Bilateral macular thickening in mild unilateral anterior uveitis: is HLA-B27 involved?
1 Department of Ophthalmology, St. Olavs University Hospital, Trondheim, Norway
2 Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Trondheim, Norway
3 Department of Neurology and Clinical Neurophysiology, St. Olavs University Hospital, Trondheim, Norway
BMC Ophthalmology 2012, 12:30 doi:10.1186/1471-2415-12-30Published: 29 July 2012
Macular thickening (MT) without clinically recognized macular edema has been described in anterior uveitis (AU). Although fellow-eyes of patients have been used as controls in several studies, little is known about macular thickness in these eyes. We studied the rate and extent of MT in both AU-affected and quiescent fellow-eyes of phakic AU patients with good visual acuity (VA). We also assessed macular thickness related to HLA-B27 presence and to recurrence, since these issues have been almost unexplored by previous optical coherence tomography (OCT) studies.
Patients with AU were prospectively included and macular thickness was measured with OCT initially and on follow up. Macular thickness in patients’ affected eyes (n = 30) as well as in their quiet fellow-eyes (n = 28) was compared with eyes of age- and gender matched controls. Inter-ocular differences in macular thickness between AU affected eyes and their fellow-eyes were assessed in patients (n = 28), also in a subgroup with visual acuity ≥ 0.8 (n = 23) by one-sample Student’s t-tests. Inter-ocular differences were also assessed related to HLA-B27 presence and related to the status of current AU episode (initial or relapse).
Subclinical MT is present in both quiet fellow-eyes and AU-affected eyes of patients. MT was found in most cases of AU, even in phakic eyes with good VA. There was a larger increase in macular thickness in HLA-B27-positive than in HLA-B27-negative patients. No differences in macular thickness were found between patients with their first AU episode and patients with recurrent episodes.
MT probably reflects systemic immune-mediated response to the inflammatory disorder in AU, and it is possible that HLA-B27-related factors are involved in the pathogenesis of AU. These observations are in line with and extend the current understanding of the mechanisms behind MT in AU.