SEVERE, ACUTE ADVERSE CUTANEOUS DRUG REACTIONS I: STEVENS–JOHNSON SYNDROME AND TOXIC EPIDERMAL NECROLYSIS

2011 ◽  
pp. 154-161 ◽  
Author(s):  
Ronni Wolf ◽  
Batya B. Davidovici
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Johnson Syndrome ◽  
Cutaneous Drug Reactions

Dermatological emergencies

2019 ◽  
pp. 691-710
Author(s):  
Punit S. Ramrakha ◽  
Kevin P. Moore ◽  
Amir H. Sam
Keyword(s):  
Herpes Zoster ◽  
Toxic Epidermal Necrolysis ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Eczema Herpeticum ◽  
Bullous Disease ◽  
Autoimmune Bullous Disease ◽  
Johnson Syndrome ◽  
Generalized Pustular Psoriasis ◽  
Cutaneous Drug Reactions

This chapter discusses dermatological emergencies, including cutaneous drug reactions, erythroderma, urticaria and angio-oedema, autoimmune bullous disease, eczema herpeticum, herpes zoster, generalized pustular psoriasis, and Stevens–Johnson syndrome and toxic epidermal necrolysis.

scholarly journals Stevens-Johnson syndrome and toxic epidermal necrolysis: a review

2016 ◽  
Vol 62 (5) ◽  
pp. 468-473 ◽  
Author(s):  
Anthony Wong ◽  
Andrey Augusto Malvestiti ◽  
Mariana de Figueiredo Silva Hafner
Keyword(s):  
High Risk ◽  
Early Diagnosis ◽  
Toxic Epidermal Necrolysis ◽  
Stevens Johnson Syndrome ◽  
Drug Reactions ◽  
Johnson Syndrome ◽  
Life Threatening ◽  
Inflammatory Drugs ◽  
Cutaneous Drug Reactions ◽  
Perilesional Skin

SUMMARY Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are uncommon, acute and potentially life-threatening adverse cutaneous drug reactions. These pathologies are considered a hypersensitivity reaction and can be triggered by drugs, infections and malignancies. The drugs most often involved are allopurinol, some antibiotics, including sulfonamides, anticonvulsants such as carbamazepine, and some non-steroid anti-inflammatory drugs (NSAIDs). Necrosis of keratinocytes is manifested clinically by epidermal detachment, leading to scalded skin appearance. The rash begins on the trunk with subsequent generalization, usually sparing the palmoplantar areas. Macular lesions become purplish, and epidermal detachment occurs, resulting in flaccid blisters that converge and break, resulting in extensive sloughing of necrotic skin. Nikolsky's sign is positive in perilesional skin. SJS and TEN are considered to be two ends of the spectrum of one disease, differing only by their extent of skin detachment. Management of patients with SJS or TEN requires three measures: removal of the offending drug, particularly drugs known to be high-risk; supportive measures and active interventions. Early diagnosis of the disease, recognition of the causal agent and the immediate withdrawal of the drug are the most important actions, as the course of the disease is often rapid and fatal.

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

scholarly journals Serum Granulysin in Differentiation of Stevens-Johnson Syndrome/toxic Epidermal Necrolysis and Erythema Multiforme

2020 ◽  
Vol 8 (B) ◽  
pp. 381-388
Author(s):  
Tran Thi Huyen ◽  
Pham Dinh Hoa ◽  
Trinh Minh Trang ◽  
Riichiro Abe ◽  
Nguyen Van Thuong ◽  
...  
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Body Surface ◽  
Erythema Multiforme ◽  
The Body ◽  
Stevens Johnson Syndrome ◽  
Enzyme Linked Immunosorbent Assay ◽  
Drug Reactions ◽  
Skin Manifestation ◽  
Johnson Syndrome ◽  
Life Threatening

BACKGROUND: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are acute, life-threatening drug reactions, which lead to massive epidermal necrolysis. Granulysin plays an important role as a key mediator for keratinocyte apoptosis in these conditions. Erythema multiforme (EM) may have skin manifestation similar to SJS/TEN. AIMS: The aim of the study was to compare serum granulysin levels in patients with SJS/TEN and EM as well as to investigate a possible association between serum granulysin levels and the severity of SJS/TEN. METHODS: In total, 48 patients with SJS/TEN, 43 patients with EM, and 20 health controls (HCs) were enrolled. We measured serum granulysin levels using enzyme-linked immunosorbent assay. RESULTS: The average level of serum granulysin in the SJS/TEN patients was 23.0 ng/ml (range 1.2–144.6 ng/ml), significantly higher than that of EM group (20.1 ng/ml; range 8.5–121 ng/ml, p < 0.05) and HCs group (20.8 ng/ml; range 10.1–46.7 ng/ml, p < 0.05). Of 48 SJS/TEN patients, the 25 samples collected <6 days after onset showed higher level of serum granulysin (27.7 ng/ml; range 2.5–144.6 ng/ml) than those collected ≥6 days after onset (17.9 ng/ml; range 1.2–59 ng/ml; p > 0.05). No significant correlation was found between serum granulysin levels and the body surface area affected and the modified-SCORTEN. At the day of re-epithelialization, serum granulysin levels were not different compared with those at the day of hospitalization. CONCLUSIONS: Serum granulysin levels are significantly higher in SJS/TEN group than in EM group. After the onset, serum granulysin levels in patients with SJS/TEN are not a good biomarker to evaluate the severity of the diseases.

Ciprofloxacin-Induced Bullae of the Lower Extremity: A Case of a Fixed Drug Reaction

2019 ◽  
Vol 109 (2) ◽  
pp. 155-158 ◽  
Author(s):  
Anthony J. Mollica ◽  
Albert J. Mollica ◽  
Elaine Grant ◽  
Ali Malik ◽  
Marc Claydon
Keyword(s):  
Drug Reaction ◽  
Adverse Drug Reactions ◽  
Hypersensitivity Syndrome ◽  
Stevens Johnson Syndrome ◽  
Adverse Side Effect ◽  
Drug Reactions ◽  
Johnson Syndrome ◽  
Fixed Drug ◽  
Cutaneous Drug Reactions ◽  
Exanthematous Pustulosis

Cutaneous adverse drug reactions make up 1% to 2% of all adverse drug reactions. From these adverse cutaneous drug reactions, 16% to 21% can be categorized as fixed drug reactions (FDR). Fixed drug reactions may show diverse morphology including but not limited to the following: dermatitis, Stevens-Johnson syndrome, urticaria, morbilliform exanthema, hypersensitivity syndrome, pigmentary changes, acute generalized exanthematous pustulosis, photosensitivity, and vasculitis. An FDR will occur at the same site because of repeated exposure to the offending agent, causing a corresponding immune reaction. There are many drugs that can cause an FDR, such as analgesics, antibiotics, muscle relaxants, and anticonvulsants. The antibiotic ciprofloxacin has been shown to be a cause of cutaneous adverse drug reactions; however, the fixed drug reaction bullous variant is rare. This case study was published to demonstrate a rare adverse side effect to a commonly used antibiotic in podiatric medicine.

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.

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