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Chokri Ben Lamine: Thread Platelet Subpopulations Leads to Therapeutic Implications
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Apr 13, 2026, 12:11

Chokri Ben Lamine: Thread Platelet Subpopulations Leads to Therapeutic Implications

Chokri Ben Lamine, Adult Hematology and SCT Assistant Consultant at Oncology Center of Excellence at King Faisal Specialist Hospital and Research Center, shared a post on X:

“Thread Platelet Subpopulations Leads to Therapeutic Implications

(Focus: actionable strategies for hematologists ans cardiologists)

Credits: Dr. Alyamany

  • High platelet turnover leads to increased reticulated platelets (RPs)
  • Use reversible P2Y12 inhibitors (ticagrelor, cangrelor) instead of clopidogrel/prasugrel
  • Continuous inhibition overcomes newly formed platelets escape
  • PLATO: decreased death/MI/stroke but increased non-procedural bleeding
  • Key concept: ‘platelet turnover: resistance to irreversible drugs’

Hyperreactive RPs in CAD

  • Target pathways: GPVI inhibition (glenzocimab, revacept)
  • with or without PI3K inhibition (LY294002 experimental)
  • Mechanism: decreased collagen-driven activation and RP hyperreactivity
  • Phase II PCI: safe with decreased bleeding but no clear MI reduction yet
  • Future: selective anti-thrombotic without bleeding penalty

COX-2–mediated thromboxane (aspirin resistance biology)

  • RPs express increased COX-2 so aspirin less effective

Strategy:

  • Adjust aspirin dosing or COX-2 inhibition (e.g., celecoxib)
  • Target: decreased TxA2 production in young platelets
  • Evidence mixed, not standard yet
  • Explains ‘high on-treatment platelet reactivity”\’

Cancer and immune evasion (PD-L1 positive platelets)

  • Target axis:
  1. VEGF / PDGF inhibition
  2. alphaIIb beta3 blockade (eptifibatide)
  • Mechanism: reverse platelet-mediated immunosuppression
  • APOLLO (NSCLC): signal for increased PFS with antiplatelet plus ICI
  • Platelets act as immune checkpoint modulators

Diabetes-associated platelet dysfunction

  • Hyperglycemia leads to increased S100A8/A9 leads to increased TPO leads to increased RPs leads to thrombosis
  • Therapeutic strategies:
  1. SGLT2 inhibitors (decrease RP production indirectly)
  2. S100A8/A9 inhibitors (ABR-215757)
  3. IL-6 / TPO modulation
  • Result: decreased platelet hyperreactivity and restored antiplatelet response
  • Precision approach: treat metabolism to fix platelets

Core clinical takeaways

  • Not all platelets are equal: ‘subpopulation-driven thrombosis’
  • Young platelets: drug resistance and higher risk
  • Future: target biology (GPVI / S100A8/A9 / PD-L1) not just aggregation
  • Move from ‘one-size antiplatelet’ to precision platelet therapy

MCQ

Which strategy best overcomes high platelet turnover–related resistance?

  1.  Increase aspirin dose
  2.  Switch to clopidogrel
  3. Use ticagrelor
  4. Add warfarin

Answer: C

Reversible P2Y12 inhibition maintains effect despite new platelet generation

OSCE scenario

Post-PCI patient with recurrent events despite DAPT and high IPF%

  • Best step: switch to ticagrelor-based strategy
  • Consider future: GPVI-targeted therapy (trial setting).”

Chokri Ben Lamine: Thread Platelet Subpopulations Leads to Therapeutic Implications

Find more posts featuring Chokri Ben Lamine on Hemostasis Today.

 

CAD Chokri Ben Lamine Health Hematology Hemostasis Hemostasis News Hemostasis Today Medicine Platelet Thromboxane TPO
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