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Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Reduced platelet function and role of drugs in acute gastrointestinal bleeding
Marianne K Kringen1, Sigrid Narum, Idar Lygren
1Department of Pharmacology, Oslo University Hospital, Ullevål, Kirkeveien 166, Oslo, Norway. m.k.kringen@medisin.uio.no
Gastrointestinal (GI) bleeding may be caused by a constitutive bleeding disposition or drug-induced inhibition of hemostasis. Platelet function in patients with ongoing GI bleeding is unknown. The aim of this study was to investigate platelet function in patients with acute GI bleeding. Patients (n=35) presenting with acute GI bleeding (hematemesis or melena) were recruited. For comparison, 13 patients treated with aspirin and 11 patients treated with clopidogrel without GI bleeding and 27 healthy controls were studied. Platelet function was measured by whole-blood aggregation and flow cytometry. Coagulation function was measured with calibrated automated thrombography. Platelet aggregation and P-selectin expression were significantly lower after arachidonic acid stimulation in GI bleeding patients than in healthy subjects (p≤0.05). Collagen-induced P-selectin expression was significantly reduced in patients using anti-platelet drugs (p=0.02) and in many patients not using anti-platelet drugs. Thrombin generation, measured by calibrated automated thrombography, was only reduced in patients on warfarin treatment. In conclusion, platelet function is reduced in acute GI bleeding patients and a considerable proportion appears to be related to drug use.
Gastrointestinal (GI) bleeding may be caused by a constitutive bleeding disposition or drug-induced inhibition of hemostasis. Platelet function in patients with ongoing GI bleeding is unknown. The aim of this study was to investigate platelet function in patients with acute GI bleeding. Patients (n=35) presenting with acute GI bleeding (hematemesis or melena) were recruited. For comparison, 13 patients treated with aspirin and 11 patients treated with clopidogrel without GI bleeding and 27 healthy controls were studied. Platelet function was measured by whole-blood aggregation and flow cytometry. Coagulation function was measured with calibrated automated thrombography. Platelet aggregation and P-selectin expression were significantly lower after arachidonic acid stimulation in GI bleeding patients than in healthy subjects (p≤0.05). Collagen-induced P-selectin expression was significantly reduced in patients using anti-platelet drugs (p=0.02) and in many patients not using anti-platelet drugs. Thrombin generation, measured by calibrated automated thrombography, was only reduced in patients on warfarin treatment. In conclusion, platelet function is reduced in acute GI bleeding patients and a considerable proportion appears to be related to drug use.
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