Report of three cases of circulating heparin‐like anticoagulants

Llamas, Pilar; Outeiriño, J; Espinoza, J; Santos, Ana Belen; Román, A; Tomás, José Francisco

doi:10.1002/ajh.1126

Cited by 23 publications

(21 citation statements)

References 4 publications

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“…Rarely, symptomatic acquired coagulopathies are due to M‐protein autoantibody behaviour targeting specific proteins including thrombin (Colwell et al , 1997), and factor VIII (FVIII) (Liebman, 2000). Another uncommon cause of bleeding in patients with plasma cell dyscrasias is detection of circulating heparin‐like activity (Palmer et al , 1984; Llamas et al , 2001). Spontaneous or post‐procedure bleeding is accompanied by laboratory findings of prolonged aPTT that is partially corrected by mixing with normal plasma, prolonged TT, with partial or complete correction following addition of protamine, normal reptilase time, and measurable heparin activity with commercial assays.…”

Section: Acquired Coagulopathiesmentioning

confidence: 99%

Pathogenesis and management of bleeding and thrombosis in plasma cell dyscrasias

Eby

2009

Br J Haematol

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Summary Unexpectedly high rates of venous thromboembolic events (VTE) concurrent with the introduction of highly effective immune modulating drugs thalidomide and lenolidomide for treatment of multiple myeloma have focused attention on the incidence and underlying pathophysiology of VTE in patients with plasma cell dyscrasias, and on thromboprophylaxis approaches. While bleeding complications are relatively uncommon in patients with lymphoproliferative disorders, acquired von Willebrand syndrome, typically occurring in patients with monoclonal gammopathy of unknown significance, and acquired coagulopathies associated with primary amyloidosis can present with haemorrhagic complications and both are challenging to manage. This review highlights these important haemostasis‐related complications of plasma cell dyscrasias and provides an overview of other uncommon bleeding and thrombotic events that can affect diagnostic and therapeutic management of clonal plasma cell disorders. Due to the infrequency of most of these haemostasis complications, available information is typically based on retrospective cases or series.

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Section: Acquired Coagulopathiesmentioning

confidence: 99%

Pathogenesis and management of bleeding and thrombosis in plasma cell dyscrasias

Eby

2009

Br J Haematol

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“…Both solid tumors and multiple myeloma have been associated with rare cases of acquired hyperfibrinolysis due to excess release of tissue plasminogen activator or urokinase-type plasminogen activator, 25 and circulating heparin-like anticoagulants. 26,27 Although the pathophysiology of both of these hemostasis disorders remains obscure, treatment with protamine infusions and antifibrinolytics respectively has been effective.…”

Section: Acquired Coagulopathies and Amyloidosismentioning

confidence: 99%

Bleeding and Thrombosis Risks in Plasma Cell Dyscrasias

Eby

2007

Hematology

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Major, spontaneous bleeding is uncommon in patients with plasma cell dyscrasias despite frequent abnormal screening hemostasis tests. However, acquired von Willebrand deficiency and light-chain (AL) amyloidosis, and amyloidosis complicating multiple myeloma can present with serious hemorrhagic complications that are challenging to manage. While patients with monoclonal gammapathy of undetermined significance and multiple myeloma share an intrinsic increased risk of venous thromboembolic events (VTE), treatment with thalidomide and lenalidomide increases the incidence of VTE in certain multiple myeloma patient subsets. Our understanding of the complex interactions among malignant plasma cells, inflammatory and hemostasis pathways, and treatment modalities that combine to produce thrombotic complications is incomplete. Prospective, randomized trials are clearly needed to assist clinicians in providing optimal VTE prophylaxis to their patients with plasma cell dyscrasias. Hemorrhagic ComplicationsWhile overt bleeding is a relatively uncommon presenting symptom of monoclonal gammopathy of undetermined significance (MGUS), multiple myeloma (MM), Waldenström macroglobulinemia, and other B-cell malignancies, pathophysiologic interactions between paraproteins and coagulation factors, platelets, and vessels can produce hemostasis abnormalities. The consequences are often incidental, abnormal hemostasis test results, but overt bleeding and thrombotic presentations occur as well. 1 IncidenceRelying on distant, retrospective surveys, bleeding complications are more likely with IgM and IgA paraproteins than with IgG, and are associated with higher concentrations of serum immunoglobins, higher serum viscosity, and prolonged bleeding time, but not with decreased platelet counts or prolonged prothrombin time (PT), activated partial thromboplastin time (aPTT), and thrombin time.2,3 More contemporary reviews report symptomatic bleeding at presentation in 0% of multiple myeloma, 4 and 17% of Waldenström's macroglobulinemia. 5 Bleeding complications are a more common cause of morbidity and death during treatment of plasma cell dyscrasias 6 due to progression of disease, renal insufficiency, infections, therapy related toxicity, and invasive procedures rather than a direct consequence of the paraprotein.

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“…These heparin-like anticoagulants have been associated with hematological malignancies, mainly with multiple myeloma or plasma cell leukemia [1][2][3][4][5][6], and other neoplastic processes [7][8][9]. Other cases were observed in infected cirrhotic and noncirrhotic patients [10].…”

Section: Introductionmentioning

confidence: 99%

Heparin-like anticoagulant associated with multiple myeloma and neutralized with protamine sulfate

Torjemane¹,

Guermazi

Ladeb³

et al. 2007

Blood Coagulation &Amp; Fibrinolysis

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A 55-year-old man with multiple myeloma developed sustained bleeding after bone marrow aspiration and cutaneous bleeding. Routine coagulation studies revealed a prolonged activated partial thromboplastin time and thrombin time (> 60 s) with a normal reptilase time. Further evaluation showed failure of the activated partial thromboplastin time to correct completely in a 1: 1 mixture with normal plasma. Treatment of the patient's plasma in vitro with protamine sulfate normalized the thrombin time. The presence of a heparin-like anticoagulant was suspected. The plasma heparin level was 0.73 IU/ml. Intravenous infusion of protamine sulfate appeared to neutralize the anticoagulant activity and stop the bleeding. The cancer cells themselves or the invasive nature of this type of cancer might result in a massive release of a heparinoid. Such coagulopathy appears to be a rare mechanism of bleeding and it is an important entity to consider since it is potentially reversible with protamine sulfate.

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Report of three cases of circulating heparin‐like anticoagulants

Cited by 23 publications

References 4 publications

Pathogenesis and management of bleeding and thrombosis in plasma cell dyscrasias

Pathogenesis and management of bleeding and thrombosis in plasma cell dyscrasias

Bleeding and Thrombosis Risks in Plasma Cell Dyscrasias

Heparin-like anticoagulant associated with multiple myeloma and neutralized with protamine sulfate

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