Reduced Platelet Function and Role of Drugs in Acute Gastrointestinal Bleeding

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). Collageninduced 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 has an incidence of 50 ⁄ 100,000 citizens per year [1], is often serious and even lethal. GI bleeding may be caused by inherited disposition, acquired bleeding diathesis, specific diseases such as Helicobacter pylori infection or oesophageal varices [2,3]. Acquired bleeding diathesis is often caused by adverse drug reaction of anti-thrombotic drugs. Both anti-coagulants and anti-platelet drugs are frequently used drugs in primary and secondary prevention of thromboembolism [4,5] and are associated with serious GI bleeding. Vitamin K antagonists, such as warfarin, interfere with the formation of functional gammacarboxylated vitamin K-dependent clotting factors (factors II, VII, IX and X) and anti-coagulants (protein C, -S and -Z) [6]. Aspirin and clopidogrel are the most commonly used anti-platelet drugs. Aspirin irreversibly acetylates cyclooxygenase (COX) -1 and inhibits thromboxane A2-mediated platelet aggregation as well as prostaglandin E 2 -mediated gastroprotection [7,8], whereas clopidogrel blocks the platelet adenosine diphosphate (ADP)-receptor P2Y 12 [9]. Non-steroidal anti-inflammatory drugs (NSAIDs) are frequently used non-selective and reversible inhibitors of both COX-1 and COX-2; however, the inhibition of COX-1 varies between the agents.Platelet count and platelet function are of vital importance for normal hemostasis. To our knowledge, no investigations have been published concerning platelet function in patients with acute GI bleeding. We hypothesized that in patients with acute GI bleeding, medications with known or possible influence on hemostasis cause a decrease in platelet and ⁄ or coagulation function. The aim of this study was therefore to investigate platelet function and the level of pro-coagulant...

Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management

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Intra‐Arterial Treatment for Massive Subcutaneous Hemorrhage in Hemodialysis Patients

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Efficacy of Intra‐Arterial Treatment for Massive Gastrointestinal Bleeding in Hemodialysis Patients

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