Myeloma patients are predisposed to thrombosis because of a number of factors which include immobilisation, hyperviscosity, low grade DIC and possibly hypercalcaemia [1]. To this list must also be added the aPL.

Myeloma is one of the B-cell disorders characterised by significant paraprotein production and most of the associated haemostatic abnormalities act to increase the risk of clinically significant bleeding rather than thrombosis [102],

7.1. Plasma Cell Dyscrasias/Multiple Myeloma

Among 10 patients with LA reviewed by Duhrsen et al. [102] were two with multiple myeloma and monoclonal gammopathy. One suffered from lym-phoplasmacytoid (LP) immunocytoma. In the one patient with myeloma, recurrent DVT preceded the diagnosis of multiple myeloma with IgG-K monoclonal gammopathy and K-light chain Bence-Jones proteinuria by 10 years. The patient died from a pulmonary embolus. Acute small bowel infarction and obliterating peripheral vascular disease had also occurred.

In the second multiple myeloma patient, with a 2-year history of the disease, both venous and arterial occlusions were seen. Pulmonary emboli also supervened in this patient. Repeated myocardial, renal and cerebral infarctions were recorded.

The patients with malignant systemic disease differ from the SLE patients in that: (a) the paraproteinemia accompanying SLE rarely, if ever, exceeded a level of 2000 mg/dl; (b) Bence-Jones proteinuria and marrow plasmacytosis were missing; (c) a revised sex ratio to SLE was evident; (d) a higher age of disease onset; and (e) a lesser frequency of serological autoimmune phenomena were seen in the malignant group of patients.

In addition, the coagulation abnormalities were not as homogeneous as those seen in the autoimmune group e.g., a powerful antithrombin effect of the LA in one patient, prolonging the PT greatly [103].

Among the 3 patients described by Bellotti et al. [101] was one patient with multiple myeloma, a 59-year-old male with the prolonged thrombin time of 18

sec (n =< 15 sec) and an activated partial thromboplastin time (aPTT) of 85 sec (n —< 50 sec). LA was demonstrable. No clinical complications were recorded in this patient.

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