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Br J Ophthalmol 2008;92:179-181 doi:10.1136/bjo.2007.127050
  • Original Article
    • Clinical science

HLA-DR17 and Mooren’s ulcer in South India

  1. J R Zelefsky1,
  2. C J Taylor2,
  3. M Srinivasan3,
  4. S Peacock2,
  5. R S Goodman2,
  6. T Key2,
  7. P G Watson2,
  8. E T Cunningham4,5
  1. 1
    New York University School of Medicine, New York, New York, USA
  2. 2
    Tissue Typing Laboratory (Box 209), Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge, CB2 0QQ UK
  3. 3
    Aravind Eye Hospital and PG Institute of Ophthalmology, Madurai, Tamil Nadu, India
  4. 4
    The Francis I Proctor Foundation, UCSF School of Medicine, San Francisco, California, USA
  5. 5
    The Uveitis Service, California Pacific Medical Center, San Francisco, CA, and Adjunct Clinical Professor of Ophthalmology, Stanford University School of Medicine, Stanford, CA, USA
  1. Dr C J Taylor, Tissue Typing Laboratory (Box 209), Addenbrooke’s Hospital, Hills Road, Cambridge CB2 0QQ, UK; craig.taylor{at}addenbrookes.nhs.uk
  • Accepted 19 August 2007
  • Published Online First 22 January 2008

Abstract

Objective: To investigate the association between Mooren’s ulcer and human leucocyte antigen (HLA) type DR17(3) in patients from the Tamil Nadu State of South India.

Methods: Blood samples from 38 patients with Mooren’s ulcer and 45 age- and sex-matched controls were obtained prospectively. HLA-DR and HLA-DQ typing was performed by PCR using sequence-specific primers.

Results: Fifteen (40%) of the patients with Mooren’s ulcer tested positive for HLA-DR17(3) compared with seven (16%) of the controls (p = 0.01). Seventeen (45%) of the patients also tested positive for the closely linked HLA-DQ2 compared with 11 (24%) of controls (p = 0.05). When adjusted for multiplicity, the correlation between HLA-DR17(3) and Mooren’s ulcer remained significant (p = 0.03).

Conclusions: These data demonstrate an association between HLA-DR17(3) and Mooren’s ulcer in South Indian patients, supporting autoimmune theories about the pathogenesis of the disorder.

Footnotes

  • Competing interests: None declared.

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