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There are countless mechanisms for causing platelet abnormalities, many of which are likely yet to be discovered. This chapter is meant to touch on additional platelet abnormalities not completely discussed in other chapters of this book—but is not by any means all inclusive. It is important to note that some platelet abnormalities may incidentally be detected in laboratory assays without an associated manifestation of clinical signs or symptoms. Such results can lead to an inappropriate (and harmful) action when interpreted without clinical context. With this in mind, consider these categories in the differential diagnosis of a platelet-like disorder workup to create a more comprehensive evaluation and continue to look further.
The effects of antiplatelet medications, aspirin, and other nonsteroidal antiinflammatory medications (NSAIDs) have already been described in other chapters. In addition to these, many drugs and herbal supplements have a platelet disorder listed in their side effect profile. Such drugs can provoke a thrombocytopathy and/or thrombocytopenia. Examples of these drugs include antiepileptics, antipsychotics, endocrine replacements, over-the-counter supplements and food ingredients ( Table 100.1 ). It is recommended to review all medications and supplements for side effects, and if clinically safe, recommend that the patient refrain from taking these medications in a reasonable time before platelet testing and/or surgical procedures to clear them from the patient’s system.
Drug Category | Common Examples |
---|---|
Neurological/antipsychotics | Selective serotonin reuptake inhibitors, valproic acid, levetiracetam (Keppra), levodopa |
Endocrine | Levothyroxine |
Antibiotics | Beta-lactam antibiotic |
Methylxanthines | Caffeine, theobromine, theophylline |
Supplements, herbs, and foods | Fish oil, garlic, ginseng, Ginkgo biloba , ginger, bilberry, dong quai, feverfew, turmeric, meadowsweet, willow, black tree fungus, alcohol |
The interaction of blood with nonbiological surfaces and/or conditions that increase turbulent flow is associated with platelet abnormalities. A resulting acquired von Willebrand disease and activation of coagulation pathways are also contributing factors. Examples of devices with artificial surfaces are often used during cardiopulmonary bypass and extracorporeal membrane oxygenation. Increased shear stress and turbulent flow is seen in heart valve disease (e.g., aortic stenosis), cavernous hemangiomata (Kasabach–Merritt syndrome), and disseminated intravascular coagulation. It is well known that thrombocytopenia ensues due to consumption, but platelets also may show signs of dysfunction. This phenomenon has been described as an “exhausted platelet syndrome” where the platelets are initially hyperactivated by injured endothelium releasing ADP, then subsequently, become unresponsive. Other studies describe mechanisms of thrombocytopathy involving alteration of platelet membrane lipid organization, loss of platelet surface integrins and receptors (integrin a2bB3, GPIbα, and GPVI shedding), and oxidative stress.
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