Abstract

Rationale: Gout is caused by the deposition of monosodium urate crystals caused by purine metabolism disorder or uric acid excretion disorder, which could be manifested as hyperuricemia, arthritis, tophus, and even renal dysfunction and other important organ damage. Gout stones to originate from crystals formed by urate and occur to joints, ears, olecranon bursa, fingers, and tendons. Bone destruction of gout stones is rare in clinic, and is easily misdiagnosed as bone tumor, and gout stones in the upper tibia is even rarer. Patient concerns: A 25-year-old male patient presented with right upper tibia pain for 2 weeks without obvious cause and had no history of alcoholism or hyper purine diet. Diagnosis: Right tibia and fibula anteroposterior and lateral radiographs showed that a round like low-density shadow at the upper end of the right tibia. CT showed bone destruction and neoplastic lesions at the right tibial tubercle. MRI showed bone destruction at the upper end of the right tibia with local oval abnormal signal, which were considered the neoplastic lesions. However, postoperative pathological diagnosis suggested gout calculi. Interventions: After examination, the patient underwent surgical treatment, curettage and bone graft fusion. Long-term oral administration of uric acid lowering drug allopurinol tablets 50 mg/time, twice/day, potassium sodium hydrogen citrate particles 2.5 g/time, 3 times/day. Outcomes: The patient took allopurinol tablets 50 mg/time, 2 times/day and Sodium Hydrogen Citrate Granules 2.5 g/time, 3 times/day for a long time after operation. As a result, the focus on gout stones was cured. Three months after operation, the bone graft healed well, the incision healed well, and the uric acid was 397 µmol/ L, which achieved satisfactory clinical efficacy. Conclusion: Tibial gout stones is rare in clinic. When hyperuricemia patients have tibial bone destruction and consider bone tumor, it should be differentiated from gout stones. The blood uric acid value should be controlled to the normal range before operation, and the drug therapy of decreasing uric acid should be continued after operation.

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