Drusen-like Deposits in Young Adults Diagnosed With Systemic Lupus Erythematosus

Abstract

Purpose: To determine the prevalence of drusen-like deposits (DLDs) and choroidal changes in patients with systemic lupus erythematosus (SLE), with or without glomerulonephritis; and to correlate ocular findings with systemic features.

Design: Case-control study.

Methods: Sixty patients with SLE (age, 18-55 years; 30 with and 30 without SLE-related glomerulonephritis) and 60 age- and sex-matched healthy controls were enrolled. All patients underwent noninvasive multimodal imaging that included fundus photography, near-infrared reflectance, blue autofluorescence, blue reflectance, and spectral-domain optical coherence tomography (SDOCT). Images were analyzed for the prevalence of DLDs. Distribution, size, and number of DLDs were measured. Correlations between ocular findings and systemic features were analyzed. Subfoveal choroidal thickness (SCT) was measured using the SDOCT.

Results: Drusen-like deposits were detected in 40% of SLE subjects and 3.33% of controls (P < .0001). Compared with other techniques, SDOCT detected the largest number of affected subjects. In eyes with DLDs, small, medium, and large lesions were found in 75%, 50%, and 42% of cases, respectively. Drusen-like deposits were located in the nasal, temporal, inferior, superior, and central regions of the posterior pole in 83%, 75%, 67%, 54%, and 25% of eyes, respectively. The prevalence of DLDs in patients with SLE was similar regardless of renal involvement, but patients with glomerulonephritis had more DLDs per eye, larger deposits, and DLDs in >3 quadrants (P < .001, P = .03, P = .009, respectively). Subfoveal choroidal thickness was greater in patients with SLE (P = .002).

Conclusions: Drusen-like deposits in patients with SLE were independent of renal disease and were best detected with SDOCT. Lupus-related glomerulonephritis was associated with more fundus abnormalities and a screening SDOCT should be considered in all patients with SLE. Drusen-like deposits in the absence of glomerulonephritis may support the recent proposal that complement alteration is the primary cause of these lesions.