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B Luderitz - One of the best experts on this subject based on the ideXlab platform.
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mean Platelet volume as marker of restenosis after percutaneous transluminal coronary angioplasty in patients with stable and unstable angina pectoris
Thrombosis Research, 2006Co-Authors: Alexander Yang, L Pizzulli, B LuderitzAbstract:Abstract Introduction Several experimental and clinical studies have demonstrated that Platelet Size and function correlate since large Platelets are hemostatically more reactive than Platelets of normal Size. Since Platelets play a crucial role in vascular remodeling after percutaneous transluminal coronary angioplasty (PTCA), we investigated the influence of the mean Platelet volume (MPV), a parameter of Platelet Size, on restenosis after PTCA. Methods The retrospective study comprised 174 patients who underwent elective PTCA and follow-up angiography within 6 months thereafter. According to the follow-up angiograms, the patients were assigned to group A (“restenosis”, n = 74) or group B (“no restenosis”, n = 100). Both groups were compared in regard to pre-procedural hematological routine parameters including MPV, Platelet count, hematocrit, white blood cell count and fibrinogen. Results MPV was significantly increased in group A, compared with that in group B (8.75 ± 0.99 fl vs. 8.04 ± 0.74 fl, p Conclusions The MPV seems to be a marker of coronary restenosis in patients undergoing PTCA. Patients with high pre-procedural MPV values might benefit from an intensified antiPlatelet therapy after coronary interventions.
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changes in Platelet Size and count in unstable angina compared to stable angina or non cardiac chest pain
European Heart Journal, 1998Co-Authors: L Pizzulli, A Yang, J F Martin, B LuderitzAbstract:Aims An increase in Platelet aggregability is associated with unstable angina and myocardial infarction. Platelet Size and activity correlate and mean Platelet volume was found to be increased before acute myocardial infarction. We measured the mean Platelet volume and Platelet count in patients with stable angina, unstable angina and non-cardiac chest pain. Methods and results We studied 981 patients (734 men; 247 women) defined clinically as stable angina (n=688), unstable angina (n=108) and unstable angina requiring immediate angioplasty (n=52). After coronary angiography the patients were subdivided into single (n=269), double (n=304) and triple-vessel disease (n=311) and the control group of non-cardiac chest pain (n=97). There was no significant difference in Platelet count between the control group and patients with 1, 2, or 3-vessel disease. However, the Platelet Size in patients with coronary artery disease was significantly larger (single: 8·7±1·19fl; double: 8·7±1·12fl; triple-vessel disease: 8·8±1·18fl) than the control group (8·2±0·95fl) ( P <0·01). Patients with stable angina similarly had no significant difference in Platelet count compared to the control group but did have a significantly increased mean Platelet volume (8·7±1·13; P <0·01). In contrast, patients with unstable angina had a decreased Platelet count (245±56×10/l) compared to either stable angina (262±62×10/l; P <0·05) or the control group (261±58×10/l; P <0·05); furthermore, the mean Platelet volume (9·4±1·23fl) was significantly greater than for stable angina ( P <0·01). Patients with unstable angina requiring immediate PTCA had an even lower Platelet count (231±55×10/l) and higher mean Platelet volume (10·4±1·03fl) ( P <0·01) than the rest of the population with unstable angina. Conclusions In stable angina the Platelet count is unchanged compared to patients with normal coronary arteries but the Platelet Size is increased. However, in unstable angina there is a decrease in Platelet count and an even larger increase in Platelet Size. We interpret this as meaning that unstable angina might be associated or preceded by an increase in Platelet destruction rate that is not completely compensated for by an increase in Platelet production rate. The large, more reactive Platelets might be causally related to an ongoing coronary artery obstruction in unstable angina.
Anders A Bengtsson - One of the best experts on this subject based on the ideXlab platform.
