be mentioned that the diagnosis was based solely on the clinical picture, histopathology was not performed. There were also features of acute generalized exanthematous pustulosis, which at that time was unknown.
Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
TCDD suppresses cell-mediated immunity and dermal hypersensitivity in both animals and humans.104 Dextran sulfate prohibits lymphoblasts from extravasating into dermal sites of delayed hypersensitivity, and suppresses TDTH cell function.105 An uncommon, life-threatening disorder that can be provocated by certain drugs, other chemicals, viruses, and bacteria is known as toxic epidermal necrolysis. The disease results in extensive shedding of the skin, and has features of autoimmunity possibly directed against keratinocytes or Langerhans’ cells.
Anti-Infective Agents
Published in Keith Struthers, Clinical Microbiology, 2017
While these drug reactions can involve other organs, cutaneous manifestations predominate. These include: Urticarial rash (usually associated with an accelerated reaction).Maculopapular exanthems.Bullous lesions.Pustules.(Stevens Johnson syndrome).(Toxic epidermal necrolysis).
Discovery of new 1H-pyrazolo[3,4-d]pyrimidine derivatives as anticancer agents targeting EGFRWT and EGFRT790M
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Ahmed A. Gaber, Mohamed Sobhy, Abdallah Turky, Hanan Gaber Abdulwahab, Ahmed A. Al-Karmalawy, Mostafa. A. Elhendawy, Mohamed. M. Radwan, Eslam B. Elkaeed, Ibrahim M. Ibrahim, Heba S. A. Elzahabi, Ibrahim H. Eissa
There are many FDA-approved EGFR-tyrosine kinase inhibitors (EGFR-TKIs). The first-generation as erlotinib I22 has a good effect against wild EGFR (EGFRWT). This class has many side effects23,24 in addition to the acquired drug resistance caused by EGFR-TK mutation25. The second-generation was discovered to overcome the resistance induced by EGFRT790M. Neratinib II26 is a one of the most famous drug in this generation. Unfortunately, latter class of drugs has a low maximal-tolerated dose producing inadequate clinical efficacy27,28. The third-generation EGFR-TKIs as olmutinib III and osimertinib IV29 showed enhanced actions against mutant EGFR (EGFRT790M). However, toxic epidermal necrolysis was associated with these drugs30. Hence, there is an urgent need to optimise the approved drugs to reach efficient and less harmful candidates.
Design, synthesis, and anti-cancer evaluation of new pyrido[2,3-d]pyrimidin-4(3H)-one derivatives as potential EGFRWT and EGFRT790M inhibitors and apoptosis inducers
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Heba S. A. Elzahabi, Eman S. Nossier, Rania A. Alasfoury, May El-Manawaty, Sara M. Sayed, Eslam B. Elkaeed, Ahmed M. Metwaly, Mohamed Hagras, Ibrahim H. Eissa
Till now, three generations of EGFR inhibitors were approved by the FDA (Figure 2). Erlotinib I27 and gefitinib II28 are examples of the first generation. The generated mutation in EGFR led to the acquired drug resistance and reduced efficacy in cancer treatment29. The mutant form of protein (EGFRT790M) resists the affinity of ATP-competitive inhibitors30. The second-generation of EGFR inhibitors was approved to overcome the drug resistance that was induced by EGFRT790M. These inhibitors can form covalent interactions with Cys797 at the ATP binding site31–33. Pelitinib III34 is a well-known example of this class. Unfortunately, low maximal-tolerated-dose, the major drawback of this class, led to poor clinical outcomes35,36. Osimertinib 537, an example of the third-generation EGFR inhibitors, exhibited greater activities against mutant form (EGFRT790M) than the wild form (EGFRWT). Recently, toxic epidermal necrolysis was reported upon the administration of olmutinib38. Hence, many efforts are still required to reach more potent and less toxic EGFR inhibitors.
Drug-induced Stevens-Johnson syndrome: a disproportionality analysis from the pharmacovigilance database of the World Health Organization
Published in Expert Opinion on Drug Safety, 2022
Yi Zheng, Wenli Zhou, Xiaojing Guo, Lijie Chi, Chenxin Chen, Zhijian Guo, Jizhou Liang, Lianhui Wei, Xiao Chen, Xiaofei Ye, Jia He
There are several limitations to our study. First, as a spontaneous reporting system, VigiBase has its own flaws. Problems such as omissions, repeated reporting, and incomplete information reporting were identified during the execution of this study. For example, 31% of final outcomes were missing. Secondly, the database is a passive detection database, making it impossible to calculate the incidence of adverse drug reactions, thus we can only provide potential signal values of IC and ROR as a dependent relationship between the drug and the SJS. Therefore, the results of this study need to be corroborated by further research. Thirdly, the study only considered the possibility of SJS caused by a single drug. Hence, we call for further research focusing on providing relevant clarifications on this. We did not include toxic epidermal necrolysis (TEN) in our study, which maybe the similar disease with over 30% body’s skin surface area detachment and mortality can be as high as 30% [22]. Finally, there are 3 drugs left to be verified in this study, which neither the relevant case on PubMed nor the corresponding ADR on the label was found.