Clinical features of and genetic predisposition to drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a single Korean tertiary institution patients - Investigating the relation between the HLA-B∗4403 allele and lamotrigine

Hye Jung Park, Sung Ryeol Kim, Dong Woo Leem, Il Joo Moon, Beom Seok Koh, Kyung Hee Park, Jungwon Park, Jae Hyun Lee

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Abstract

Purpose: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but fatal adverse mucocutaneous reactions to certain drugs. Recent studies suggest that ethnicity and genetic predisposition may play a crucial role in the manifestation of the reaction. In this study, we described the role of human leukocyte antigen (HLA)-B alleles in the development of clinical characteristics and treatment outcomes of SJS/TEN in a single Korean tertiary hospital. Methods: We retrospectively reviewed the medical records (from March 1, 2010 to February 28, 2014) of 30 patients diagnosed with SJS and/or TEN. Results: The main causative drugs were anticonvulsants (26.7 %) and allopurinol (26.7 %), followed by antibiotics (16.7 %), acetazolamide (10.0 %), acetaminophen (10.0 %), and herbal medication (6.7 %). The mean latencies of these drugs were variable. Liver damage was the most common symptom (observed in 63.3 % of the patients). Of the five patients with lamotrigine-induced SJS/TEN, three expressed the HLA-B∗4403 allele (60.0 %). Of the seven patients with allopurinol-induced SJS/TEN, five expressed the HLA-B∗5801 allele (71.4 %). Conclusions: The major SJS/TEN-inducing drugs were found to be allopurinol and anticonvulsants (such as lamotrigine). We speculated that Korean individuals expressing the HLA-B∗4403 allele may be highly susceptible to lamotrigine-induced SJS/TEN.

Original languageEnglish
Pages (from-to)35-41
Number of pages7
JournalEuropean Journal of Clinical Pharmacology
Volume71
Issue number1
DOIs
Publication statusPublished - 2015 Jan 1

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Stevens-Johnson Syndrome
Genetic Predisposition to Disease
HLA Antigens
Alleles
Allopurinol
Anticonvulsants
Pharmaceutical Preparations
Acetazolamide
Acetaminophen
lamotrigine
Tertiary Care Centers
Medical Records
Anti-Bacterial Agents
Liver

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmacology (medical)

Cite this

@article{01046c846a1748e19e2f30878e78bbd4,
title = "Clinical features of and genetic predisposition to drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a single Korean tertiary institution patients - Investigating the relation between the HLA-B∗4403 allele and lamotrigine",
abstract = "Purpose: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but fatal adverse mucocutaneous reactions to certain drugs. Recent studies suggest that ethnicity and genetic predisposition may play a crucial role in the manifestation of the reaction. In this study, we described the role of human leukocyte antigen (HLA)-B alleles in the development of clinical characteristics and treatment outcomes of SJS/TEN in a single Korean tertiary hospital. Methods: We retrospectively reviewed the medical records (from March 1, 2010 to February 28, 2014) of 30 patients diagnosed with SJS and/or TEN. Results: The main causative drugs were anticonvulsants (26.7 {\%}) and allopurinol (26.7 {\%}), followed by antibiotics (16.7 {\%}), acetazolamide (10.0 {\%}), acetaminophen (10.0 {\%}), and herbal medication (6.7 {\%}). The mean latencies of these drugs were variable. Liver damage was the most common symptom (observed in 63.3 {\%} of the patients). Of the five patients with lamotrigine-induced SJS/TEN, three expressed the HLA-B∗4403 allele (60.0 {\%}). Of the seven patients with allopurinol-induced SJS/TEN, five expressed the HLA-B∗5801 allele (71.4 {\%}). Conclusions: The major SJS/TEN-inducing drugs were found to be allopurinol and anticonvulsants (such as lamotrigine). We speculated that Korean individuals expressing the HLA-B∗4403 allele may be highly susceptible to lamotrigine-induced SJS/TEN.",
author = "Park, {Hye Jung} and Kim, {Sung Ryeol} and Leem, {Dong Woo} and Moon, {Il Joo} and Koh, {Beom Seok} and Park, {Kyung Hee} and Jungwon Park and Lee, {Jae Hyun}",
year = "2015",
month = "1",
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doi = "10.1007/s00228-014-1764-0",
language = "English",
volume = "71",
pages = "35--41",
journal = "European Journal of Clinical Pharmacology",
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Clinical features of and genetic predisposition to drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a single Korean tertiary institution patients - Investigating the relation between the HLA-B∗4403 allele and lamotrigine. / Park, Hye Jung; Kim, Sung Ryeol; Leem, Dong Woo; Moon, Il Joo; Koh, Beom Seok; Park, Kyung Hee; Park, Jungwon; Lee, Jae Hyun.

