Figure 3.
Patients with WM have delayed and reduced thrombin generation. Thrombin generation in (A-G) EDTA-anticoagulated PPP, (H) EDTA-anticoagulated PPP + PAR-1–activated HD WPs, or (I-M) trisoidium citrate-anticoagulated PPP + PAR1–activated HD or WM WPs in HDs (n = 6-25, blue), patients with WM not on therapy (n = 5-13, red) and receiving BTKis (n = 1-3, green). For panels A,H, representative thrombograms, mean of duplicates. For panels B-F,I-M, mean ± SD. For panel G, correlation between ETP and IgM levels of patients with WM. P values were determined by Kruskal-Wallis 1-way ANOVA with Dunn's multiple comparisons test for the panels B-F, or Wilcoxon matched-pairs signed rank test for the panels I-M. R2 values were determined by simple linear regression.

Patients with WM have delayed and reduced thrombin generation. Thrombin generation in (A-G) EDTA-anticoagulated PPP, (H) EDTA-anticoagulated PPP + PAR-1–activated HD WPs, or (I-M) trisoidium citrate-anticoagulated PPP + PAR1–activated HD or WM WPs in HDs (n = 6-25, blue), patients with WM not on therapy (n = 5-13, red) and receiving BTKis (n = 1-3, green). For panels A,H, representative thrombograms, mean of duplicates. For panels B-F,I-M, mean ± SD. For panel G, correlation between ETP and IgM levels of patients with WM. P values were determined by Kruskal-Wallis 1-way ANOVA with Dunn's multiple comparisons test for the panels B-F, or Wilcoxon matched-pairs signed rank test for the panels I-M. R2 values were determined by simple linear regression.

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