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Editor,—Recent research has shown that cell adhesion molecules are integral to the homing and migration of leucocytes into areas of inflammation. Soluble forms of cell adhesion molecules can be detected in the sera after shedding from activated vascular endothelium.1 2 Increased levels of soluble ICAM-1 have been found in the serum of patients with a number of autoimmune and inflammatory disorders including uveitis.3 4 We hypothesised that circulating levels of cell adhesion molecules should be higher in patients with uveitis associated with an underlying systemic disease, where there are greater amounts of activated vascular endothelium. We therefore compared the sICAM-1 levels in the sera of patients with uveitis associated with underlying systemic disease with uveitis patients with disease limited to the eye and to normal controls.
Sera were collected from 19 patients with active uveitis and from 15 age and sex matched controls and stored at −70°C. Recorded information included medical history, physical and ophthalmological examination, and diagnostic tests. Soluble ICAM-1 levels in the serum were measured at the same time using ELISA (Bender MedSystems, Vienna, Austria).
Patient characteristics including age, sex, and diagnosis are listed in Table 1. There was no statistically significant difference between patients with uveitis and controls. Ten of the 19 patients had uveitis without associated underlying systemic disease. Six of these patients had idiopathic retinal vasculitis and four had birdshot retinochoroidopathy. Nine of the 19 patients with uveitis had an underlying systemic disease. Six patients had Behçet’s disease and three patients had biopsy proved sarcoidosis. At the time that the sera were drawn, all uveitis patients had active ocular disease based on the presence of an increased vitritis, retinal vasculitis, or retinal infiltrates. The underlying systemic disease was not active in any of the patients with uveitis. Of the 19 patients with uveitis, six were treated with prednisone, one with cyclosporine, and three with prednisone and cyclosporine; nine patients were on no systemic anti-inflammatory medications.
The sICAM-1 levels (mean (SE)) were significantly higher in the sera from patients with uveitis (270.3 (23.2) ng/ml) than in normal controls (167.9 (18.9) ng/ml; p=0.002; Student’s ttest). sICAM-1 levels were also higher in uveitis patients with an associated systemic disease (315.2 (41.9) ng/ml) than in uveitis patients with no systemic disease (229.9 (16.0) ng/ml; p=0.04; Student’s t test) (Fig 1). sICAM-1 levels were higher in patients with sarcoidosis than in patients with idiopathic retinal vasculitis (p=0.0007), Behçet’s disease (p=0.005), birdshot retinochoroiditis (p=0.06), or normal controls (Fisher’s test). Serum levels of sICAM-1were slightly higher in uveitis patients receiving systemic anti-inflammatory medications (290.7 (39.0) ng/ml) than in uveitis patients without systemic treatment (247.6 (22.8) ng/ml); however, the difference was not statistically significant (p=0.3; Student’st test).
Our data show that levels of sICAM-1 were higher in the sera of patients with uveitis than in normal controls. Importantly, sICAM-1 levels were significantly higher in sera of patients with uveitis associated with an underlying systemic disease. In contrast, Zamanet al reported that patients with accompanying systemic disease had similar sICAM-1 levels to these with isolated ocular disease.3 Our study showed no significant difference in sICAM-1 levels in patients receiving or not receiving systemic anti-inflammatory medications. Droogan et al similarly reported that methylprednisolone did not affect sICAM-1 levels in patients with multiple sclerosis.5Therefore, it is unclear whether sICAM-1 levels could be used to assess or predict therapeutic effect. In summary, our data suggest that elevated sICAM-1 levels in the sera of patients with uveitis may predict the presence of an underlying systemic disease and warrant a diagnostic evaluation in these patients.
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