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Cutaneous necrosis as a terminal paraneoplastic thromboembolic event in a patient with non‐Hodgkin’s lymphoma
Author(s) -
Luboshitz J.,
Bairey O.,
Blickstein D.,
Vaknin H.,
Okon E.,
Lahav J.,
Prokocimer M.
Publication year - 1999
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1046/j.1365-2796.1999.00475.x
Subject(s) - medicine , thrombosis , lymphoma , pathology , monoclonal antibody , necrosis , complement system , complement membrane attack complex , antibody , immunology
. Luboshitz J, Bairey O, Blickstein D, Vaknin H, Okon E, Lahav J, Prokocimer M (Rabin Medical Center, Belinson Campus, Petah‐Tikva and Sackler Faculty of Medicine, Tel Aviv University, Israel). Cutaneous necrosis as a terminal paraneoplastic thromboembolic event in a patient with non‐Hodgkin’s lymphoma (Case Report). J Intern Med 1999; 245: 301–5. Thrombotic complications in non‐Hodgkin’s lymphoma often originate in the large veins. We describe a patient with refractory advanced high‐grade lymphoma who presented with the rare complication of extensive cutaneous necrosis due to thrombosis of dermal vessels; there was also a recent new peak of monoclonal IgM‐κ protein. Direct immunofluorescence demonstrated immune deposits with complement in the dermal vessel wall. Based on these observations and on published data, we suggest that these complexes were the trigger for the thrombotic events and that the monoclonal IgM acted as xenoreactive antibodies, initiating a cascade of events. The first step of this cascade was activation of the complement and the membrane attack complex, which caused secretion of IL‐1α by endothelial cells, followed by overexpression of tissue factor on the surface of the dermal vessel wall endothelium. Dermal vessel thrombosis was the final event in this cascade.