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p28 decreased Platelet Size in systemic lupus erythematosus is associated with up regulation of type i interferon proteins
Lupus science & medicine, 2020Co-Authors: Petrus Linge, Andreas Jonsen, Robin Kahn, Lina Wirestam, Sabine Arve, Anders A BengtssonAbstract:Background Dysregulated apoptosis is of major importance in Systemic Lupus Erythematosus (SLE) pathogenesis, linked to the development of autoantibodies, immune complex formation and type I interferon signaling. Platelets from SLE patients are smaller in Size, compared to Platelets from healthy individuals, which may suggest an increased rate of apoptosis, a known cause of Platelet shrinkage. Our aim with this project was to investigate if decreased Platelet Size could be explained by increased apoptosis rates. Methods Platelet activation markers; CD62P, CD41, CD154, CD32, PAC-1 and PAR1 and apoptosis; Annexin V, Caspase 3 activation, mitochondrial content (MitoTracker) and mitochondrial depolarization (JC-1) where analyzed in 23 SLE patients and 10 healthy controls (HC) by flow cytometry. Analysis of the total protein content in Platelets from SLE patients of normal (n=5) and decreased (n=5) Size were made using mass spectrometry (MS). Results The level of CD41 (p=0.001) positive Platelets and mean expression of CD154 (p=0.004) were higher in SLE patients. A JC-1 ratio (p=0.0001) indicting increased mitochondrial depolarization was significantly associated with Platelets from SLE patients. MS analysis revealed 32 proteins with ≥ 1.5-fold difference and a p-value of less than 0.05 (Abundance Ratio Adjusted). STAT1, ISG15, NMI and TRIM25 were among 19 proteins expressed at higher levels in small Platelets and unbiased enrichments analyses showed a significant overrepresentation of proteins related to type I interferon signaling. Conclusions The increased mitochondrial depolarization in Platelets from SLE patients is an indication but not conclusive evidence of increased Platelet apoptosis. Interestingly, decreased Sized Platelets from SLE patients showed an up regulation of type I interferon related proteins, suggesting direct or indirect influence of IFN. This is a novel finding that may suggest that Platelet Size is related to IFN signaling. Further studies will be conducted to investigate the mechanistic and potential clinical role of this finding.
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decreased Platelet Size is associated with Platelet activation and anti phospholipid syndrome in systemic lupus erythematosus
Rheumatology, 2016Co-Authors: Christian Lood, Helena Tyden, Birgitta Gullstrand, Christoffer Tandrup Nielsen, Niels H H Heegaard, Petrus Linge, Andreas Jonsen, Roger Hesselstrand, Robin Kahn, Anders A BengtssonAbstract:Objectives: . SLE is an autoimmune disease with increased cardiovascular morbidity and Platelet activation. In the general population, increased Platelet Size predicts Platelet reactivity and cardiovascular disease. The aim of this study was to investigate whether Platelet Size related to Platelet activation and cardiovascular disease in SLE.Methods: . Fresh blood samples from SLE patients ( n = 148), healthy volunteers ( n = 79) and disease controls ( n = 40) were analysed for Platelet Size and activation by flow cytometry, ELISA and cell count. Associations to manifest cardiovascular disease, venous thrombosis and APS were adjusted for traditional cardiovascular risk factors using logistic regression analysis.Results: . SLE patients had decreased Platelet Size as compared with healthy controls ( P = 0.003). In SLE, decreased Platelet Size was related to increased Platelet activation, in particular microparticle formation ( P < 0.0001, r = -0.46) and release of serotonin from dense granules ( P < 0.001, r = 0.57). SLE patients with aCL had decreased Platelet Size ( P = 0.02) and aCL decreased Platelet Size in vitro ( P = 0.007). In contrast to the general population, increased Platelet Size was not associated with cardiovascular disease. Instead, decreased Platelet Size was associated with secondary APS, even after adjusting for traditional cardiovascular risk factors ( P = 0.01, odds ratio 3.58).Conclusion: . Platelet Size is decreased in SLE patients and associated with microparticle formation and APS. Future studies are needed to determine the underlying mechanism(s) as well as the potential predictive value of small Platelets for disease complications in SLE.
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decreased Platelet Size is associated with Platelet activation and anti phospholipid syndrome in systemic lupus erythematosus
Rheumatology, 2016Co-Authors: Christian Lood, Helena Tyden, Birgitta Gullstrand, Christoffer Tandrup Nielsen, Niels H H Heegaard, Petrus Linge, Andreas Jonsen, Roger Hesselstrand, Robin Kahn, Anders A BengtssonAbstract:Objectives: . SLE is an autoimmune disease with increased cardiovascular morbidity and Platelet activation. In the general population, increased Platelet Size predicts Platelet reactivity and cardiovascular disease. The aim of this study was to investigate whether Platelet Size related to Platelet activation and cardiovascular disease in SLE.Methods: . Fresh blood samples from SLE patients ( n = 148), healthy volunteers ( n = 79) and disease controls ( n = 40) were analysed for Platelet Size and activation by flow cytometry, ELISA and cell count. Associations to manifest cardiovascular disease, venous thrombosis and APS were adjusted for traditional cardiovascular risk factors using logistic regression analysis.Results: . SLE patients had decreased Platelet Size as compared with healthy controls ( P = 0.003). In SLE, decreased Platelet Size was related to increased Platelet activation, in particular microparticle formation ( P < 0.0001, r = -0.46) and release of serotonin from dense granules ( P < 0.001, r = 0.57). SLE patients with aCL had decreased Platelet Size ( P = 0.02) and aCL decreased Platelet Size in vitro ( P = 0.007). In contrast to the general population, increased Platelet Size was not associated with cardiovascular disease. Instead, decreased Platelet Size was associated with secondary APS, even after adjusting for traditional cardiovascular risk factors ( P = 0.01, odds ratio 3.58).Conclusion: . Platelet Size is decreased in SLE patients and associated with microparticle formation and APS. Future studies are needed to determine the underlying mechanism(s) as well as the potential predictive value of small Platelets for disease complications in SLE.
