ArticleBlood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis2026
Thrombin generation profiling in multiple myeloma: a comprehensive evaluation of prothrombotic state.
Article in Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveVenous thromboembolism is a major complication in patients with multiple myeloma (MM), with treatment strategies further increasing thrombotic risk. Conventional coagulation tests (CCT) fail to reflect the in vivo hemostatic balance, whereas thrombin generation assay (TGA) provides a global assessment of thrombin dynamics and may better identify hypercoagulable states in MM.
methodsTo this aim, to evaluated thrombin generation, we enrolled 20 MM patients during follow-up while receiving active MM-treatment: sixteen had immunoglobulin G (IgG) MM, one immunoglobulin A (IgA) MM, one light-chain MM, and two biclonal MM (IgG and IgA). Citrated blood samples were collected under standardized conditions for CCT and TGA. Thrombin generation was measured in platelet poor plasma, both in the absence and presence of thrombomodulin (TM) using the ST Genesia system.
resultsTGA revealed increased peak height (139.75%; r.v. 40-69%), endogenous thrombin potential (107.80%; r.v. 58-78%), and velocity index (153.10%; r.v. 31-62%), along with shortened time to peak (ratio 1.04; r.v. 1.2-1.5). Notably, TM-mediated inhibition of thrombin generation was reduced (16.20%; r.v. 60-76%), indicating protein C pathway dysfunction despite preserved natural anticoagulant levels. This procoagulant state was further supported by elevated fibrinogen and D-dimer, together with increased factor VIII and von Willebrand levels.
conclusionOur findings confirm a hypercoagulable state in MM patients, likely related to endothelial injury and systemic inflammation. Impairment of the protein C pathway, as highlighted by TGA, further contributes to this imbalance. In light of the limitations of prothrombin time and activated partial thromboplastin time, TGA provides a more sensitive and informative evaluation of coagulation dynamics in MM patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.