drug-induced delayed multiorgan hypersensitivity syndrome (2023)

Klimas, N., Quintanilla-Dieck, J.(2015).Drug-induced delayed multiorgan hypersensitivity syndrome. EmSkin eruptions caused by drugs: diagnosis, histopathology and treatment(pp. 271-279). Springer-Verlag Londres Ltda.https://doi.org/10.1007/978-1-4471-6729-7_25

Drug-induced delayed multiorgan hypersensitivity syndrome./ Klimas, Natascha; Quintanilla-Dieck, Josephine; Vandergrif, Travis Vandergrif.

Drug eruptions: diagnosis, histopathology and treatment. Springer-Verlag London Ltd, 2015. p. 271-279.

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Klimas, N., Quintanilla-Dieck, J.2015,Drug-induced delayed multiorgan hypersensitivity syndrome. EmDrug eruptions: diagnosis, histopathology and treatment.Springer-Verlag London Ltd, S. 271-279.https://doi.org/10.1007/978-1-4471-6729-7_25

Klimas N, Quintanilla-Dieck J, Vandergriff-TV.Drug-induced delayed multiorgan hypersensitivity syndrome. For drug rashes: diagnosis, histopathology and therapy. Springer Verlag London Ltd. 2015. p. 271-279 doi: 10.1007/978-1-4471-6729-7_25

Klimas, Natascha; Quintanilla-Dieck, Josephine; Vandergrif, Travis Vandergrif. /Drug-induced delayed multiorgan hypersensitivity syndrome. Drug eruptions: diagnosis, histopathology and treatment. Springer-Verlag London Ltd, 2015. pp. 271-279

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title="Drug-Induced Delayed Multiorgan Hypersensitivity Syndrome",

abstract = "Drug-Induced Delayed Multiorgan Hypersensitivity Syndrome (DIDMOHS), also known as Drug Reaction (or Rash) with Eosinophilia and Systemic Symptoms (DRESS), Drug-Induced Hypersensitivity Syndrome (DIHS) or Anticonvulsant Drug-Induced Hypersensitivity Syndrome such as carbamazepine, phenytoin, lamotrigine, and phenobarbital, as well as anticonvulsants such as carbamazepine, phenytoin, lamotrigine, and phenobarbital, such as allopurinol and sulfonamides, are the most common causes of DIDMOHS drug detoxification, and herpes virus reactivation plays a key role in the pathogenesis of DIDMOHS Leukocyte antigen (HLA) haplotypes also contribute Initial skin findings usually include a morbilliform rash characterized by diffuse, erythematous, and pruritic s characterized on the upper face, trunk, and upper extremities with posterior extension to the lower extremities es, rapid confluence and progression are characteristic. DIDMOHS commonly affects the lymphatic, hematologic and hepatic systems. Renal, pulmonary and cardiac dysfunctions can also occur. Early detection and diagnosis, with immediate discontinuation of the offending drug, are of paramount importance. Corticosteroid therapy is widely recognized as the cornerstone of the treatment of DIDMOHS. In the future, haplotyping and assays such as the lymphocyte transformation test (LTT) will help in the primary prevention and diagnosis of DIDMOHS. New steroid-sparing immunomodulatory agents also have significant therapeutic potential.",

keywords="Corticosteroids, Cytochrome P450, Drug allergy, Drug rash, Drug reaction with eosinophilia and systemic symptoms (DRESS), Drug-induced multiorgan delayed hypersensitivity syndrome (DIDMOHS), Drug-induced hypersensitivity syndrome (DIHS), Eosinophilia, Erythrodermic herpesvirus, human leukocyte antigen (HLA) haplotype,

autor = "Natasha Klimas e Josephine Quintanilla-Dieck e Vandergriff, {Travis Vandergrif}",

