![]() Clinical utilization of MPV in cardiovascular disease, DM, and malignancy is open to discussion.Ī low MPV is usually related to inflammatory states. Mean platelet volume level was significantly higher in malignant tumors than in healthy subjects and decreased with therapy, according to a recent meta-analysis ( 8). MPV is augmented in patients with type 2 diabetes mellitus (DM) and might associate with risk of cardiovascular events in this population ( 7). The test might behave as a prognostic biomarker in individuals with cardiovascular disease ( 6). In a 2010 meta-analysis, an elevated MPV associated with acute myocardial infarction (AMI), mortality after AMI, as well as restenosis following coronary angioplasty. There has also been a body of interest for MPV in patients with normal platelet counts. In patients with high platelet counts, a high MPV is suggestive of primary thrombocytosis, while a low MPV characterizes a reactive thrombocytosis, seen in infection, inflammation, or malignancy ( 5). Thrombocytopenia with low MPV is typical of patients with low platelet production, i.e., aplastic anemia. Thrombocytopenia with high MPV is seen in immune thrombocytopenic purpura (ITP), disseminated intravascular coagulation (DIC), sepsis, and preeclampsia. The test is particularly useful in patients with thrombocytopenia and thrombocytosis. MPV cutoff has not been fully validated so far, and standardization is a major need. Clinical utility of MPV has been a matter of debate for the last few years. It is also regarded as a useful surrogate marker of platelet activation or reactivity ( 4, 5). MPV correlates with platelet function and may be more sensitive than platelet count as a biomarker in a variety of disorders. It is meant to show the relationship between platelet synthesis in bone marrow and cell destruction. Mean platelet volume, normally measured using automated blood analysers, reflects the average size of platelets in circulation. We will particularly approach the clinical applicability of MPV and IPF in such a context. In this review, we will be focusing on the “non-hemostatic” functions of platelets in rheumatic and non-rheumatic autoimmune disorders. Among them, the mean platelet volume (MPV), routinely measured in blood cell count, and the immature platelet fraction (IPF) are tests of current interest ( 5). Size correlates with cell activity and can be assessed by volume indices ( 4). Platelet size heterogeneity is mostly determined by variations in territory growth and demarcation, but not accurately upon aging in circulation. Moreover, serotonin released by platelets enhances vascular permeability within the inflamed synovium ( 3). ![]() IL-1-containing platelet-derived vesicles are abundant in synovial fluid and stimulate synovial fibroblast to produce inflammatory mediators. In autoimmune diseases such as systemic lupus erythematosus (SLE), immune complexes activate platelets by interacting with Fc receptors in RA, the platelet is a well-known source of prostaglandins within the inflamed synovium. Also, they release granular contents (growth factors) active in wound repair ( 2). Knowingly, platelets can recognize bacteria and attract immune cells to inflammatory sites. Platelet receptors such as CD40, GPIb/IX/V, and selectins have all been implicated in perpetuation of atherosclerosis, rheumatoid arthritis (RA), and tumors. Platelets have also been linked to inflammation, atherosclerosis, autoimmunity, and tumor immunology ( 1). Nowadays, the biological functions of platelets are considered to be far beyond hemostasis and thrombosis. Approximately one trillion platelets circulate in blood to provide vascular regulation. Platelets are intriguing and complex cells. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |