Visual improvement with corticosteroid therapy in giant cell arteritis. Report of a large study and review of literature.

Abstract

OBJECTIVES (1) To report the incidence and extent of visual improvement achieved by high-dose systemic corticosteroid treatment in eyes with visual loss due to giant-cell arteritis (GCA). (2) To understand the cause of the discrepancies between visual improvement revealed by routine visual acuity (VA) and by the central visual field in kinetic perimetry. (3) To review critically the contradictory literature on the effectiveness of corticosteroid therapy on visual recovery in GCA and to attempt to reconcile differences in the reported results. METHODS Clinical data were collected systematically on 84 consecutive patients (114 eyes) with visual loss, all of whom had GCA confirmed by temporal artery biopsy and treated by us with high-dose systemic corticosteroid therapy. The patients were treated between 1974 and 1999 and data were compiled retrospectively. All patients underwent a detailed visual and ophthalmic evaluation at the initial visit and at every follow-up. This included visual field testing (with a Goldmann perimeter). All were treated with systemic corticosteroid therapy (intravenous followed by oral in 41 patients and oral only in 43 patients). RESULTS Visual loss was due to anterior ischaemic optic neuropathy (91%), central retinal artery occlusion (10.5%), cilioretinal artery occlusion (10%), and/or posterior ischaemic optic neuropathy (4%), either alone or in different combinations. Improvement in both VA (>or= 2 lines) and central visual field was found in only five (4%) eyes of five patients (three treated with intravenous and two with oral steroid therapy). Improvement in VA >or= 2 lines but not in the central visual field was found in seven eyes (in six patients). Visual improvement was seen in 7% of 41 patients treated initially with intravenous steroids versus 5% (p = 0.672) of 43 patients treated with oral steroids only. Comparison of patients with visual improvement in both VA and fields versus those with no improvement suggested a shorter interval (p = 0.065) between onset of visual loss and start of therapy in the improved patients. CONCLUSIONS In our study, only 4% of eyes with visual loss due to GCA improved, as judged by improvement in both VA and central visual field (by kinetic perimetry and Amsler grid). The data also suggest that there is a better (p = 0.065) chance of visual improvement with early diagnosis and immediate start of steroid therapy. Improvement in VA without associated improvement in the central visual field or Amsler grid may simply represent a learned ability to fixate eccentrically with more effective use of remaining vision: this factor could help explain a number of reported cases in the literature of improved VA after steroid treatment for GCA. To prevent further visual loss in either eye and for management of systemic manifestations of GCA, all patients must be treated on a long-term basis with adequate amounts of systemic corticosteroids.