Neal S. Kleiman - One of the best experts on this subject based on the ideXlab platform.
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Platelet activation patterns in Platelet Size sub populations differential responses to aspirin in vitro
Journal of Thrombosis and Thrombolysis, 2010Co-Authors: Kiran Kumar R Mangalpally, Jing Fei Dong, Muthiah Vaduganathan, Neal S. Kleiman, Alan Siqueirosgarcia, Sasidhar GuthikondaAbstract:Circulating Platelets are heterogeneous in Size and structure. Whether this translates into differences in Platelet function and efficacy of antiPlatelet therapy is unclear. Hence, we decided to investigate the activation patterns among different Platelet populations differentiated by Size, and to compare the inhibitory effects of aspirin in these populations. Circulating Platelets from 9 healthy volunteers were separated by Size and stratified into the largest and smallest quintiles. Platelets were stimulated with 75 μM arachidonic acid (AA), 10 μM ADP or 25 μM TRAP. Alpha-granule protein secretion and expression (P-selectin, VWF, fibrinogen), surface-protein activation (activated integrin αIIbβ3) were assessed. Platelet thromboxane B2 (TxB2) synthesis following AA stimulation was measured in vitro before and after incubation with 265 μM aspirin. Reticulated (juvenile) Platelets were assessed using thiazole orange staining. A greater number of large Platelets in the largest quintile were reticulated compared with the smallest quintile (6.1 ± 2.8% vs. 1.2 ± 1.5% respectively, p < 0.001). Larger Platelets also syntheSized more TxB2 than small Platelets both before (1348 ± 276 pg/mL vs. 1023 ± 214 pg/mL, respectively, p = 0.01) and after aspirin (1029 ± 190 pg/mL vs. 851 ± 159 pg/mL, respectively, p = 0.03). After stimulation with each agonist, a greater proportion of large Platelets bound fibrinogen, VWF, P-selectin and activated integrin αIIbβ3 than small Platelets both in the presence and in the absence of in vitro aspirin. In an in vitro setting, large Platelets appear to be more active than small Platelets and continue to be more active even after in vitro aspirin. Platelets exhibit heterogeneity in Size and structure. Whether this translates into Platelet function and efficacy of antiPlatelet therapy is unclear. We evaluated Platelet functional properties and the effects of aspirin on separated Platelet subpopulations in an in vitro setting. Platelets were sorted into the largest and smallest Size quintiles using flow cytometry forward scatter. Alpha-granule protein release, dense granule content, surface protein activation and thromboxane synthesis were significantly greater in large Platelets compared with small Platelets, before and after stimulation with arachidonic acid, ADP and TRAP. Even after incubation with aspirin, large Platelets continued to be more active than small Platelets. In conclusion, large Platelets are more active than small Platelets and aspirin fails to eliminate these differential activation properties.
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role of reticulated Platelets and Platelet Size heterogeneity on Platelet activity after dual antiPlatelet therapy with aspirin and clopidogrel in patients with stable coronary artery disease
Journal of the American College of Cardiology, 2008Co-Authors: Sasidhar Guthikonda, Mehmet E Arikan, Timothy Delao, Carlos L Alviar, Armando Tellez, Jing Fei Dong, Muthiah Vaduganathan, Juan F Granada, Neal S. KleimanAbstract:Objectives The aim of this study was to evaluate the relationship between reticulated Platelets (RPs), Platelet Size, and Platelet function in patients with stable coronary artery disease (CAD) taking aspirin and clopidogrel. Background Reticulated Platelets are young Platelets that are larger and possibly more active than non-RPs. Methods Flow cytometry was used to measure RPs after staining with thiazole orange and to define the upper 20% and lower 20% of Platelets by Size. Platelet aggregation was measured with light transmission aggregometry (LTA); Platelet activation was assessed by measuring activated Platelet surface expression of P-selectin and glycoprotein (GP) IIb/IIIa. Results Ninety patients were recruited and stratified into tertiles of %RPs. Patients in the upper tertile displayed greater Platelet aggregation to 5-μmol/l adenosine diphosphate (ADP) (50.7 ± 16.4% vs. 34.2 ± 17.3%, p 20%) was higher in the upper tertile (53% vs. 17%, p 50%) was also elevated in the upper tertile (50% vs. 13%, p = 0.003). The larger Platelet gate had a higher % of RPs compared with the smaller gate (15.4 ± 16.7% vs. 1.7 ± 2.3%, p Conclusions The proportion of circulating RPs strongly correlates with response to antiPlatelet therapy in patients with stable CAD. Large Platelets exhibit increased reactivity despite dual antiPlatelet therapy, compared with smaller Platelets.
