An elderly patient with a chronic history of myelofibrosis with recent myeloproliferative phase presented to the emergency room with swelling and erythema of the right hand.
Two images of the right hand were obtained in posteroanterior and oblique views. These demonstrate pathognomonic changes of gout with focal thenar swelling, first metacarpal base and trapezium juxta-articular erosions, and overhanging edges. There is a background of diffuse osteopenia.
An elderly patient with a chronic history of myelofibrosis with recent myeloproliferative phase presented to the emergency room with swelling and erythema of the right hand.
Physical examination revealed a swollen, tender, warm, and erythematous right hand with a decreased range of motion. Hematological evaluations demonstrated leukopenia with elevated C-reactive protein and uric acid level.
Two images of the right hand were obtained in posteroanterior and oblique views. These demonstrate pathognomonic changes of gout with focal thenar swelling, first metacarpal base and trapezium juxta-articular erosions, and overhanging edges. There is a background of diffuse osteopenia.
A bone marrow biopsy revealed myeloid precursor with atypical megakaryocytes. This myleoproliferative phase resulted in excessive clonal proliferation, secondary destruction of abnormal platelets, and subsequent uremia.
Gouty arthritis stems from three basic pathways: idiopathic, familial, or high cellular turnover (usually cancer or chemotherapy)[1]. Most common pathophysiology is biochemical derangement of monosodium urate regulation and subsequent deposition within the soft tissue and joints over time leading to juxta-articular erosions [2].
Late manifestations of gout were revealed in hand radiographs in the background of thrombocytosis (with platelet counts over 700, 000/mm3) and elevated chronic uric acid levels (measuring over 12mg/dL).
Prophylactic use of uricosuric agents and xanthine oxidase inhibitors should be considered early to prevent gouty arthritis in patients diagnosed with lymphoproliferative disorders and elevated uric acid levels [3].
Secondary gout
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• The posteroanterior (PA) and oblique X-ray views show soft tissue swelling in the right thenar eminence, with a pronounced soft tissue protrusion in that area.
• Erosive lesions can be seen near the articular surfaces of the base of the first metacarpal and the adjacent carpal bone (e.g., the trapezium), with a characteristic “overhanging edge” appearance at the margins.
• Generalized bone demineralization (osteopenia) is observed in the background.
• Combined with clinical examination showing local redness, swelling, warmth, and pain, and laboratory results (e.g., elevated C-reactive protein, decreased white blood cells but elevated uric acid), there is a correlation between joint inflammation and hyperuricemia.
1. Gouty Arthritis
• Caused by long-term elevated serum uric acid leading to monosodium urate crystal deposition in articular surfaces and soft tissues, triggering local inflammatory responses.
• Typical imaging findings include erosions near the joint surface with an “overhanging edge,” accompanied by surrounding soft tissue swelling, tophi, etc.
2. Septic Arthritis
• Clinically, it can also cause local redness, swelling, warmth, and pain. However, it is often accompanied by a significant increase in white blood cells or markedly abnormal inflammatory indicators. In this case, normal white blood cell counts can be a distinguishing factor.
3. Rheumatoid Arthritis
• Typically presents as symmetric erosions of small joints in both hands, often involving the proximal interphalangeal and metacarpophalangeal joints. X-ray may show marginal erosions and soft tissue swelling, but the “overhanging edge” appearance in this case is more characteristic of gout.
4. Osteoarthritis
• Primarily involves degenerative changes of articular cartilage and proliferative changes. In late stages, joint space narrowing and osteophyte formation can be seen. However, it most commonly affects weight-bearing joints (e.g., knees) and differs from the characteristics in this case.
Considering the patient’s history of chronic myelofibrosis and recent myeloproliferative phase (high cell turnover leading to hyperuricemia), continuous significant elevation of uric acid (＞12 mg/dL) in laboratory tests, and the typical imaging findings of near-articular erosions with an “overhanging edge,” the most likely diagnosis is: Gouty Arthritis with Chronic Myelofibrosis and Hyperuricemia in the Myeloproliferative Phase.
1. Pharmacological Treatment
• Acute Attack Management: Non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids can be used to alleviate acute joint inflammation.
• Long-Term Uric Acid Lowering Therapy: Utilize xanthine oxidase inhibitors such as allopurinol or febuxostat, and if necessary, combine with uricosuric agents (e.g., probenecid).
• Underlying Cause Management: Aggressively address issues related to myelofibrosis and myeloproliferative conditions, and monitor blood counts and complications in a timely manner.
2. General Conservative and Supportive Measures
• Elevation and rest of the affected limb to reduce local swelling.
• Appropriate application of ice packs during the acute inflammatory phase to relieve pain and swelling.
• Correct dietary habits, limit high-purine foods, and increase fluid intake.
3. Rehabilitation and Exercise Prescription
Given the patient’s advanced age and fragile bones, rehabilitation exercises should be introduced gradually and tailored to individual conditions. The main goals are to improve joint mobility and muscle strength while avoiding excessive local stress.
This report is based solely on the patient’s provided medical history, imaging, and laboratory findings, and serves as a comprehensive reference. It should not replace in-person diagnostic and treatment advice. If you have any questions or experience symptom changes, please seek medical attention and follow the guidance of a qualified healthcare professional.
Secondary gout
