Common risk allele in aromatic antiepileptic-drug induced Stevens–Johnson syndrome and toxic epidermal necrolysis in Han Chinese

2010 ◽  
Vol 11 (3) ◽  
pp. 349-356 ◽  
Author(s):  
Shuen-Iu Hung ◽  
Wen-Hung Chung ◽  
Zhi-Sheng Liu ◽  
Chien-Hsiun Chen ◽  
Mo-Song Hsih ◽  
...  
Keyword(s):  
Antiepileptic Drug ◽  
Toxic Epidermal Necrolysis ◽  
Risk Allele ◽  
Han Chinese ◽  
Stevens Johnson Syndrome ◽  
Drug Induced ◽  
Johnson Syndrome

scholarly journals HLA-A*24:02 as a common risk factor for antiepileptic drug–induced cutaneous adverse reactions

Neurology ◽  
2017 ◽  
Vol 88 (23) ◽  
pp. 2183-2191 ◽  
Author(s):  
Yi-Wu Shi ◽  
Fu-Li Min ◽  
Dong Zhou ◽  
Bin Qin ◽  
Juan Wang ◽  
...  
Keyword(s):  
Risk Factor ◽  
Antiepileptic Drug ◽  
Antiepileptic Drugs ◽  
Adverse Reactions ◽  
Han Chinese ◽  
Stevens Johnson Syndrome ◽  
Drug Induced ◽  
Maculopapular Eruption ◽  
Johnson Syndrome ◽  
Cutaneous Adverse Reactions

Objective:To investigate the involvement of human leukocyte antigen (HLA) loci in aromatic antiepileptic drug–induced cutaneous adverse reactions.Methods:A case-control study was performed to detect HLA loci involved in aromatic antiepileptic drug–induced Stevens-Johnson syndrome in a southern Han Chinese population. Between January 1, 2006, and December 31, 2015, 91 cases of Stevens-Johnson syndrome induced by aromatic antiepileptic drugs and 322 matched drug-tolerant controls were enrolled from 8 centers. Important genotypes were replicated in cases with maculopapular eruption and in the meta-analyses of data from other populations. Sequence-based typing determined the HLA-A, HLA-B, HLA-C, and HLA-DRB1 genotypes.Results:HLA-B*15:02 was confirmed as strongly associated with carbamazepine-induced Stevens-Johnson syndrome (p = 5.63 × 10−15). In addition, HLA-A*24:02 was associated significantly with Stevens-Johnson syndrome induced by the aromatic antiepileptic drugs as a group (p = 1.02 × 10−5) and by individual drugs (carbamazepine p = 0.015, lamotrigine p = 0.005, phenytoin p = 0.027). Logistic regression analysis revealed a multiplicative interaction between HLA-B*15:02 and HLA-A*24:02. Positivity for HLA-A*24:02 and/or HLA-B*15:02 showed a sensitivity of 72.5% and a specificity of 69.0%. The presence of HLA-A*24:02 in cases with maculopapular exanthema was also significantly higher than in controls (p = 0.023). Meta-analysis of data from Japan, Korea, Malaysia, Mexico, Norway, and China revealed a similar association.Conclusions:HLA-A*24:02 is a common genetic risk factor for cutaneous adverse reactions induced by aromatic antiepileptic drugs in the southern Han Chinese and possibly other ethnic populations. Pretreatment screening is recommended for people in southern China.

Specific HLA types are associated with antiepileptic drug-induced Stevens–Johnson syndrome and toxic epidermal necrolysis in Japanese subjects

2013 ◽  
Vol 14 (15) ◽  
pp. 1821-1831 ◽  
Author(s):  
Nahoko Kaniwa ◽  
Emiko Sugiyama ◽  
Yoshiro Saito ◽  
Kouichi Kurose ◽  
Keiko Maekawa ◽  
...  
Keyword(s):  
Antiepileptic Drug ◽  
Toxic Epidermal Necrolysis ◽  
Stevens Johnson Syndrome ◽  
Drug Induced ◽  
Johnson Syndrome ◽  
Japanese Subjects

scholarly journals Stevens - Johnson Syndrome and Toxic Epidermal Necrolysis; Extensive Review of Reports of Drug-Induced Etiologies, and Possible Therapeutic Modalities

2018 ◽  
Vol 6 (4) ◽  
pp. 730-738 ◽  
Author(s):  
Adegbenro Omotuyi John Fakoya ◽  
Princess Omenyi ◽  
Precious Anthony ◽  
Favour Anthony ◽  
Precious Etti ◽  
...  
Keyword(s):  
Adverse Drug Reaction ◽  
Toxic Epidermal Necrolysis ◽  
Stevens Johnson Syndrome ◽  
Hypersensitivity Reactions ◽  
Extensive Review ◽  
Drug Induced ◽  
Therapeutic Modalities ◽  
Johnson Syndrome ◽  
Mucous Membranes ◽  
Degrees Of Severity

Stevens - Johnson Syndrome and Toxic Epidermal Necrolysis are adverse hypersensitivity reactions that affect the skin and mucous membranes. They are characterised by erythematous macules and hemorrhagic erosions of the mucous membranes. Epidermal detachments of varying degrees of severity also occur in these conditions. Various aetiologies are associated with these conditions, with adverse drug reaction being the most common. Though the worldwide incidence of these conditions is recorded as low, diverse types of medication are being observed to lead to these conditions. This review compiles information on the details of Stevens-Johnson syndrome and Toxic Epidermal Necrolysis, the pathophysiology, therapeutic management, and largely considers the drug-induced etiologies associated with these conditions.

