Introduction: Chronic tophaceous gout is a rare cause of parathyroid hormone (PTH)-independent hypercalcemia. This is due to increased 1-alpha hydroxylase activity within granulomatous inflammation surrounding gouty tophi, resulting in excess calcitriol production. In advanced disease, immobilization from pain and joint deformity may further exacerbate hypercalcemia due to immobilizationrelated bone resorption, leading to clinically significant symptoms and complications. Case: A 59-year-old male with chronic tophaceous gout complicated with CKD and nephrocalcinosis was referred for inpatient evaluation of hypercalcemia. He had an episode of acute pancreatitis attributed to hypercalcemia 1 month prior. Serum calcium levels have risen progressively over the preceding year, from 2.48 mmol/L (reference 2.0–2.65) to 3.17 mmol/L. His gout was poorly controlled with uric acid levels ranging 641–709 umol/L, with extensive tophi over the upper and lower limbs and gluteal regions. He had been maintained on low-dose allopurinol 150 mg/day for 2 years. Functionally, he was largely bedbound and wheelchair-dependent. On admission, corrected calcium was 3.48 mmol/L with suppressed intact parathyroid hormone (<0.6 pmol/L) consistent with PTH-independent hypercalcemia. Malignancy and myeloma workup, including tumor markers, was unremarkable. Serum phosphate (0.9 mmol/L) and alkaline phosphatase (152 IU/L) were normal. Hypercalcemia persisted despite intravenous hydration and calcitonin. Low-dose prednisolone was then initiated, followed by pamidronate, resulting in normalization of corrected calcium to 2.17 mmol/L. He remained normocalcemic while on tapering prednisolone for a month. However, calcium rebounded months after cessation. Gradual escalation of allopurinol to 900 mg/day improves uric acid levels to 389–429 umol/L with better functional status (standing unsupported briefly and mobilizing with assistance). However, calcium remains moderately elevated 2.65–2.85 mmol/L. Conclusion This case highlights severe tophaceous gout as a rare but significant cause of PTH-independent hypercalcemia, in which glucocorticoids can be effective in treating refractory hypercalcemia. It also underscores the importance of addressing the underlying disease through optimization of urate-lowering therapy and functional rehabilitation.