A European study of HLA-B in Stevens–Johnson syndrome and toxic epidermal necrolysis related to five high-risk drugs

@article{Lonjou2008AES,
  title={A European study of HLA-B in Stevens–Johnson syndrome and toxic epidermal necrolysis related to five high-risk drugs},
  author={Christine Lonjou and Nicolas Borot and Peggy Sekula and Neil Ledger and Laure Thomas and Sima Halevy and Luigi Naldi and Jan-Nico Bouwes-Bavinck and Alexis Sidoroff and Claudia de Toma and Martin Schumacher and Jean Claude Roujeau and Alain Hovnanian and Maja Mockenhaupt},
  journal={Pharmacogenetics and Genomics},
  year={2008},
  volume={18},
  pages={99-107}
}
BACKGROUND Stevens-Johnson syndrome (SJS) and its severe form, toxic epidermal necrolysis (TEN), are rare but life-threatening cutaneous adverse reactions to drugs, especially to allopurinol, carbamazepine, lamotrigine, phenobarbital, phenytoine, sulfamethoxazole, oxicam and nevirapine. [] Key MethodMETHODS HLA-B genotyping was performed on 150 patients included in a European study (RegiSCAR) of SJS and TEN.
Specific HLA types are associated with antiepileptic drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Japanese subjects.
TLDR
The data suggest that HLA-A*02:07 and Hla-B*51:01 are potential biomarkers for zonisamide- and phenobarbital-induced SJS/TEN, respectively, in Japanese individuals.
Carbamazepine-induced Stevens-Johnson syndrome/toxic epidermal necrolysis overlap in a Filipino with positive HLA-B75 serotype
TLDR
A case of Filipino with SJS/TEN overlap probably induced by carbamazepine is reported, and the patient tested positive for the HLA-B75 serotype, suggesting that carbamazepsine-induced SJS-TEN may be serotype specific.
HLA-B locus in Japanese patients with anti-epileptics and allopurinol-related Stevens-Johnson syndrome and toxic epidermal necrolysis.
TLDR
While HLA-B*1502 is unlikely to be associated with carbamazepine-related or aromatic anti-epileptic agent-related SJS/TEN in Japanese, HLA*5801 was significantly associated with allopurinol- related S JS/T EN in Japanese.
Strong association between HLA-B*5801 and allopurinol-induced Stevens–Johnson syndrome and toxic epidermal necrolysis in a Thai population
TLDR
It is suggested that HLA-B*5801 is a valid genetic marker for screening Thai individuals who may be at risk for allopurinol-induced life-threatening SJS and TEN.
Common risk allele in aromatic antiepileptic-drug induced Stevens-Johnson syndrome and toxic epidermal necrolysis in Han Chinese.
TLDR
OXC, PHT and LTG, which possess an aromatic ring just as CBZ does, when causing SJS/TEN, share a common risk allele, suggesting that aromatic antiepileptic drugs, including CBZ, OXC and PHT, should be avoided in the B*1502 carrier and caution should also be exercised for LTG.
Association between HLA-B*5901 and methazolamide-induced Stevens-Johnson syndrome/toxic epidermal necrolysis: a systematic review and meta-analysis
TLDR
Genetic screening prior to methazolamide therapy in Asian populations is warranted, since HLA-B*5901 and Hla-B-Cw*0102 haplotype are associated with methzolamide-induced SJS/TEN.
HLA-B*5801 Should Be Used to Screen for Risk of Stevens-Johnson Syndrome in Family Members of Han Chinese Patients Commencing Allopurinol Therapy
TLDR
An observational study in the immediate family members of a male patient who experienced allopurinol-induced SJS in 1997 (index case) and the clinical utility of HLA-B*5801 is unclear is unclear.
Association of HLA-B*5801 allele and allopurinol-induced stevens johnson syndrome and toxic epidermal necrolysis: a systematic review and meta-analysis
TLDR
A strong and significant association between HLA-B* 5801 and allopurinol-induced SJS/TEN is found and HLA*5801 allele screening may be considered in patients who will be treated with allopURinol.
HLA‐B*58:01 is strongly associated with allopurinol‐induced severe cutaneous adverse reactions in Han Chinese patients: a multicentre retrospective case–control clinical study
TLDR
A multicentre retrospective case–control study of Han Chinese patients to elucidate the relationship between allopurinol-induced SCARs and HLA-B alleles and found that SJS and TEN are more severe reactions and commonly overlap in the clinic.
A study of HLA class I and class II 4‐digit allele level in Stevens–Johnson syndrome and toxic epidermal necrolysis
TLDR
HLA molecules behave as a strong risk factor for SCAR‐related to allopurinol even when a limited number of patients are considered, and haplotype analysis indicated that B*58:01, DRB 1*13:02 and DRB1*15:02 alleles, that in a single allele analysis lost statistical significance after P correction, may still confer susceptibility.
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References

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A marker for Stevens-Johnson syndrome …: ethnicity matters
TLDR
Preliminary results from a European study of 12 carbamazepine-induced SJS/TEN cases (RegiSCAR) show that although the HLA region may contain important genes for SJS, the Hla-B*1502 allele is not a universal marker for this disease and that ethnicity matters.
Stevens-Johnson syndrome and toxic epidermal necrolysis: assessment of medication risks with emphasis on recently marketed drugs. The EuroSCAR-study.
TLDR
A multinational case-control study conducted in Europe between 1997 and 2001 evaluated the risk of medications to induce SCAR, finding that many cases were still related to a few "old" drugs with a known high risk, and risk was restricted to the first few weeks of drug intake.
HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol.
TLDR
The results indicated that allopurinol-SCAR is strongly associated with a genetic predisposition in Han Chinese, and in particular, HLA-B*5801 allele is an important genetic risk factor for this life-threatening condition.
Genetic susceptibility to carbamazepine-induced cutaneous adverse drug reactions
TLDR
The data suggest that HLA-B*1502 could contribute to the pathogenesis ofCBZ-SJS/TEN, and that genetic susceptibility to CBZ-induced cADRs is phenotype-specific.
Medication use and the risk of Stevens-Johnson syndrome or toxic epidermal necrolysis
TLDR
Risks were increased for trimethoprim–sulfamethoxazole and other sulfonamide antibiotics, chlormezanone, quinolones, and aminopenicillins among drugs usually used for short periods.
Nevirapine and the risk of Stevens–Johnson syndrome or toxic epidermal necrolysis
TLDR
In European countries the risk of SJS or TEN in the context of HIV infection appears to be associated with nevirapine, and it is suggested discontinuation of the drug as soon as any eruption occurs.
Medical genetics: A marker for Stevens–Johnson syndrome
TLDR
It is shown that there is a strong association in Han Chinese between a genetic marker, the human leukocyte antigen HLA–B*1502, and Stevens–Johnson syndrome induced by carbamazepine, a drug commonly prescribed for the treatment of seizures.
HLA phenotypes and bullous cutaneous reactions to drugs.
Drug induced toxic epidermal necrolysis and Stevens-Johnson syndrome are weakly associated with HLA-B12. Among patients reacting to a given drug we observed stronger links, especially for HLA-A29;
HLA-B locus in Caucasian patients with carbamazepine hypersensitivity.
TLDR
HLA-B*1502 does not seem to be a marker for all forms of CBZ-induced hypersensitivity in a Caucasian population, and HLA- B*0702 allele may protect against severe CBZ hypersensitivity but warrants further study.
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