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Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

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Abstract

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered a delayed-type hypersensitivity reaction to drugs. They represent true medical emergencies and an early recognition and appropriate management is decisive for the survival. SJS/TEN manifest with an “influenza-like” prodromal phase (malaise, fever), followed by painful cutaneous and mucous membrane (ocular, oral, and genital) lesions, and other systemic symptoms. The difference between SJS, SJS/TEN overlap, and TEN is defined by the degree of skin detachment: SJS is defined as skin involvement of < 10%, TEN is defined as skin involvement of > 30%, and SJS/TEN overlap as 10–30% skin involvement. The diagnosis of different degrees of epidermal necrolysis is based on the clinical assessment in conjunction with the corresponding histopathology. The mortality rates for SJS and TEN have decreased in the last decades. Today, the severity-of-illness score for toxic epidermal necrolysis (SCORTEN) is available for SJS/TEN severity assessment. Drugs with a high risk of causing SJS/TEN are anti-infective sulfonamides, anti-epileptic drugs, non-steroidal anti-inflammatory drugs of the oxicam type, allopurinol, nevirapine, and chlormezanone. Besides conventional drugs, herbal remedies and new biologicals should be considered as causative agents. The increased risk of hypersensitivity reactions to certain drugs may be linked to specific HLA antigens. Our understanding of the pathogenesis of SJS/TEN has improved: drug-specific T cell-mediated cytotoxicity, genetic linkage with HLA- and non-HLA-genes, TCR restriction, and cytotoxicity mechanisms were clarified. However, many factors contributing to epidermal necrolysis still have to be identified, especially in virus-induced and autoimmune forms of epidermal necrolysis not related to drugs. In SJS/TEN, the most common complications are ocular, cutaneous, or renal. Nasopharyngeal, esophageal, and genital mucosal involvement with blisters, erosions as well as secondary development of strictures also play a role. However, in the acute phase, septicemia is a leading cause of morbidity and fatality. Pulmonary and hepatic involvement is frequent. The acute management of SJS/TEN requires a multidisciplinary approach. Immediate withdrawal of potentially causative drugs is mandatory. Prompt referral to an appropriate medical center for specific supportive treatment is of utmost importance. The most frequently used treatments for SJS/TEN are systemic corticosteroids, immunoglobulins, and cyclosporine A.

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Abbreviations

ACSR:

Anti-folate cytotoxic skin reaction

AGEP:

Acute generalized exanthematous pustulosis

ALDEN:

Algorithm for assessment of drug causality in epidermal necrolysis

Anti PD-L1:

Anti programmed death-ligand 1

APACHE:

Acute physiology and chronic health evaluation

BSA:

Body surface area

BSLE:

Bullous systemic lupus erythematosus

CBZ:

Carbamazepine

CsA:

Cyclosporine A

DIHS:

Drug-induced hypersensitivity syndrome

DRESS:

Drug reaction with eosinophilia and systemic symptoms

EBA:

Epidermolysis bullosa acquisita

EM:

Erythema multiforme

FACS:

Fluorescence-activated cell sorting

FasL:

Fas ligand

GBFDE:

Generalized bullous fixed drug eruption

GSTM1:

Glutathione S-transferase Mu 1

GvHD:

Graft versus host disease

HLA:

Human leukocyte antigen

ICNARC:

Intensive Care National Audit & Research Center

IVIG:

Intravenous immunoglobulins

LABD:

Linear IgA bullous dermatosis

LTT:

Lymphocyte transformation test

MIEN:

Methotrexate-induced epidermal necrolysis

MRR:

Mortality risk ratio

NK cells:

Natural killer cells

NSAIDs:

Nonsteroidal anti-inflammatory drugs

PCR:

Polymerase chain reaction

SCORTEN:

Severity-of-illness score for toxic epidermal necrolysis

SJS:

Stevens-Johnson syndrome

SMR:

Standardized mortality rate

SMX/TMP:

Sulfamethoxazole/trimethoprim

SSSS:

Staphylococcal scalded skin syndrome

TBSA:

Total body surface area

TEN:

Toxic epidermal necrolysis

TNF:

Tumor necrosis factor

TRAIL:

TNF-related apoptosis-inducing ligand

TWEAK:

TNF-like weak inducer of apoptosis

VBDS:

Vanishing bile duct syndrome

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Authors and Affiliations

  1. Allergy/Dermatology Unit, Department of Internal Medicine, Kantonsspital Winterthur, Winterthur, Switzerland

    Marianne Lerch

  2. Department of Dermatology, Bellinzona Regional Hospital, Bellinzona, Switzerland

    Carlo Mainetti

  3. Epatocentro Ticino, Lugano, Switzerland

    Benedetta Terziroli Beretta-Piccoli

  4. Unité d’allergologie, Service d’immunologie et d’allergologie, Hôpitaux Universitaires de Genève HUG, Genève, Switzerland

    Thomas Harr

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Lerch, M., Mainetti, C., Terziroli Beretta-Piccoli, B. et al. Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. Clinic Rev Allerg Immunol 54, 147–176 (2018). https://doi.org/10.1007/s12016-017-8654-z

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