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Patients With Multiple Myeloma Have a Disbalanced Whole Blood Thrombin Generation Profile.
Li, Li; Roest, Mark; Sang, Yaqiu; Remijn, Jasper A; Fijnheer, Rob; Smit, Karel; Huskens, Dana; Wan, Jun; de Laat, Bas; Konings, Joke.
Afiliação
  • Li L; Department of Platelet Pathophysiology, Synapse Research Institute, Maastricht, Netherlands.
  • Roest M; Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
  • Sang Y; Department of Platelet Pathophysiology, Synapse Research Institute, Maastricht, Netherlands.
  • Remijn JA; Department of Platelet Pathophysiology, Synapse Research Institute, Maastricht, Netherlands.
  • Fijnheer R; Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, Netherlands.
  • Smit K; Department of Clinical Chemistry, Meander Medical Center, Amersfoort, Netherlands.
  • Huskens D; Department of Internal Medicine, Meander Medical Center, Amersfoort, Netherlands.
  • Wan J; Department of Internal Medicine, Meander Medical Center, Amersfoort, Netherlands.
  • de Laat B; Department of Platelet Pathophysiology, Synapse Research Institute, Maastricht, Netherlands.
  • Konings J; Department of Functional Coagulation, Synapse Research Institute, Maastricht, Netherlands.
Front Cardiovasc Med ; 9: 919495, 2022.
Article em En | MEDLINE | ID: mdl-35833182
ABSTRACT

Background:

Multiple myeloma (MM) is associated with a high prevalence of bleeding and an increased risk of thrombo-embolism. MM patients have reduced platelet- and red blood cell (RBC) numbers in blood, which may indicate that the paradoxical hemostasis profile is a consequence of a disturbed platelet and RBC homeostasis.

Objectives:

To get better insight in the disbalanced hemostasis of MM patients.

Methods:

We conducted a case-control study on the whole blood (WB) coagulation profiles of 21 MM patients and 21 controls. We measured thrombin generation (TG) in WB and platelet poor plasma (PPP) of MM patients and controls.

Results:

In WB-TG, we observed that the median time to the thrombin Peak was 52% longer in MM patients than in controls, while the median endogenous thrombin potential until the Peak (ETPp) was 39% higher in MM-patients than in controls. In line with these findings, the levels of platelets, RBCs, white blood cells and agonist induced platelet activation were decreased in MM patients compared to controls. The plasma TG experiments showed no differences between MM-patients and controls.

Conclusion:

Patients with MM have a disturbed blood cell metabolism and a disbalanced WB-TG profile. This disbalance may explain the paradoxically high prevalence of bleeding symptoms in MM patients vs. an increased thrombosis risk. There was no disturbance observed in plasma TG, indicating that blood cells are the major determinants for the disbalanced hemostasis in MM patients.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article