Granulocyte colony-stimulating factor in toxic epidermal necrolysis (TEN) and Chelsea &amp; Westminster TEN protocol

Sica-Chapman, A. De; Williams, G.; Soni, N. K.; Bunker, C.B.

doi:10.1111/j.1365-2133.2009.09585.x

Cited by 40 publications

(27 citation statements)

References 23 publications

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“…G-CSF was reported to have beneficial clinical results in two cases of severe TEN affecting over 80% body surface area (BSA) and concurrent neutropenia [50]. In both cases, the patients made full recovery.…”

Section: Managementmentioning

confidence: 99%

Review of Toxic Epidermal Necrolysis

Harris

Jackson

Cooper

2016

IJMS

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Toxic epidermal necrolysis (TEN) is a rare but life threatening mucocutaneous reaction to drugs or their metabolites. It is characterised by widespread keratinocyte apoptosis and sloughing of the skin, erosions of the mucous membranes, painful blistering, and severe systemic disturbance. The pathophysiology of TEN is incompletely understood. Historically, it has been regarded as a drug-induced immune reaction initiated by cytotoxic lymphocytes via a human leukocyte antigen (HLA)-restricted pathway. Several mediators have been identified as contributors to the cell death seen in TEN, including; granulysin, soluble Fas ligand, perforin/granzyme, tumour necrosis factor-α (TNF-α), and TNF-related apoptosis-inducing ligand. Currently, granulysin is accepted as the most important mediator of T cell proliferation. There is uncertainty around the accepted management of TEN. The lack of definitive management guidelines for TEN is explained in part by the rarity of the disease and its high mortality rate, which makes it difficult to conduct randomised control trials on emerging therapies. Developments have been made in pharmacogenomics, with numerous HLA alleles identified; however, these have largely been ethnically specific. These associations have translated into screening recommendations for Han Chinese.

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Section: Managementmentioning

confidence: 99%

Review of Toxic Epidermal Necrolysis

Harris

Jackson

Cooper

2016

IJMS

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“…The mechanism is not known. Delayed re-epithelialization has been observed in GM-CSF "knock-out mice" compared with wild types (9).…”

Section: Discussionmentioning

confidence: 99%

“…In the bone marrow, it regulates the production of neutrophils (10) and induces immunotolerance by activating CD4* CD 25* regulatory T cells (Tregs) fi-om the bone marrow. This seems to prevent further tissue damage and facilitate faster recovery (9).…”

Section: Discussionmentioning

confidence: 99%

Successful Treatment of Toxic Epidermal Necrolysis/Stevens-Johnson Syndrome Overlap with Human Granulocyte Colony Stimulating Factor: A Case Report

Pallesen¹,

Robinson²,

Toft³

et al. 2012

Acta Derm Venerol

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“…In patients with severe neutropenia, Granulocyte colony-stimulating factor which is a glycoprotein that stimulates the bone marrow to produce stem cells and granulocytes and release them to the blood stream was given as supportive therapy. Later it is suggested in patients without neutropenia [54,55,56].…”

Section: Other Therapiesmentioning

confidence: 99%

Study of Stevens - Johnson syndrome

2018

IJASRE

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Granulocyte colony-stimulating factor in toxic epidermal necrolysis (TEN) and Chelsea & Westminster TEN protocol

Abstract: G-CSF has been used for severe neutropenia in TEN, but we recommend and explain why, as in our Chelsea and Westminster protocol, G-CSF should be considered in treating severe TEN irrespective of the severity of neutropenia.

Cited by 40 publications

References 23 publications

Review of Toxic Epidermal Necrolysis

Review of Toxic Epidermal Necrolysis

Successful Treatment of Toxic Epidermal Necrolysis/Stevens-Johnson Syndrome Overlap with Human Granulocyte Colony Stimulating Factor: A Case Report

Study of Stevens - Johnson syndrome

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