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Platelets are relatively small blood cells that facilitate clotting and maintenance of blood volume, especially during vascular injury. A balance of healthy mature platelets is vital to homeostasis. Low platelets may be associated with bone marrow failure, hemorrhage, certain anemias, lupus, leukemia, and increased all-cause mortality.
Excessively high platelets, especially large immature ones, are detrimental and can be associated with thrombosis, malignancy, rheumatoid arthritis, inflammation, iron-deficiency anemia, and increased all-cause mortality
Standard Range: 140 - 400 10E3/uL
Optimal Dx’s Optimal Range: 190 - 300 10E3/uL
Low platelet count (thrombocytopenia) is seen with decreased platelet production due to bone marrow failure or damage, platelet destruction, hemorrhage, acute or chronic infection, pernicious anemia, some hemolytic anemias, myelofibrosis, leukemia, lupus, hypersplenism, disseminated intravascular coagulation, chemotherapy, dilution due to transfusion, or medication use including antibiotics and diuretics (Pagana 2021). A decreasing platelet count is associated with increasing fibrosis in NAFLD (Yoneda 2011).
High platelet count (thrombocytosis or thrombocythemia) is seen with thrombosis, malignancy, iron-deficiency anemia, polycythemia vera, rheumatoid arthritis, inflammation, post-splenectomy, living at high altitudes, strenuous exercise, some infections, and oral contraceptive use (Pagana 2021). A high platelet count may be associated with significantly lower bone mineral density (Kristjansdottir 2021). Increased activated platelets can contribute to the progression and pathogenicity of atherosclerosis (Badimon 2012).
Platelets, also called thrombocytes, are essential to blood clotting and vascular function. Platelets stick together and adhere to an injury site, creating a “platelet plug” in order to stop bleeding. Once activated, platelets promote the coagulation cascade to further enhance clotting and maintain blood volume during vascular injury. They are also involved in the immune response, inflammation, and tissue growth. Platelets store many vital compounds including serotonin, ATP, ADP, calcium, and potassium (Fountain 2021).
The platelet count reflects how many platelets are found in a cubic millimeter of blood. It is important to assess the platelet count in those individuals with spontaneous bleeding, heavy menstrual periods. or petechiae (Pagana 2021). Petechiae are pinpoint hemorrhages under the skin that can be caused by vitamin C deficiency.
Platelets play an active role in the innate immune system and help reduce risk of infection following an injury. When platelets bind bacteria, they release antimicrobial peptides along with hundreds of active compounds. These include serotonin which facilitates vasoconstriction to minimize blood loss, and ADP which recruits more platelets to the site (Cox 2011).
Chronic cigarette smoking, a source of toxic heavy metals, can impair platelet function via oxidative stress. Research indicates that oral administration of 2 grams of vitamin C reduced the oxidative and toxic effects of smoking on platelet function (Takajo 2001).
A decreased platelet count is associated with all-cause mortality as demonstrated in population and cohort studies. A 12-year follow-up study of 29,526 angiography patients suggests that individuals with a platelet count of 182 or below had increased risk of all-cause mortality while those with a count of 264 and above had reduced risk (Anderson 2007).
The association between lower platelet count and increased all-cause mortality was also observed in a comprehensive evaluation that included patient and general populations comprising 138,309 subjects. Platelet counts of 183 or below, calculated into the Intermountain Risk Score, contributed the most to all-cause mortality compared to higher platelets (Horne 2009).
Anderson, Jeffrey L et al. “Usefulness of a complete blood count-derived risk score to predict incident mortality in patients with suspected cardiovascular disease.” The American journal of cardiology vol. 99,2 (2007): 169-74. doi:10.1016/j.amjcard.2006.08.015
Badimon, Lina et al. “Atherosclerosis, platelets and thrombosis in acute ischaemic heart disease.” European heart journal. Acute cardiovascular care vol. 1,1 (2012): 60-74. doi:10.1177/2048872612441582
Cox, D et al. “Platelets and the innate immune system: mechanisms of bacterial-induced platelet activation.” Journal of thrombosis and haemostasis : JTH vol. 9,6 (2011): 1097-107. doi:10.1111/j.1538-7836.2011.04264.x
Fountain, J. H., & Lappin, S. L. (2021). Physiology, Platelet. In StatPearls. StatPearls Publishing.
Horne, Benjamin D et al. “Exceptional mortality prediction by risk scores from common laboratory tests.” The American journal of medicine vol. 122,6 (2009): 550-8. doi:10.1016/j.amjmed.2008.10.043
Kristjansdottir, H L et al. “High platelet count is associated with low bone mineral density: The MrOS Sweden cohort.” Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA vol. 32,5 (2021): 865-871. doi:10.1007/s00198-020-05766-6
Pagana, Kathleen Deska, et al. Mosby's Diagnostic and Laboratory Test Reference. 15th ed., Mosby, 2021.
Podda, Gian Marco et al. “Measurement of platelet count with different anticoagulants in thrombocytopenic patients and healthy subjects: accuracy and stability over time.” Haematologica vol. 104,12 (2019): e570-e572. doi:10.3324/haematol.2019.222265
Takajo, Y et al. “Augmented oxidative stress of platelets in chronic smokers. Mechanisms of impaired platelet-derived nitric oxide bioactivity and augmented platelet aggregability.” Journal of the American College of Cardiology vol. 38,5 (2001): 1320-7. doi:10.1016/s0735-1097(01)01583-2
Yoneda, Masato et al. “Platelet count for predicting fibrosis in nonalcoholic fatty liver disease.” Journal of gastroenterology vol. 46,11 (2011): 1300-6. doi:10.1007/s00535-011-0436-4