Recurrent fatal drug-induced toxic epidermal necrolysis (Lyell’s syndrome) after putative β-lactam cross-reactivity: Case report and scrutiny of antibiotic imputability

Paquet, Philippe; Jacob, Eric; Damas, Pierre; Pierard, Gérald

doi:10.1097/00003246-200211000-00029

Cited by 33 publications

(11 citation statements)

References 60 publications

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“…However, cross reactivity resulting in TEN can occur within different classes of beta-lactam antibiotics, such as penicillins and cephalosporins. 55 A reaction to sulfonamide antibiotics does not mean sensitivity to sulfonamide nonantibiotic drugs, such as thiazide diuretics, sufonylureas, furosemide, or cyclooxygenase-2 inhibitors. All of these medications have a sulfonamide moiety, but only sulfonamide antibiotics have an arylamine group at the N4 position.…”

Section: Clinical Aspects Of Sjs/tenmentioning

confidence: 99%

Toxic epidermal necrolysis

Pereira

Mudgil

Rosmarin

2007

Journal of the American Academy of Dermatology

287

237

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Section: Clinical Aspects Of Sjs/tenmentioning

confidence: 99%

Toxic epidermal necrolysis

Pereira

Mudgil

Rosmarin

2007

Journal of the American Academy of Dermatology

287

237

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“…Drugs showing any chemical resemblance to the primary culprit compound should be strictly avoided in the management of TEN [43]. …”

Section: Ten Treatmentsmentioning

confidence: 99%

Novel Treatments for Drug-Induced Toxic Epidermal Necrolysis (Lyell’s Syndrome)

Paquet

Pierard

Quatresooz³

2005

Int Arch Allergy Immunol

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Drug-induced toxic epidermal necrolysis (TEN) is a life-threatening disease characterized by extensive destruction of the epidermis. It apparently results from the formation of specific toxic drug metabolites by the keratinocytes. The mortality rate which averages 25–30% is mainly due to secondary septicemia, and to ionic and metabolic disturbances following loss of epidermal integrity. Apoptosis is the likely mechanism leading to massive keratinocyte death in TEN. Dysregulations in the tumor necrosis factor-α (TNF-α) pathway, CD95 system (Fas ligand, CD95L; Fas receptor, CD95R) and calcium homeostasis in the epidermis are involved in this apoptotic process. An active role has also been ascribed to T lymphocytes, macrophages and factor XIIIa-positive dermal dendrocytes. Despite progress, treatment of TEN remains controversial. In the past, systemic glucocorticoids were used in order to target the inflammatory reaction in TEN. However, there was no evidence for improvement of the healing process, while corticosteroids worsened the prognosis by increasing the risk of septicemia. Only a few cases have been treated with other drugs including cyclophosphamide, pentoxyfilline, thalidomide, anti-TNF-α antibodies and cyclosporin A. In the recent past, some TEN patients were treated with intravenous human immunoglobulins (IVIG). The rationale for such a treatment was to block the CD95 system on keratinocytes. The early promising clinical results of IVIG treatment in TEN were subsequently challenged. This review compares the effectiveness and drawbacks of the major drugs presently used in TEN treatment. Some future prospects in TEN management are also discussed.

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“…The aromatic anticonvulsants carbamazepine, phenytoin and phenobarbitol cross react with one another. Cross reactivity resulting in SJS/TEN can also occur across different classes of beta-lactam antibiotics, such as penicillins, cephalosporins and carbapenems [176]. Administration of a structurally related drug can also result in different reactions.…”

Section: Restricted Use Of Related Medicationsmentioning

confidence: 99%

Severe Cutaneous Adverse Reactions

Fernando¹

2013

Skin Biopsy - Diagnosis and Treatment

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Recurrent fatal drug-induced toxic epidermal necrolysis (Lyell’s syndrome) after putative β-lactam cross-reactivity: Case report and scrutiny of antibiotic imputability

Cited by 33 publications

References 60 publications

Toxic epidermal necrolysis

Toxic epidermal necrolysis

Novel Treatments for Drug-Induced Toxic Epidermal Necrolysis (Lyell’s Syndrome)

Severe Cutaneous Adverse Reactions

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