© 2003 BMJ Publishing Group
LETTER
Mooren’s ulcer resolved with campath-1H
Department of Ophthalmology, Aberdeen Royal Infirmary, Aberdeen, UK
Correspondence to:
Correspondence to:
Augusto Azuara Blanco, MD PhD, Ophthalmology Department, Aberdeen Royal Infirmary, The Eye Clinic, Foresterhill, Aberdeen AB25 2ZN, UK;
aazblanco@aol.com
Accepted 13 December 2002
Keywords: Mooren’s ulcer; campath-1H
| The first 150 words of the full text of this article appear below. |
Mooren’s ulcer is a rare idiopathic peripheral ulcerative keratitis. The diagnosis is usually based on characteristic clinical features and absence of other causes of peripheral keratitis. The clinical course can be unremitting, particularly in bilateral disease, occasionally leading to total loss of stroma.1,2
An autoimmune process is recognised as being central to the pathogenesis.
Calgranulin-C (CaGC), produced by granulocytes and also expressed by keratocytes, appears to be the target protein for the autoimmune response that leads to Mooren’s ulcer. Previous corneal trauma2 and a higher prevalence of HLA class II subtypes have been associated with Mooren’s ulcer.
The disease responds to immunosuppression with variable success. Surgical treatments such as conjunctival recession have been proposed. Campath-1H is a humanised lymphocytotoxic monoclonal antibody (mAb) that targets the CD52 antigen on T lymphocytes. Successful mAb therapy using campath-1H has been reported in serious ophthalmic inflammatory conditions that were unresponsive to maximum conventional immunosuppression.1–5
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