title: Analysis of Ocular Manifestation and Genetic Association of Allopurinol-Induced Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis in South Korea.
abstract: OBJECTIVE
  To describe the clinical characteristics and genetic background of allopurinol-induced Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) in South Korea.
  
  
  METHODS
  This is a prospective, noncomparative case series. Visual acuity, detailed medical history, ocular findings, and systemic manifestations of 5 patients (10 eyes) with allopurinol-induced SJS/TEN were recorded. The acute ocular involvement score and the chronic ocular manifestation score were graded on scales of 0-3 and 0-39, respectively, based on severity. Human leukocyte antigen (HLA) genotyping was also performed during the hospitalization.
  
  
  RESULTS
  Three patients were diagnosed with SJS, and 2 with TEN. Mild ocular involvement with only conjunctival hyperemia (acute ocular involvement score ≤ 1) was present in all 10 eyes during the acute stage. Patients were treated with systemic steroids and topical antibiotics, steroids, and preservative-free artificial tears, with rinsing of the ocular surface, in the acute stages of SJS/TEN. In the final follow-up, none of the patients had developed severe chronic ocular complications (chronic ocular manifestation score ≤ 8), including keratinization, corneal conjunctivalization, mucocutaneous junction involvement, or symblepharon. One patient developed bilateral persistent epithelial defects 3 months after the disease onset, which healed after conservative treatment, leaving a bilateral central corneal haze. HLA genotyping showed that 4 of the 5 patients (80%) were positive for HLA-B*58:01.
  
  
  CONCLUSIONS
  Allopurinol-induced SJS/TEN might not cause serious acute or chronic complications of the ocular surface. In addition, our HLA genotyping results are consistent with previous studies reporting a strong association between HLA-B*58:01 and allopurinol-induced SJS/TEN among Koreans.
authors.affiliation: *Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju, South Korea; Departments of †Frontier Medical Science and Technology for Ophthalmology, and ‡Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan; §Department of Ophthalmology, Seoul National University College of Medicine, Seoul, South Korea; and ¶Department of Ophthalmology, Institute of Vision Research, Yonsei University College of Medicine, Seoul, South Korea.
authors.forename: Hyo Seok
authors.initials: HS
authors.lastname: Lee
authors.forename: Mayumi
authors.initials: M
authors.lastname: Ueta
authors.forename: Mee Kum
authors.initials: MK
authors.lastname: Kim
authors.forename: Kyoung Yul
authors.initials: KY
authors.lastname: Seo
authors.forename: Chie
authors.initials: C
authors.lastname: Sotozono
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kinoshita
authors.forename: Kyung Chul
authors.initials: KC
authors.lastname: Yoon
mesh_terms: D000368:Aged; D000493:Allopurinol / Q000009:adverse effects*; D044466:Asian People / Q000208:ethnology; D003229:Conjunctival Diseases / Q000139:chemically induced* / Q000188:drug therapy / Q000208:ethnology / Q000235:genetics*; D003875:Drug Eruptions / Q000188:drug therapy / Q000208:ethnology / Q000209:etiology / Q000235:genetics*; D005260:Female; D005838:Genotype; D060005:Genotyping Techniques; D005938:Glucocorticoids / Q000627:therapeutic use; D006074:Gout Suppressants / Q000009:adverse effects*; D006680:HLA Antigens / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011239:Prednisolone / Q000627:therapeutic use; D011446:Prospective Studies; D056910:Republic of Korea / Q000453:epidemiology; D013262:Stevens-Johnson Syndrome / Q000188:drug therapy / Q000208:ethnology / Q000209:etiology / Q000235:genetics*
chemical_list: D005938:Glucocorticoids; D006074:Gout Suppressants; D006680:HLA Antigens; D000493:Allopurinol; D011239:Prednisolone