A right-hand-dominant, 62-year-old obese man presented to our department due to progressive right shoulder pain and weakness. There was no history of recent trauma to the right shoulder. He had a 2-year history of intermittent pain in the right shoulder. Nine months prior, he started to experience worsening pain and weakness in the right shoulder with the restriction of active shoulder motion. He had been treated with conservative treatment (acupuncture, physical therapy, and subacromial steroid injections), which provided short periods of relief. The pain did not disappear, and he visited our hospital for further examination and treatment.
His past medical history included right clavicle fracture, hypertension, and gout. Thirty-six years prior, he suffered a right clavicle middle-shaft fracture that was treated conservatively with a figure-of-eight bandage. The patient recalled that there was no abnormality in the right shoulder at that time. He had a 20-year history of long-standing but suboptimally treated gout, and the gout intermittently led to redness and pain in the feet, which occurred 4-5 times a year. The symptoms were relieved by colchicine during acute episodes, and no systemic treatment was given. The patient had a body mass index of 31.9 kg/m2 and no previous history of tuberculosis. The patient consumed excessive alcohol and had an alcohol consumption history of 250 ml/day for 30 years; additionally, he smoked 20 cigarettes a day for 35 years and followed no particular diet.
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A clinical evaluation revealed that his right shoulder joint had a limited active range of motion, and the passive range of motion was nearly normal. On palpation, tenderness was noted in the anterior and posterior aspects of the shoulder joint, and there was no warmth, erythema, swelling, or redness. When the patient’s upper limb was raised, abducted, and externally rotated, the shoulder joint had a sense of movement, and there were a popping sound and a feeling of shoulder reduction. Gouty tophi were observed on the dorsal aspect of the bilateral great toe and extensor aspect of the bilateral elbows; all of the patient’s other joints were clinically normal, and the examination revealed nothing else of note. Plain radiographs of the affected shoulder showed glenohumeral joint space narrowing, erosions of the glenoid, and osteophyte formation on the inferior aspect of the glenoid. At the superolateral point of the humeral head, a lytic lesion (arrow) was detected, and malunion of the right clavicle fracture was also seen (Fig. 1). To assess the integrity of the soft tissue of the shoulder joint, we ordered a magnetic resonance imaging (MRI) examination, which revealed that the axial and coronal proton density-weighted, fat-suppressed MRI exhibited an intact rotator cuff, joint effusion, synovial proliferation, effusion within the biceps long head tendon sheath, humoral head superolateral cystic erosion, posterior humeral head subluxation, and severe glenoid erosion (Fig. 2). A laboratory examination revealed an elevated uric acid level of 594 µmol/L (normal range 208.00-428.00 µmol/L), erythrocyte sedimentation rate (ESR) of 65 mm/h, C-reactive protein level of 34 mg/L, leukocyte count of 8.35 × 109/L, and hemoglobin level of 12.8 g/dL. The patient had a negative test for rheumatoid factor and anti-citrullinated protein antibodies (ACPAs). The liver and kidney function of the patient were normal. No abnormalities were found on electromyography of the upper extremities. In consideration of the possibility of shoulder joint infection or malignancy, arthrocentesis was performed, and 20 ml of fluid was aspirated. The fluid was macroscopically cloudy and yellow. The synovial analysis revealed an inflammatory cell count with leukocytes 5200/mm3, which were predominantly neutrophils. Gram staining of the fluid was negative, and no organisms were cultured. A cytology analysis and the joint fluid Xpert MTB/RIF test were negative. A polarizing microscope was not available in our hospital; therefore, we could not examine the synovial fluid for crystals.
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The plain radiograph of the chest showed no neoplastic or tuberculous changes. Serendipitously, the radiograph revealed a round contour lytic lesion in the left humeral head with sclerotic borders near the articular surface (Fig. 3). Therefore, a bilateral shoulder joint computed tomography (CT) scan and left shoulder MRI examination were performed. An infectious shoulder etiology appeared unlikely, and differential diagnoses included destructive arthritis or neoplastic lesions. Ultrasound and dual-energy CT imaging of the shoulder joints were not performed on this patient.
The CT scan demonstrated severe destructive lytic changes at the glenoid and erosive lesions and posterior subluxation of the humeral head in the right shoulder. A faint amorphous opacity could also be seen at the posterior capsule of the right shoulder. Circular lytic lesions in the left humeral head with sclerotic borders near the articular surface broke through the articular cartilage (Fig. 4). Left shoulder MRI revealed that the axial and coronal proton density-weighted, fat-suppressed MRI showed effusion, lytic destruction of the subchondral bone of the humeral head, erosion, and collapse of the articular cartilage medial to the lesion (Fig. 5). However, we still could not determine the cause of the bony destruction of the shoulder joint. Therefore, several biopsies were taken from the capsule and synovial membrane of the right shoulder. The biopsy showed inflammatory cells and gout crystals, and there was no evidence of malignancy or tuberculosis (Fig. 6). Based on these findings, we made a diagnosis of gouty arthritis of the bilateral shoulder. Etoricoxib and febuxostat treatment improved the patient’s clinical condition. The patient refused surgical intervention and decided to continue receiving physical therapy and medication for symptom control. After physical therapy and medication, the pain in the right shoulder diminished further but was not eliminated.
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