Figure 1.
18F-fluorodeoxyglucose positron emission tomography in a patient with VEXAS syndrome demonstrating hypermetabolic activity in bone marrow (yellow). Somatic mutations in UBA1 in hematopoietic cells lead to myeloid-driven inflammation that is often refractory to treatment in patients with VEXAS syndrome.

18F-fluorodeoxyglucose positron emission tomography in a patient with VEXAS syndrome demonstrating hypermetabolic activity in bone marrow (yellow). Somatic mutations in UBA1 in hematopoietic cells lead to myeloid-driven inflammation that is often refractory to treatment in patients with VEXAS syndrome.

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