Literature DB >> 29400697

Randomized, controlled trial of TNF-α antagonist in CTL-mediated severe cutaneous adverse reactions.

Chuang-Wei Wang1,2, Lan-Yan Yang3, Chun-Bing Chen1, Hsin-Chun Ho1,4, Shuen-Iu Hung5, Chih-Hsun Yang1,4, Chee-Jen Chang6,7, Shih-Chi Su1,8, Rosaline Chung-Yee Hui1,4, See-Wen Chin1, Li-Fang Huang3, Yang Yu-Wei Lin1, Wei-Yang Chang3, Wen-Lang Fan8, Chin-Yi Yang1, Ji-Chen Ho4,9, Ya-Ching Chang1,4, Chun-Wei Lu1,4, Wen-Hung Chung1,2,4,8.   

Abstract

BACKGROUND: Cytotoxic T lymphocyte-mediated (CTL-mediated) severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), are rare but life-threatening adverse reactions commonly induced by drugs. Although high levels of CTL-associated cytokines, chemokines, or cytotoxic proteins, including TNF-α and granulysin, were observed in SJS-TEN patients in recent studies, the optimal treatment for these diseases remains controversial. We aimed to evaluate the efficacy, safety, and therapeutic mechanism of a TNF-α antagonist in CTL-mediated SCARs.
METHODS: We enrolled 96 patients with SJS-TEN in a randomized trial to compare the effects of the TNF-α antagonist etanercept versus traditional corticosteroids.
RESULTS: Etanercept improved clinical outcomes in patients with SJS-TEN. Etanercept decreased the SCORTEN-based predicted mortality rate (predicted and observed rates, 17.7% and 8.3%, respectively). Compared with corticosteroids, etanercept further reduced the skin-healing time in moderate-to-severe SJS-TEN patients (median time for skin healing was 14 and 19 days for etanercept and corticosteroids, respectively; P = 0.010), with a lower incidence of gastrointestinal hemorrhage in all SJS-TEN patients (2.6% for etanercept and 18.2% for corticosteroids; P = 0.03). In the therapeutic mechanism study, etanercept decreased the TNF-α and granulysin secretions in blister fluids and plasma (45.7%-62.5% decrease after treatment; all P < 0.05) and increased the Treg population (2-fold percentage increase after treatment; P = 0.002), which was related to mortality in severe SJS-TEN.
CONCLUSIONS: The anti-TNF-α biologic agent etanercept serves as an effective alternative for the treatment of CTL-mediated SCARs. TRIAL REGISTRATION: ClinicalTrials.gov NCT01276314. FUNDING: Ministry of Science and Technology of Taiwan.

Entities:  

Keywords:  Allergy; Clinical Trials; Immunology; Immunotherapy

Mesh:

Substances:

Year:  2018        PMID: 29400697      PMCID: PMC5824923          DOI: 10.1172/JCI93349

Source DB:  PubMed          Journal:  J Clin Invest        ISSN: 0021-9738            Impact factor:   14.808


  58 in total

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Journal:  J Am Acad Dermatol       Date:  2013-12       Impact factor: 11.527

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Journal:  Ann Pharmacother       Date:  2014-11-18       Impact factor: 3.154

Review 4.  Severe cutaneous adverse drug reactions.

Authors:  Wen-Hung Chung; Chuang-Wei Wang; Ro-Lan Dao
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5.  Prevention of toxic epidermal necrolysis by regulatory T cells.

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6.  HLA-B*13:01 and the dapsone hypersensitivity syndrome.

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7.  Correlations between clinical patterns and causes of erythema multiforme majus, Stevens-Johnson syndrome, and toxic epidermal necrolysis: results of an international prospective study.

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8.  Randomised comparison of thalidomide versus placebo in toxic epidermal necrolysis.

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9.  Human leukocyte antigen class I-restricted activation of CD8+ T cells provides the immunogenetic basis of a systemic drug hypersensitivity.

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Review 10.  Transcriptional regulation by steroid hormones.

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5.  Treatment of severe cutaneous adverse reaction with tocilizumab.

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7.  Stevens-Johnson syndrome/toxic epidermal necrolysis induced by pirfenidone.

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8.  Clinical Aspects of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis With Severe Ocular Complications in Taiwan.

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