Suprachoroidal effusion with angle-closure glaucoma in a patient with active systemic lupus erythematosus: a case report

BACKGROUND: Systemic lupus erythematosus (SLE) uncommonly presents with ocular manifestations as the initial feature. Uveal effusion syndrome (UES) is typically described in eyes with nanophthalmos and scleral abnormalities. This case is noteworthy for two reasons. First, the patient had normal axial length and no marked diffuse scleral thickening on ultrasound biomicroscopy(UBM), with a massive annular uveal/suprachoroidal effusion resembling a type III UES-like phenotype; however, concurrent active SLE, hypoalbuminaemia and polyserositis suggested a secondary systemic trigger. Second, ocular recovery appeared to accelerate after periocular corticosteroid therapy, despite inadequate response to systemic immunosuppression. CASE PRESENTATION: A 38-year-old woman presented with three days of bilateral ocular pain and visual deterioration. Initial examination revealed intraocular pressure of 38.7 mmHg in the right eye and 32.7 mmHg in the left, shallow anterior chambers, and axial length of 21.85 mm bilaterally. Bilateral angle-closure glaucoma was diagnosed, and laser peripheral iridotomy was performed along with topical antiglaucoma agents and corticosteroids. One week later, systemic symptoms including fever and polyarthralgia developed. Laboratory tests showed strongly positive autoimmune markers (ANA: antinuclear antibody, ANSA༚anti-nucleosome antibody, ARPA༚anti-ribosomal P protein antibody), low complement levels (C3༚complement 3, C4༚complement 4). Inflammatory markers were elevated (CRP༚C-reactive protein 84.08 mg/L, ESR༚erythrocyte sedimentation rate 83 mm/h), severe hypoalbuminaemia (27.4 g/L). Imaging revealed pleural, pericardial, and peritoneal effusions. Active SLE with polyserositis and lupus nephritis was diagnosed. Intravenous methylprednisolone, cyclophosphamide, hydroxychloroquine and telitacicept were initiated. However, ultrasonography showed progressive 360-degree annular choroidal detachment with anterior displacement of the lens-iris diaphragm. Bilateral periocular triamcinolone acetonide 20 mg was administered, followed by periocular dexamethasone 5 mg. Choroidal detachment rapidly resolved, anterior chamber depth increased from 1.57 mm to 2.93 mm, and the retina reattached spontaneously. One month later, best-corrected visual acuity improved from 20/500 to 20/50 in both eyes, and intraocular pressure normalised. CONCLUSIONS: This case illustrates that systemic serous leakage in SLE can cause massive suprachoroidal effusion with secondary angle-closure glaucoma, even in eyes with normal axial length. Periocular corticosteroid therapy may serve as a useful adjunct by increasing local ocular drug exposure and promoting fluid resorption.