A case of calcium pyrophosphate deposition disease in a young patient’s knee joint

Abstract Background Calcium pyrophosphate deposition disease (CPPD) is a crystal-associated arthropathy that predominantly affects elderly individuals. Presentation in young adults is exceptionally rare and poses significant diagnostic challenges. We report a case of extensive CPPD in a 27-year-old male patient that was initially misdiagnosed as gout, highlighting the importance of considering this condition in the differential diagnosis of chronic calcific knee arthropathy in young patients. Case presentation A 27-year-old male patient of Asian ethnicity presented with a three-year history of progressive left knee pain. He was initially misdiagnosed with gout and treated unsuccessfully with allopurinol (300 mg daily) and febuxostat (40 mg daily) for four months, with no symptomatic improvement. Upon referral, laboratory investigations revealed an erythrocyte sedimentation rate of 12 mm/hour and C-reactive protein of 8 mg/L, both within normal limits, effectively excluding an active inflammatory arthropathy. Comprehensive metabolic screening, including serum magnesium and thyroid function tests (free triiodothyronine, free thyroxine, and thyroid-stimulating hormone), demonstrated unremarkable findings, thereby ruling out common secondary causes of calcium pyrophosphate deposition disease. Preoperative imaging revealed joint space narrowing, irregular periarticular calcification, and characteristic magnetic resonance imaging (MRI) findings: abnormal signals that were isointense to slightly hyperintense on T1-weighted images, slightly hyperintense on T2-weighted images, and markedly hypointense on proton density-weighted images. Open knee arthrotomy with complete synovectomy and debridement confirmed extensive crystal infiltration of the joint cavity, tendons, and ligaments. Histopathology demonstrated positively birefringent rhomboid-shaped calcium pyrophosphate dihydrate crystals, confirming CPPD. Postoperative indomethacin (25 mg three times daily) and structured rehabilitation yielded complete pain resolution at six-month follow-up, with functional range of motion from 0 to 110 degrees flexion and no radiological recurrence. Conclusions This case highlights the importance of including CPPD in the differential diagnosis of chronic monoarticular knee pain with calcific imaging abnormalities, even in young adults. Surgical debridement with complete synovectomy and crystal removal can provide both definitive diagnosis and long-term symptomatic relief when pharmacological therapy fails. Clinicians should maintain a high index of suspicion for CPPD in young patients presenting with chronic calcific arthropathy refractory to conventional treatment.