Arterial thrombosis is becoming increasingly recognized as a complication of malignant lymphoma.1,2 Here we present a case of radial and ulnar arterial thrombosis in a patient with diffuse large B-cell… Click to show full abstract
Arterial thrombosis is becoming increasingly recognized as a complication of malignant lymphoma.1,2 Here we present a case of radial and ulnar arterial thrombosis in a patient with diffuse large B-cell lymphoma (DLBCL) and a history of repetitive blunt hand trauma caused by frequent handgun use. A 66-year-old male with a history of smoking, premorbid digital cold sensitivity, and chronic kidney disease awoke with joint and finger swelling. He was an avid marksman, and reported using a high-caliber revolver with substantial recoil 1 week prior to symptom onset. Days later an eschar developed on his index finger and he sought emergency care. Catheterbased digital subtraction angiography revealed an occlusion of the distal ulnar and radial arteries (Panel A, black arrowhead, and black arrow), including the superficial palmar arch (Panel A, white arrowhead). His right digital vessels were also thrombosed (Panel A, gray arrowheads), with ‘corkscrew’ collaterals and absent flow to the distal index finger where his lesion had progressed to an eschar (Panel B). Nitroglycerin infusion improved flow; however, occlusion of the digital vessels persisted. He was hospitalized for 21 days with a heparin infusion prior to transferring care to our health system. Laboratory evaluation revealed normal prothrombin time, partial thromboplastin time, lupus anticoagulant, and negative cryoglobulin, cryofibrinogen, beta-2 glycoprotein and cardiolipin antibodies. No prothrombin or Factor V Leiden mutations were detected. However, serum protein electrophoresis showed an M protein spike of 1.5 g with immunoglobulin M (IgM) kappa monoclonality. IgG and IgA were within normal limits. A positron emission tomography–computed tomography scan showed hypermetabolic activity in several cervical lymph nodes. Pathological review was consistent with non-germinal center DLBCL after which chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone was started. Flow cytometry demonstrated no polyclonal cell populations. A bone marrow biopsy was unrevealing. The patient was started on apixaban prior to diagnosis of malignancy, and remained on apixaban throughout his chemotherapy course. A main driver of thrombosis in the setting of malignancy is the expression of tissue factor on the surface of circulating tumor cells.3 Expression of tissue factor on tumor and endothelial cells is induced by tumor cell-secreted inflammatory cytokines and leukocytes responding to the malignancy. Additionally, many chemotherapies contribute to the pro-inflammatory milieu.3 The present case suggests that the combination of frequent handgun use, premorbid digital cold sensitivity, and Distal radial and ulnar artery thrombosis in a cancer patient with a history of chronic handgun use
               
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