Reduced Platelet Function and Role of Drugs in Acute Gastrointestinal Bleeding
: 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...
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Published in | Basic & clinical pharmacology & toxicology Vol. 108; no. 3; pp. 194 - 201 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.03.2011
Blackwell |
Subjects | |
Online Access | Get full text |
ISSN | 1742-7835 1742-7843 1742-7843 |
DOI | 10.1111/j.1742-7843.2010.00643.x |
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Abstract | : 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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AbstractList | 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. 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 less than or equal to 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. |
Author | Holthe, Mette R. Sandset, Per‐Morten Kringen, Marianne K. Brørs, Odd Narum, Sigrid Lygren, Idar Trøseid, Anne‐Marie S. Johansen, Per W. Seljeflot, Ingebjørg |
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Keywords | Drug Digestive diseases Intestinal disease Gastrointestinal bleeding Acute Platelet function |
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SubjectTerms | Adult Aged Aged, 80 and over Anticoagulants - adverse effects Antigens, CD - blood Arachidonic acid Arachidonic Acid - pharmacology Aspirin Biological and medical sciences Bleeding Blood Coagulation - drug effects Blood Platelets - drug effects Blood Platelets - metabolism Clopidogrel Coagulation Collagen Collagen - pharmacology Disposition Drugs Female Flow cytometry Gastrointestinal Hemorrhage - chemically induced Gastrointestinal Hemorrhage - metabolism Gastrointestinal Hemorrhage - physiopathology Hematemesis - etiology hemostasis Hemostasis - drug effects Humans Male Medical sciences Melena - etiology Middle Aged P-selectin P-Selectin - blood Pharmacology. Drug treatments Platelet aggregation Platelet Aggregation - drug effects Platelet Aggregation Inhibitors - adverse effects Platelet Membrane Glycoproteins Severity of Illness Index Tetraspanin 30 Thrombin Warfarin |
Title | Reduced Platelet Function and Role of Drugs in Acute Gastrointestinal Bleeding |
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