LAUSR

Dear Editor, Allopurinol hypersensitivity among susceptible individuals is widely reported. Nevertheless, ocular manifestations caused by allopurinol are rarely encountered. Here, we describe a case of a young Chinese woman diagnosed with gout and metabolic syndrome, who developed crystalline maculopathy after allopurinol was initiated. A 33-year-old Chinese woman was referred to our center in 2012 at 24 weeks period of gestation. Her presenting complaint was recurrent multiple joint pain for the past 3 years. It was poly-articular, involving both big and small joints. Each episode was associated with swelling and hyperemic skin changes. Attacks were precipitated by intake of high purine diet. The pain resolved gradually without specific treatment. Her attacks became more frequent as her pregnancy progressed. In addition, she had type II diabetes mellitus diagnosed since the age of 30 and had been on treatment since then. There was strong family history of diabetes mellitus. On examination, she was obese with body mass index of 35.2. At presentation, she was normotensive. There were neither skin rashes nor tophi deposits. Joint examinations revealed asymmetry, poly-articular tenderness and swelling involving hands, knees, ankles and feet, with clinical evidence of effusion over both knee joints. There were no joint deformities. Her initial investigations showed elevated C-reactive protein of 11.6 mg/L and erythrocyte sedimentation rate of 86 mm/h. Her fasting blood sugar was 7.6 mmol/L. Fasting lipid profile showed elevated total cholesterol (6.20 mmol/L), elevated triglyceride (4.04 mmol/L), with low high-density lipoprotein-cholesterol (0.90 mmol/L). Otherwise, full blood count, renal profile, liver function test, and thyroid function test showed normal ranges. Rheumatoid factor, anti-cyclic citrullinated peptide antibodies, and anti-nuclear antibodies were all negative. Ultrasound of kidneys showed increased echogenicity in keeping with renal parenchymal disease, with no evidence of renal calculi. Musculoskeletal ultrasound of both knees showed presence of suprapatellar effusion, with power Doppler signals 1+. There was no synovial hypertrophy. Microscopy examinations of the aspirates from the left knee joint showed presence of monosodium urate crystals, thus confirming the diagnosis of gouty arthritis. Serum uric acid (SUA) level was 575 lmol/L. She continued her pregnancy and delivered at term. Post-delivery, she continued to have recurrent arthritis. She was started on allopurinol 150 mg every night with subsequent dose increment to 300 mg every night. Treatment was tolerated well. Follow-up clinics showed decreasing SUA trend. Her other medications included Metformin XR 1500 mg every night, ascorbic acid 500 mg once daily, fenofibrate 145 mg once daily, gliclazide MR 90 mg once daily and URAL sachets. Her SUA level reduced to < 360 lmol/L without further gout attack. Six months after initiation of allopurinol, she developed gradual blurring of vision. She was referred for ophthalmological assessment (Figs 1a,b,2a,b). Provisional diagnosis of crystalline maculopathy was made. Crystalline maculopathy refers to the deposition of refractile crystals in the superficial retina around the perifoveal region. It normally involves both eyes, affecting the posterior pole of the fundus. Vision is commonly not affected. However, visual acuity can be reduced due to subfoveal or perifoveal cyst formation. There are numerous causes of crystalline maculopathy: systemic disorders (oxalosis, cystinosis); primary ocular disorders; embolic diseases (calcium emboli, cholesterol emboli); and drug-induced. Numerous literatures have reported on ocular and visual side effects of systemic drugs. Crystalline maculopathy has been reported among patients on tamoxifen, cisplatin, canthaxanthine, clofazamin, aminoglycosides, nitrofurantoin, and talc. Dr. Gerald Pinnas had reported a case of possible association