In: European Journal of Clinical Pharmacology, Vol. 71, No. 1, 01.01.2015, p. 35-41.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Clinical features of and genetic predisposition to drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a single Korean tertiary institution patients - Investigating the relation between the HLA-B∗4403 allele and lamotrigine

AU - Park, Hye Jung

AU - Kim, Sung Ryeol

AU - Leem, Dong Woo

AU - Moon, Il Joo

AU - Koh, Beom Seok

AU - Park, Kyung Hee

AU - Park, Jungwon

AU - Lee, Jae Hyun

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Purpose: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but fatal adverse mucocutaneous reactions to certain drugs. Recent studies suggest that ethnicity and genetic predisposition may play a crucial role in the manifestation of the reaction. In this study, we described the role of human leukocyte antigen (HLA)-B alleles in the development of clinical characteristics and treatment outcomes of SJS/TEN in a single Korean tertiary hospital. Methods: We retrospectively reviewed the medical records (from March 1, 2010 to February 28, 2014) of 30 patients diagnosed with SJS and/or TEN. Results: The main causative drugs were anticonvulsants (26.7 %) and allopurinol (26.7 %), followed by antibiotics (16.7 %), acetazolamide (10.0 %), acetaminophen (10.0 %), and herbal medication (6.7 %). The mean latencies of these drugs were variable. Liver damage was the most common symptom (observed in 63.3 % of the patients). Of the five patients with lamotrigine-induced SJS/TEN, three expressed the HLA-B∗4403 allele (60.0 %). Of the seven patients with allopurinol-induced SJS/TEN, five expressed the HLA-B∗5801 allele (71.4 %). Conclusions: The major SJS/TEN-inducing drugs were found to be allopurinol and anticonvulsants (such as lamotrigine). We speculated that Korean individuals expressing the HLA-B∗4403 allele may be highly susceptible to lamotrigine-induced SJS/TEN.

AB - Purpose: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but fatal adverse mucocutaneous reactions to certain drugs. Recent studies suggest that ethnicity and genetic predisposition may play a crucial role in the manifestation of the reaction. In this study, we described the role of human leukocyte antigen (HLA)-B alleles in the development of clinical characteristics and treatment outcomes of SJS/TEN in a single Korean tertiary hospital. Methods: We retrospectively reviewed the medical records (from March 1, 2010 to February 28, 2014) of 30 patients diagnosed with SJS and/or TEN. Results: The main causative drugs were anticonvulsants (26.7 %) and allopurinol (26.7 %), followed by antibiotics (16.7 %), acetazolamide (10.0 %), acetaminophen (10.0 %), and herbal medication (6.7 %). The mean latencies of these drugs were variable. Liver damage was the most common symptom (observed in 63.3 % of the patients). Of the five patients with lamotrigine-induced SJS/TEN, three expressed the HLA-B∗4403 allele (60.0 %). Of the seven patients with allopurinol-induced SJS/TEN, five expressed the HLA-B∗5801 allele (71.4 %). Conclusions: The major SJS/TEN-inducing drugs were found to be allopurinol and anticonvulsants (such as lamotrigine). We speculated that Korean individuals expressing the HLA-B∗4403 allele may be highly susceptible to lamotrigine-induced SJS/TEN.

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JO - European Journal of Clinical Pharmacology

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