PB0780 - Patients with multiple myeloma have an increased prevalence of acquired platelet secretion defects and a disbalanced whole blood thrombin generation profile

Monday, July 11, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: In-Person

Co-Author(s)

Mark Roest, PhD

Clinical Director
Department of Platelet pathophysiology, Synapse Research Institute, Maastricht, the Netherlands
Maastricht, Limburg, Netherlands
YS

Yaqiu Sang

PhD
Blood Research Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Chapel Hill, North Carolina, United States
LL

Li Li

PhD
Department of Platelet pathophysiology, Synapse Research Institute, Maastricht, the Netherlands
Maastricht, Limburg, Netherlands
JR

Jasper A. Remijn, PhD

Clinical Chemist - Hematologist
Department of Clinical Chemistry. Meander Medical Center, Amersfoort
Amersfoort, Utrecht, Netherlands
RF

Rob Fijnheer

Professor
Department for Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht University, Utrecht
Utrecht, Utrecht, Netherlands
RU

Rolf T. Urbanus

Associate professor
Center for Benign Haematology, Thrombosis and Haemostasis, Van Creveldkliniek, University Medical Center Utrecht, Utrecht University, Utrecht, the Netherlands
Utrecht, Utrecht, Netherlands
Dana Huskens, PhD

PhD, Research Project Leader
Synapse research insitute
MAASTRICHT, Limburg, Netherlands
JW

Jun Wan

PhD
Blood Research Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Chapel Hill, North Carolina, United States
Bd

Bas de Laat, MD, PhD

General Director
Department of Functional Coagulation, Synapse Research Institute, Maastricht, the Netherlands
Maastricht, Limburg, Netherlands

Presenting Author(s)

JK

Joke Konings, PhD

Senior Scientist
Synapse Research Institute
Maastricht, Limburg, Netherlands

Background: Multiple myeloma (MM) is associated with a mild thrombocytopenia and/or anemia as well as an increased risk of thrombo-embolism.

Aims: To determine if the disbalanced platelets and erythrocyte state play a role in the high thrombosis risk in patients with MM.

Methods: To study platelet and erythrocyte dependent haemostasis in MM patients, we conducted a case-control study in 21 MM patients and 21 related controls and measured thrombin generation in whole blood (WB-TG) and platelet poor plasma (PPP-TG), and the platelet activation profiles and platelet vitality in WB. Mann-Whitney U test was used to compare the groups. The study was approved by the Medical Ethical Committee of Maastricht University Medical Center, and patients and volunteers gave full informed consent according to the Helsinki declaration.

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 (Fig. 1). In line with these findings, platelet response to agonists, agonist induced platelet granule release, as well as the whole blood cell counts (platelets, erythrocytes and white blood cells) were decreased in MM patients compared to controls. The plasma TG experiments showed no differences between MM-patients and controls.

Conclusion(s): Our results show that patients with MM have a disturbed blood cell count, a disturbed platelet phenotype and a disbalanced WB-TG profile. This disbalance may explain the paradoxical high prevalence of thrombosis in MM patients, despite low platelet counts and impaired function.