Toxic Epidermal Necrolysis

Toxic epidermal necrolysis (TEN) is the most severe form of drug-induced skin reaction and includes denudation of >30% of total body surface area. The mechanism of disease is not completely understood, but immunologic mechanisms, cytotoxic reactions, and delayed hypersensitivity seem to be invol...

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Main Authors: Syed Naveed Ali Shah, Ifaza Tariq, Muhammad Nauman Zafar
Format: Article
Language:English
Published: Rawalpindi Medical University 2020-11-01
Series:Journal of Rawalpindi Medical College
Subjects:
Online Access:https://www.journalrmc.com/index.php/JRMC/article/view/1514
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spelling doaj-c0e5fa69700d430b983a63406c9bde122021-04-20T05:39:22ZengRawalpindi Medical UniversityJournal of Rawalpindi Medical College1683-35621683-35702020-11-01212Toxic Epidermal NecrolysisSyed Naveed Ali ShahIfaza TariqMuhammad Nauman Zafar Toxic epidermal necrolysis (TEN) is the most severe form of drug-induced skin reaction and includes denudation of >30% of total body surface area. The mechanism of disease is not completely understood, but immunologic mechanisms, cytotoxic reactions, and delayed hypersensitivity seem to be involved. Drug-induced toxic epidermal necrolysis (TENS), also known as Lyell’s syndrome, remains one of the most dramatic dermatological emergencies characterized by extensive destruction of epidermis and mucosal epithelia that often can be caused by drugs. TEN affects between 0.4 and 1.5 cases per million people every year with a mortality rate between 15% to 40%, with a large portion of patients dying from infections or multi-organ failure.1-4 The pathogenesis of drug-induced TEN is unknown, although several theories have been developed. Recent discoveries have shown that keratinocytes in TEN undergo apoptosis, not simply necrosis.5,6 Further research has elucidated that this apoptosis can be induced by interactions between cell surface death receptor Fas and its ligand, FasL or CD95L. The management of these patients is primarily supportive, although the use of corticosteroids and intravenous immunoglobulin (IVIG) therapy has been widely used with controversy. We report a case of risperidone induced toxic epidermal necrolysis with excellent response to corticosteroid. https://www.journalrmc.com/index.php/JRMC/article/view/1514toxic epidermal necrolysis(TENS),
collection DOAJ
language English
format Article
sources DOAJ
author Syed Naveed Ali Shah
Ifaza Tariq
Muhammad Nauman Zafar
spellingShingle Syed Naveed Ali Shah
Ifaza Tariq
Muhammad Nauman Zafar
Toxic Epidermal Necrolysis
Journal of Rawalpindi Medical College
toxic epidermal necrolysis(TENS),
author_facet Syed Naveed Ali Shah
Ifaza Tariq
Muhammad Nauman Zafar
author_sort Syed Naveed Ali Shah
title Toxic Epidermal Necrolysis
title_short Toxic Epidermal Necrolysis
title_full Toxic Epidermal Necrolysis
title_fullStr Toxic Epidermal Necrolysis
title_full_unstemmed Toxic Epidermal Necrolysis
title_sort toxic epidermal necrolysis
publisher Rawalpindi Medical University
series Journal of Rawalpindi Medical College
issn 1683-3562
1683-3570
publishDate 2020-11-01
description Toxic epidermal necrolysis (TEN) is the most severe form of drug-induced skin reaction and includes denudation of >30% of total body surface area. The mechanism of disease is not completely understood, but immunologic mechanisms, cytotoxic reactions, and delayed hypersensitivity seem to be involved. Drug-induced toxic epidermal necrolysis (TENS), also known as Lyell’s syndrome, remains one of the most dramatic dermatological emergencies characterized by extensive destruction of epidermis and mucosal epithelia that often can be caused by drugs. TEN affects between 0.4 and 1.5 cases per million people every year with a mortality rate between 15% to 40%, with a large portion of patients dying from infections or multi-organ failure.1-4 The pathogenesis of drug-induced TEN is unknown, although several theories have been developed. Recent discoveries have shown that keratinocytes in TEN undergo apoptosis, not simply necrosis.5,6 Further research has elucidated that this apoptosis can be induced by interactions between cell surface death receptor Fas and its ligand, FasL or CD95L. The management of these patients is primarily supportive, although the use of corticosteroids and intravenous immunoglobulin (IVIG) therapy has been widely used with controversy. We report a case of risperidone induced toxic epidermal necrolysis with excellent response to corticosteroid.
topic toxic epidermal necrolysis(TENS),
url https://www.journalrmc.com/index.php/JRMC/article/view/1514
work_keys_str_mv AT syednaveedalishah toxicepidermalnecrolysis
AT ifazatariq toxicepidermalnecrolysis
AT muhammadnaumanzafar toxicepidermalnecrolysis
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