Fulminant Liver Failure After Vancomycin in a Sulfasalazine-Induced DRESS Syndrome: Fatal Recurrence After Liver Transplantation

Mennicke, M; Zawodniak, Anna; Keller, M.; Wilkens, Ludwig; Yawalkar, Nikhil; Stickel, Felix; Keogh, Anne; Inderbitzin, Devdas Thomas; Candinas, Daniel; Pichler, Werner J.

doi:10.1111/j.1600-6143.2009.02788.x

Cited by 105 publications

(74 citation statements)

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“…Histological examination of inflamed liver tissue from a patient with a sulfasalazine-induced drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome revealed infiltration of granzyme B secreting T lymphocytes. 69 This finding supports a direct role of drugresponsive T lymphocytes in the pathogenesis of DILI.…”

Section: Immunologic Basis For the Pathogenesis Of Dilisupporting

confidence: 73%

Update on Advances in Research on Idiosyncratic Drug-Induced Liver Injury

Kim

Naisbitt

2016

Allergy Asthma Immunol Res

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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.Drug-induced liver injury (DILI) is a major concern for public health, as well as for drug development in the pharmaceutical industry, since it can cause liver failure and lead to drug withdrawal from the market and black box warnings. Thus, it is important to identify biomarkers for early prediction to increase our understanding of mechanisms underlying DILI that will ultimately aid in the exploration of novel therapeutic strategies to prevent or manage DILI. DILI can be subdivided into 'intrinsic' and 'idiosyncratic' categories, although the validity of this classification remains controversial. Idiosyncratic DILI occurs in a minority of susceptible individuals with a prolonged latency, while intrinsic DILI results from drug-induced direct hepatotoxicity over the course of a few days. The rare occurrence of idiosyncratic DILI requires multicenter collaborative investigations and phenotype standardization. Recent progress in research on idiosyncratic DILI is based on key developments in 3 areas: (1) newly developed highthroughput genotyping across the whole genome allowing for the identification of genetic susceptibility markers, (2) new mechanistic concepts on the pathogenesis of DILI revealing a key role of drug-responsive T lymphocytes in the immunological response, and (3) broad multidisciplinary approaches using different platform "-omics" technologies that have identified novel biomarkers for the prediction of DILI. An association of a specific human leukocyte antigen (HLA) allele with DILI has been reported for several drugs. HLA-restricted T-cell immune responses have also been investigated using lymphocytes and T-cell clones isolated from patients. A microRNA, miR-122, has been discovered as a promising biomarker for the early prediction of DILI. In this review, we summarize recent advances in research on idiosyncratic DILI with an understanding of the key role of adaptive immune systems.

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Section: Immunologic Basis For the Pathogenesis Of Dilisupporting

confidence: 73%

Update on Advances in Research on Idiosyncratic Drug-Induced Liver Injury

Kim

Naisbitt

2016

Allergy Asthma Immunol Res

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“…More recently, histological examination of an inflamed liver from a single patient exposed to sulfasalazine revealed an infiltration of granzyme B secreting T-lymphocytes. 9 The discovery of HLA alleles as risk factors for DILI (e.g., flucloxacillin [B*57:01], 10 ximelagatran [DRB1*07:01], 11 lumiracoxib [DRB1*15:01] 12 ) is supportive of an immune mechanism; however, biological data showing HLA restriction of drug-responsive cytotoxic T cells is lacking. The strength of the association described for flucloxacillin-approximately 85% of cases carry at least one copy of HLA-B*57:01-prompted us to investigate (1) the cellular response in patients with flucloxacillin-induced liver injury, and (2) whether flucloxacillin activates naive CD8þ T cells from HLA-B*57:01-positive volunteers.…”

mentioning

confidence: 99%

Human leukocyte antigen (HLA)-B*57:01-restricted activation of drug-specific T cells provides the immunological basis for flucloxacillin-induced liver injury

et al. 2013

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“…Sulfasalazine bağlı İİHS ve DRESS, geç dönemde akut interstisyel nefrit ve karaciğer transplantasyonu ile sonuçlanan karaciğer yetmezliğine neden olabilir. Hatta karaciğer transplantasyonu sonrası karaciğer yetmezliği tablosu tekrarlayan bir olgu bildirilmiştir [10][11][12] . İlaç reaksiyonlarında klinik görünüm patogenezde daha baskın olan mekanizmayı yansıtmaktadır.…”

Section: Discussionunclassified

Sulfasalazin İle Tetiklenen İlaçla İlişkili Hipersensitivite Sendromu

Saral¹,

Akay²,

Şanlı³

2013

Turkderm

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Türk derm-De ri Has ta lık la rı ve Fren gi Ar şi vi Der gi si, Ga le nos Ya yı ne vi ta ra f›n dan ba s›l m›fl t›r. Turk derm-Arc hi ves of the Tur kish Der ma to logy and Ve ne ro logy, pub lis hed by Ga le nos Pub lis hing. Özetİlaçla ilişkili hipersensitivite sendromu (İİHS), ilaç reaksiyonları arasında en tehlikelilerinden biridir. Sistemik organ tutulumları bu reaksiyonun mortalite ve morbiditesini arttırmaktadır. Lezyonlar en sık makülopapüler döküntü şeklinde ortaya çıkmakla birlikte, lezyon morfolojisi farklılık gösterebilir. Çoğunlukla aromatik antikonvulzanlarla ortaya çıkar. Ancak başka ilaçların da bu ilaç reaksiyonu patogenezinde rol oynayabileceği unutulmamalıdır. Erken tanı tedavide en önemli basamaktır. Burada sulfasalazin ile tetiklenen ve klinik olarak makülopapüler döküntüye eşlik eden püstüler lezyonlarla prezente olan bir İİHS olgusu sunmaktayız. Sum maryDrug-induced hypersensitivity syndrome (DIHS) is one of the most dangerous drug reactions. Mortality and morbidity is increased by consequent systemic organ involvement. Maculopapular eruptions are the most common lesions accompanying DIHS, however, the morphology of skin lesions may vary. The most common cause of DIHS is the use of aromatic anticonvulsant drugs. However, one must not forget that other drugs may also cause DIHS. Early recognition of the condition is the most important step in the treatment. Herein, we present a case of DIHS triggered by sulphasalazine and associated with pustular eruption and maculopapular eruption. (Turkderm 2013; 47: 123-5)

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Fulminant Liver Failure After Vancomycin in a Sulfasalazine-Induced DRESS Syndrome: Fatal Recurrence After Liver Transplantation

Cited by 105 publications

References 20 publications

Update on Advances in Research on Idiosyncratic Drug-Induced Liver Injury

Update on Advances in Research on Idiosyncratic Drug-Induced Liver Injury

Human leukocyte antigen (HLA)-B*57:01-restricted activation of drug-specific T cells provides the immunological basis for flucloxacillin-induced liver injury

Sulfasalazin İle Tetiklenen İlaçla İlişkili Hipersensitivite Sendromu

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