again="2015",

month = August,

Label = "21",

doi = "10.1007/978-1-4471-6729-7_25",

language = "English (United States)",

isbn = "9781447167297",

pages="271--279",

booktitle = "Drug eruptions: diagnosis, histopathology and treatment",

editor = "Springer-Verlag London Ltd",

}

YOU-CHAP

T1 - Drug-induced delayed multiorgan hypersensitivity syndrome

AU-Klimas, Natasha

AU - Quintanilla-Dieck, Josephine

Australia - Vandergriff, Travis Vandergrif

PJ - 21/08/2015

Update 1 - 2015/08/21

N2: Drug-induced delayed multiorgan hypersensitivity syndrome (DIDMOHS), also known as drug reaction (or rash) with eosinophilia and systemic symptoms (DRESS), drug-induced hypersensitivity syndrome (DIHS), or drug hypersensitivity syndrome (DHS) . a rare and potentially fatal drug-induced hypersensitivity reaction characterized by rash, fever, lymphadenopathy, haematological abnormalities, and visceral manifestations. Anticonvulsants such as carbamazepine, phenytoin, lamotrigine, and phenobarbital, as well as allopurinol and sulfonamides, are the most common causes of DIDMOHS. Impaired drug detoxification and herpesvirus reactivation play a key role in the pathogenesis of DIDMOHS. Human leukocyte antigen (HLA) haplotypes also contribute. Initial skin findings usually include a morbilliform rash characterized by diffuse, erythematous, itchy patches on the face, upper trunk, and upper extremities, which then spread to the lower extremities. Rapid confluence and progression are characteristic. DIDMOHS commonly affects the lymphatic, hematologic and hepatic systems. Renal, pulmonary and cardiac dysfunctions can also occur. Early detection and diagnosis, with immediate discontinuation of the offending drug, are of paramount importance. Corticosteroid therapy is widely recognized as the cornerstone of the treatment of DIDMOHS. In the future, haplotyping and assays such as the lymphocyte transformation test (LTT) will help in the primary prevention and diagnosis of DIDMOHS. New steroid-sparing immunomodulatory agents also have significant therapeutic potential.

AB: Drug-induced delayed multiorgan hypersensitivity syndrome (DIDMOHS), also known as drug reaction (or rash) with eosinophilia and systemic symptoms (DRESS), drug-induced hypersensitivity syndrome (DIHS), or drug hypersensitivity syndrome (DHS) . a rare and potentially fatal drug-induced hypersensitivity reaction characterized by rash, fever, lymphadenopathy, haematological abnormalities, and visceral manifestations. Anticonvulsants such as carbamazepine, phenytoin, lamotrigine, and phenobarbital, as well as allopurinol and sulfonamides, are the most common causes of DIDMOHS. Impaired drug detoxification and herpesvirus reactivation play a key role in the pathogenesis of DIDMOHS. Human leukocyte antigen (HLA) haplotypes also contribute. Initial skin findings usually include a morbilliform rash characterized by diffuse, erythematous, itchy patches on the face, upper trunk, and upper extremities, which then spread to the lower extremities. Rapid confluence and progression are characteristic. DIDMOHS commonly affects the lymphatic, hematologic and hepatic systems. Renal, pulmonary and cardiac dysfunctions can also occur. Early detection and diagnosis, with immediate discontinuation of the offending drug, are of paramount importance. Corticosteroid therapy is widely recognized as the cornerstone of the treatment of DIDMOHS. In the future, haplotyping and assays such as the lymphocyte transformation test (LTT) will help in the primary prevention and diagnosis of DIDMOHS. New steroid-sparing immunomodulatory agents also have significant therapeutic potential.

KW - Corticosteroids

KW - Citocromo P450

KW - drug allergy

KW - drug rash

KW - Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

KW - Delayed Drug-Induced Multiple Organ Hypersensitivity Syndrome (DIDMOHS)

KW - Drug-Induced Hypersensitivity Syndrome (DIHS)

KW - Eosinophilia

KW – Erythroderma-Herpesvirus

KW - Human leukocyte antigen (HLA) haplotype.

URL: http://www.scopus.com/inward/record.url?scp=84955364818&partnerID=8YFLogxK

URL: http://www.scopus.com/inward/citedby.url?scp=84955364818&partnerID=8YFLogxK

U2-10.1007/978-1-4471-6729-7_25

DO - 10.1007/978-1-4471-6729-7_25

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SN - 9781447167297

SN - 9781447167280

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BT - Drug eruptions: diagnosis, histopathology and therapy

PB - Springer-Verlag Londres Ltda

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