scholarly journals Causative drugs and HLA-B polymorphism in drug-induced Stevens-Johnson syndrome - toxic epidermal necrolysis: A study in five hospitals in Jakarta

2019 ◽  
Author(s):  
Anesia Tania ◽  
Evita Halim Effendi ◽  
Inge Ade Krisanti ◽  
Yulia Ariani
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Drug Eruption ◽  
Stevens Johnson Syndrome ◽  
Allele Polymorphism ◽  
Exclusion Criteria ◽  
Drug Induced ◽  
Causative Drug ◽  
Johnson Syndrome ◽  
Luminex Technology ◽  
Referral Hospitals

Stevens-Johnson syndrome and toxic epidermal necrolysis is a very rare but lifethreatening form of cutaneous drug eruption. In recent years, several countries in Asia had succeded in preventing carbamazepine induced SJS/TEN by screening for HLA-B*15:02 before prescribing carbamazepine. This study aimed to acquire data regarding causative drugs and HLA-B allele polymorphism in SJS/TEN patient in Jakarta. We acquired data from 5 referral hospitals from March 2015 to March 2017. Subject fulfilling the inclusion and exclusion criteria was interviewed and blood sample was taken for DNA extraction. The DNA was examined with PCR SSOP and Luminex technology for high resolution HLA-B typing. We studied 22 subjects. The median age was 45,4 years old (14-74). The most common causative drug in this study is carbamazepine. HLA-B*15:02 and HLAB* 18:01 were the most common allele in all subjects. HLA-B*15:02 was found in five (72%) out of seven subjects whose condition was caused by carbamazepine. The most common causative drug of SJS/TEN in five hospitals in Jakarta is carbamazepine, with five (72%) out seven subjects had HLA-B*15:02 allele.

scholarly journals Drug-induced liver injury associated with stevens-Johnson syndrome/toxic epidermal necrolysis: Patient characteristics, causes, and outcome in 36 cases

Hepatology ◽  
2015 ◽  
Vol 63 (3) ◽  
pp. 993-999 ◽  
Author(s):  
Harshad Devarbhavi ◽  
Sujata Raj ◽  
Venu H. Aradya ◽  
Vijaykumar T. Rangegowda ◽  
Girish P. Veeranna ◽  
...  
Keyword(s):  
Liver Injury ◽  
Toxic Epidermal Necrolysis ◽  
Patient Characteristics ◽  
Stevens Johnson Syndrome ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Johnson Syndrome

Drug-Induced Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis Call for Optimum Patient Stratification and Theranostics via Pharmacogenomics

2018 ◽  
Vol 19 (1) ◽  
pp. 329-353 ◽  
Author(s):  
Chonlaphat Sukasem ◽  
Theodora Katsila ◽  
Therdpong Tempark ◽  
George P. Patrinos ◽  
Wasun Chantratita
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Clinical Care ◽  
Genomic Medicine ◽  
Stevens Johnson Syndrome ◽  
Future Research ◽  
Great Promise ◽  
Patient Stratification ◽  
Clinical Implementation ◽  
Drug Induced ◽  
Johnson Syndrome

The Global Genomic Medicine Collaborative, a multinational coalition of genomic and policy experts working to implement genomics in clinical care, considers pharmacogenomics to be among the first areas in genomic medicine that can provide guidance in routine clinical practice, by linking genetic variation and drug response. Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe life-threatening reactions to medications with a high incidence worldwide. Genomic screening prior to drug administration is a key opportunity and potential paradigm for using genomic medicine to reduce morbidity and mortality and ultimately eliminate one of the most devastating adverse drug reactions. This review focuses on the current understanding of the surveillance, pathogenesis, and treatment of SJS/TEN, including the role of genomics and pharmacogenomics in the etiology, treatment, and eradication of preventable causes of drug-induced SJS/TEN. Gaps, unmet needs, and priorities for future research have been identified for the optimal management of drug-induced SJS/TEN in various ethnic populations. Pharmacogenomics holds great promise for optimal patient stratification and theranostics, yet its clinical implementation needs to be cost-effective and sustainable.

scholarly journals DRUG-INDUCED STEVENS-JOHNSON SYNDROME AND TOXIC EPIDERMAL NECROLYSIS

2016 ◽  
Vol 65 (4) ◽  
pp. 377-381
Author(s):  
Dalia Dop ◽  
◽  
Desdemona Stepan ◽  
Cristian Gheonea ◽  
Elena Carmen Niculescu ◽  
...  
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Rare Diseases ◽  
Intravenous Immunoglobulins ◽  
Stevens Johnson Syndrome ◽  
Drug Induced ◽  
Johnson Syndrome ◽  
Medical Emergencies ◽  
Steven Johnson Syndrome ◽  
Restitutio Ad Integrum

Steven-Johnson Syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare diseases that appear following the administration of risk drugs. Both are severity grades of the same condition and are considered medical emergencies, because they are potentially lethal. They are characterized by mucocutaneous tenderness, erythema, necrosis and bullous detachment similar to extended burns. We report 3 cases of SJS/TEN in which the etiology was probably drug-related (Paracetamol, Atomoxetinum, Sulfamethoxazolum + trimethoprinum), with restitutio ad integrum following the administration of intravenous immunoglobulins.

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