Cutaneous Adverse Drug Reactions: Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

2016 ◽  
pp. 393-404 ◽  
Author(s):  
Riichiro Abe
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Johnson Syndrome

Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis

1996 ◽  
Vol 35 (4) ◽  
pp. 234-236 ◽  
Author(s):  
Pierre Wolkenstein ◽  
Oliver Chosidow ◽  
Marie-Laure Fléchet ◽  
Odile Robbiola ◽  
Muriel Paul ◽  
...  
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Patch Testing ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Johnson Syndrome

Neutrophils initiate and exacerbate Stevens-Johnson syndrome and toxic epidermal necrolysis

2021 ◽  
Vol 13 (600) ◽  
pp. eaax2398
Author(s):  
Manao Kinoshita ◽  
Youichi Ogawa ◽  
Natsumi Hama ◽  
Inkin Ujiie ◽  
Akito Hasegawa ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Cytotoxic T Cells ◽  
Formyl Peptide Receptor ◽  
Stevens Johnson Syndrome ◽  
Lipocalin 2 ◽  
Drug Reactions ◽  
Johnson Syndrome

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening mucocutaneous adverse drug reactions characterized by massive epidermal detachment. Cytotoxic T cells and associated effector molecules are known to drive SJS/TEN pathophysiology, but the contribution of innate immune responses is not well understood. We describe a mechanism by which neutrophils triggered inflammation during early phases of SJS/TEN. Skin-infiltrating CD8+ T cells produced lipocalin-2 in a drug-specific manner, which triggered the formation of neutrophil extracellular traps (NETs) in early lesional skin. Neutrophils undergoing NETosis released LL-37, an antimicrobial peptide, which induced formyl peptide receptor 1 (FPR1) expression by keratinocytes. FPR1 expression caused keratinocytes to be vulnerable to necroptosis that caused further release of LL-37 by necroptotic keratinocytes and induced FPR1 expression on surrounding keratinocytes, which likely amplified the necroptotic response. The NETs-necroptosis axis was not observed in less severe cutaneous adverse drug reactions, autoimmune diseases, or neutrophil-associated disorders, suggesting that this was a process specific to SJS/TEN. Initiation and progression of SJS/TEN keratinocyte necroptosis appear to involve a cascade of events mediated by innate and adaptive immune responses, and understanding these responses may contribute to the identification of diagnostic markers or therapeutic targets for these adverse drug reactions.

scholarly journals A rare case of oxcarbazepine induced Stevens Johnson Syndrome: toxic epidermal necrosis overlap

2017 ◽  
Vol 6 (2) ◽  
pp. 466
Author(s):  
Aditi Maitra ◽  
Shashwat Bhattacharyya ◽  
Shatavisa Mukherjee ◽  
Nikhil Era
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Rare Case ◽  
Stevens Johnson Syndrome ◽  
Toxicity Profile ◽  
Drug Reactions ◽  
Clinical Safety ◽  
Drug Eruptions ◽  
Johnson Syndrome ◽  
Epidermal Necrosis

Oxcarbazepine is a closely related analogue of carbamazepine and is useful in the monotherapy of seizures with an improved toxicity profile. Its clinical safety has been recently put under scrutiny as evidence has emerged about its adverse drug reactions and it is increasingly being reported to cause cutaneous drug eruptions. Here we report a rare case of oxcarbazepine induced Stevens Johnson - toxic epidermal necrolysis overlap.

