Acquired platelet dysfunction, which is common, may result from aspirin, other nonsteroidal anti-inflammatory drugs (NSAIDs), or systemic disorders.
(See also Overview of Platelet Disorders.)
Acquired abnormalities of platelet function are very common. Causes include
Medications
Systemic disorders
Cardiopulmonary bypass
Acquired platelet dysfunction is suspected and diagnosed when unusual or prolonged bleeding is observed and other possible diagnoses (eg, thrombocytopenia, coagulation abnormalities) have been eliminated. Platelet aggregation studies are unnecessary.
Лікарські препарати
Aspirin, other NSAIDs, inhibitors of the platelet P2Y12 adenosine diphosphate (ADP) receptor (eg, clopidogrel, prasugrel, ticagrelor), and glycoprotein IIb/IIIa receptor inhibitors (eg, abciximab, eptifibatide, tirofiban) may induce platelet dysfunction. Sometimes this effect is incidental (eg, when the medications are used to relieve pain and inflammation) and sometimes therapeutic (eg, when aspirin or the P2Y12 inhibitors are used for prevention of stroke or coronary thrombosis).
Aspirin and NSAIDs prevent cyclooxygenase-mediated production of thromboxane A2. The aspirin effect lasts 5 to 7 days and that of NSAIDs for under a day. Aspirin modestly increases bleeding in healthy people but may markedly increase bleeding in older patients and those with underlying platelet dysfunction or a severe coagulation disturbance (eg, patients receiving heparin, patients with severe hemophilia). Aspirin, clopidogrel, prasugrel, and ticagrelor all can markedly reduce platelet function and increase bleeding.
A number of other medications can also cause platelet dysfunction (1).
Системні порушення
Many disorders (eg, myeloproliferative neoplasms, myelodysplastic disorders, uremia, macroglobulinemia, multiple myeloma, cirrhosis, systemic lupus erythematosus) can impair platelet function.
Of the systemic disorders, uremia is probably the most common and significant; uremia prolongs bleeding via unknown mechanisms. If bleeding is observed clinically in patients with uremia, bleeding may be reduced with vigorous dialysis, cryoprecipitate administration, or desmopressin infusion. If necessary, increasing the hemoglobin concentration to > 10 g/dL (> 100 g/L) by transfusion or by giving erythropoietin can also reduce bleeding. No high-quality data are available on the efficacy of these alternatives.
Серцево-легеневе шунтування
As blood circulates through a pump oxygenator during cardiopulmonary bypass, platelets may become dysfunctional, prolonging bleeding. The mechanism appears to be activation of fibrinolysis on the platelet surface with resultant loss of the glycoprotein Ib/IX binding site for von Willebrand factor. Regardless of platelet count, patients who bleed excessively after cardiopulmonary bypass are often transfused with platelets; this is a weak recommendation by the AABB (formerly, the American Association of Blood Banks) based on very low quality evidence (2). Giving an antifibrinolytic agent during bypass may preserve platelet function and reduce the need for transfusion (3).
Довідкові матеріали
1. Scharf RE: Drugs that affect platelet function. Semin Thromb Hemost 38(8): 865–883, 2012. doi: 10.1055/s-0032-1328881
2. Kaufman RM, Djulbegovic B, Gernsheimer T, et al: Platelet transfusion: a clinical practice guideline from the AABB. Ann Intern Med 162(3):205–213, 2015. doi:10.7326/M14-1589
3. Brown JR, Birkmeyer NJ, O'Connor GT: Meta-analysis comparing the effectiveness and adverse outcomes of antifibrinolytic agents in cardiac surgery. Circulation 115(22):2801–2813, 2007. doi:10.1161/CIRCULATIONAHA.106.671222
