Malignant olecranon bursitis in the setting of multiple myeloma relapse

Multiple myeloma is the most common plasma cell neoplasm, with an estimated 24,000 cases occurring annually.1 Symptomatic multiple myeloma most commonly presents with one or more of the cardinal CRAB phenomena of hypercalcemia, renal dysfunction, anemia, or lytic bone lesions.2 Less commonly, patients may present with plasmacytomas (focal lesions of malignant plasma cells), which may involve bony or soft tissues.1 Plasma cell neoplasms occasionally involve the joints, including the elbows, typically as plasmacytomas. ‚e elbow is an unusual but reported location of plasmacytomas.3,4 A case of multiple myeloma and amyloid light-chain (AL) amyloidosis has been reported, with manifestations including pseudomyopathy, bone marrow plasmacytosis, and bilateral trochanteric bursitis.5 Bursitis is de…ned as in†ammation of the synovial-†uid–containing sacs that lubricate joints. ‚e olecranon bursa is commonly aˆected. Etiologies include infection, in†ammatory disease, trauma, and malignancy. Furthermore, there is an association between bursitis and immunosuppression.6,7 ‚e most common modes of therapy used to treat bursitis are nonsteroidal anti-in†ammatory drugs, corticosteroid injections, and surgical management. Trochanteric bursitis has been attributed to multiple myeloma in one previous case report, but we are not aware of any previous cases of olecranon bursitis caused by multiple myeloma. Here, we present the case of a 46-year-old man with heavily pretreated multiple myeloma and amyloidosis who developed left olecranon bursitis contemporaneously with disease relapse; †ow cytometric analysis of the bursal †uid demonstrated an abnormal plasma cell population, establishing the etiology. Case presentation and summary A 46-year-old man with a longstanding history of multiple myeloma developed swelling of the left elbow that was initially painless in September 2016. He had been diagnosed with IgA kappa multiple myeloma and AL deposition in 2011. Over the course of his disease, he was treated with the following sequence of therapies: cyclophosphamide, bortezomib, and dexamethasone, followed by melphalanconditioned autologous peripheral blood stem cell transplant; lenalidomide and dexamethasone; car…lzomib and dexamethasone; pomalidomide, bortezomib, and dexamethasone; and bortezomib, lenalidomide, dexamethasone, doxorubicin, cyclophosphamide, and etoposide, followed by second melphalan-conditioned autologous peripheral blood stem cell transplant. In addition to treatment with numerous novel and chemotherapeutic agents, his disease course was notable for amyloid deposition in the liver, bone marrow, and kidneys, which resulted in dialysis dependence. After the second autologous transplant, he achieved a very good partial response and experienced about 9 months of remission, after which laboratory evaluation indicated recurrence of IgA kappa monoclonal protein and free kappa light-chains, which increased slowly over several months without focal symptoms, cytopenias, or decline in organ function (Figure 1). Twelve months after his second transplant, he presented in September 2016 with 4 weeks of left elbow swelling, with the appearance suggesting a †uid collection over the left olecranon process (Figure 2). ‚e †uid collection was not painful unless bumped or pushed. ‚e maximum pain level was 1-2 on a scale of 0-10. His daughter drained the †uid collection on 2 occasions, but it reaccumulated over 2 to 3 days. He reported no fevers, chills, or sweats. He did not