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The association of HLA B*15:02 allele and Stevens–Johnson syndrome/toxic epidermal necrolysis induced by aromatic anticonvulsant drugs in a South Indian population
Author(s) -
Devi Keerankulangara
Publication year - 2018
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.13812
Subject(s) - toxic epidermal necrolysis , carbamazepine , phenytoin , medicine , anticonvulsant , population , allele , human leukocyte antigen , epilepsy , pharmacology , dermatology , immunology , genetics , psychiatry , biology , antigen , environmental health , gene
Background The presence of HLA ‐B*15:02 allele is considered a risk factor for development of Stevens–Johnson syndrome/toxic epidermal necrolysis ( SJS / TEN ) in patients taking aromatic anticonvulsant drugs like carbamazepine and phenytoin. The genetic association is ethnicity specific. Testing for HLA ‐B*15:02 allele is suggested as a prerequisite before starting carbamazepine in certain ethnic groups. There are only a few/no studies from south India on HLA association of SJS / TEN . Aims To identify any association between HLA ‐B*15:02 allele and SJS / TEN induced by carbamazepine/phenytoin among native population. Methods (including settings, design, and statistical analysis used) A case–control study done in a tertiary care center at Kottayam in Kerala state of south India. Cases were 12 native patients who developed SJS / TEN owing to aromatic anticonvulsant drugs (phenytoin – 8; carbamazepine – 4), and controls were 11 persons tolerant to these drugs from unrelated families of the same ethnic group. HLA ‐B typing was done by PCR SSP method. Results There was only one HLA ‐B*15:02 carrier among cases and controls. He/she had SJS / TEN induced by carbamazepine. Conclusions Association of HLA ‐B*15:02 with phenytoin‐induced SJS / TEN is rare in the population studied. The one limitation of the study was the small sample size.

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