Cutaneous adverse drug reactions

2020 ◽  
pp. 347-358
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Clinical Manifestations ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Practical Advice ◽  
Johnson Syndrome ◽  
Causative Agents

Cutaneous adverse drug reactions considers the principle types of unwanted responses to drugs seen on the skin. The most common exanthematous rash is examined as are serious eruptions such as Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) along with other reactions. The clinical manifestations are discussed along with likely causative agents. Practical advice about severity, worrying features, and management is given.

scholarly journals Implementation of Pharmacogenomic Information on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

2021 ◽  
Vol 8 ◽  
Author(s):  
Eri Tsukagoshi ◽  
Yoichi Tanaka ◽  
Yoshiro Saito
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Adverse Drug Reactions ◽  
Stevens Johnson Syndrome ◽  
Future Perspectives ◽  
Drug Reactions ◽  
Johnson Syndrome ◽  
Label Information

Drug-related Stevens-Johnson syndrome and toxic epidermal necrolysis (SJS/TEN) are rare but severe adverse drug reactions, termed as idiosyncratic reactions; however, predicting their onset remains challenging. Pharmacogenomic information associated with SJS/TEN has accumulated on several drugs in the last 15 years, with clinically useful information now included on drug labels in several countries/regions or guidelines of the Clinical Pharmacogenetics Implementation Consortium (CPIC) for implementation. However, label information might be different among countries. This mini-review summarizes pharmacogenomic information on drug labels of five drugs in six countries and compared descriptions of drug labels and CPIC guidelines. Finally, we discuss future perspectives of this issue. Pharmacogenomic information on drug labels is not well-harmonized across countries/regions, but CPIC guidelines are a scientifically sound goal for future pharmacogenomic implementation.

scholarly journals Pediatric SJS-TEN: Where are we now?

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 982
Author(s):  
Michele Ramien ◽  
Jennifer L. Goldman
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Mycoplasma Pneumoniae ◽  
Adverse Drug Reactions ◽  
Response To Treatment ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Skin Reactions ◽  
Recent Advances ◽  
Johnson Syndrome

Stevens–Johnson syndrome and toxic epidermal necrolysis are rare severe blistering skin reactions triggered by medications or infections. Over the last 5 to 10 years, a number of important publications have advanced understanding of these diseases and their response to treatment. Importantly, a subset of patients with disease triggered by infection has been identified as having Mycoplasma pneumoniae–induced rash and mucositis, suggesting a reconsideration of the diagnostic paradigm. We present an update on pediatric Stevens–Johnson syndrome and toxic epidermal necrolysis in the broader context of cutaneous adverse drug reactions and focus on challenges and recent advances in diagnosis, management, and prevention.

scholarly journals Intravenous N-acetylcysteine in severe cutaneous drug reaction treatment: A case series

2020 ◽  
Vol 8 ◽  
pp. 2050313X2093470 ◽  
Author(s):  
Md Jahidul Hasan ◽  
Raihan Rabbani
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Intravenous Immunoglobulin ◽  
Adverse Drug Reactions ◽  
Therapeutic Option ◽  
Case Series ◽  
High Rate ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Drug Induced ◽  
Johnson Syndrome

Drug-induced serious adverse reaction is an unpleasant event with high rate of mortality. Stevens–Johnson Syndrome and toxic epidermal necrolysis are most common among the serious adverse drug reactions. There is no selective drug therapy for the management of serious adverse drug reactions-associated mucocutaneous blisters. The use of N-acetylcysteine in the treatment of mucocutaneous blisters has limited evidence worldwide. Three cases of toxic epidermal necrolysis or Stevens–Johnson Syndrome-associated mucocutaneous blisters are presented in this study where intravenous N-acetylcysteine (600 mg, every 8 h) was given in early hospitalization hours for the treatment of mucocutaneous fluid-filled blisters. Here, one patient with toxic epidermal necrolysis received intravenous immunoglobulin along with intravenous N-acetylcysteine and the other two patients (toxic epidermal necrolysis/Stevens–Johnson Syndrome) received only N-acetylcysteine intravenously. In response, mucocutaneous fluid-filled blisters stopped progressing within 48 h and were healed within 2 weeks of admission in the intensive care unit. Thus, intravenous N-acetylcysteine with or without having intravenous immunoglobulin in the treatment of serious adverse drug reactions-associated mucocutaneous blisters may be an effective therapeutic option for better clinical outcome.

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