Patrizia Noris - One of the best experts on this subject based on the ideXlab platform.
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clinical and pathogenic features of etv6 related thrombocytopenia with predisposition to acute lymphoblastic leukemia
Haematologica, 2016Co-Authors: Federica Melazzini, Patrizia Noris, Flavia Palombo, Alessandra Balduini, Daniela De Rocco, Caterina Marconi, Chiara Gnan, Tommaso Pippucci, Valeria BozziAbstract:ETV6-related thrombocytopenia is an autosomal dominant thrombocytopenia that has been recently identified in a few families and has been suspected to predispose to hematologic malignancies. To gain further information on this disorder, we searched for ETV6 mutations in the 130 families with inherited thrombocytopenia of unknown origin from our cohort of 274 consecutive pedigrees with familial thrombocytopenia. We identified 20 patients with ETV6-related thrombocytopenia from seven pedigrees. They have five different ETV6 variants, including three novel mutations affecting the highly conserved E26 transformation-specific domain. The relative frequency of ETV6-related thrombocytopenia was 2.6% in the whole case series and 4.6% among the families with known forms of inherited thrombocytopenia. The degree of thrombocytopenia and bleeding tendency of the patients with ETV6-related thrombocytopenia were mild, but four subjects developed B-cell acute lymphoblastic leukemia during childhood, resulting in a significantly higher incidence of this condition compared to that in the general population. Clinical and laboratory findings did not identify any particular defects that could lead to the suspicion of this disorder from the routine diagnostic workup. However, at variance with most inherited thrombocytopenias, Platelets were not enlarged. In vitro studies revealed that the maturation of the patients' megakaryocytes was defective and that the patients have impaired proPlatelet formation. Moreover, Platelets from patients with ETV6-related thrombocytopenia have reduced ability to spread on fibrinogen. Since the dominant thrombocytopenias due to mutations in RUNX1 and ANKRD26 are also characterized by normal Platelet Size and predispose to hematologic malignancies, we suggest that screening for ETV6, RUNX1 and ANKRD26 mutations should be performed in all subjects with autosomal dominant thrombocytopenia and normal Platelet Size.
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new roles for mean Platelet volume measurement in the clinical practice
Platelets, 2016Co-Authors: Patrizia Noris, Federica Melazzini, Carlo L BalduiniAbstract:AbstractSeveral hundreds of studies recently investigated mean Platelet volume (MPV) as measured by electronic cell counters in a wide variety of acquired diseases, and most of them found that Platelet Size was significantly increased with respect to healthy subjects. On this basis, it has been suggested that MPV can be used for diagnostic purposes. Moreover, investigation of subjects with arterial thrombosis not only revealed that their Platelets were larger than those of controls, but also found that a high MPV predicted poor prognosis. Despite the large amount of available data, the pathogenesis of increased Platelet Size in these conditions is unclear. In particular, we do not know whether the increased Platelet Size is the cause or the consequence of thrombosis. Differences in MPV between patients and controls are usually very small and they reach the statistical significance because of the large number of investigated patients and the standardized methodology for MPV measurement. In real life, the w...
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Platelet Size for distinguishing between inherited thrombocytopenias and immune thrombocytopenia a multicentric real life study
British Journal of Haematology, 2013Co-Authors: Patrizia Noris, Federica Melazzini, Catherine Klersy, Alessandro Pecci, Paolo Gresele, Fiorina Giona, Paola Giordano, Pietro Minuz, Giuseppe Loffredo, Elisa CivaschiAbstract:The most frequent forms of inherited thrombocytopenia (IT) are characterized by Platelet Size abnormalities and it has been suggested that this parameter is useful for their differentiation from immune thrombocytopenia (ITP). Recently, a monocentric study identified cut-off values for mean Platelet volume (MPV) and mean Platelet diameter (MPD) with good diagnostic accuracy in this respect. To validate these cut-off values in a different and larger case series of patients, we enrolled 130 subjects with ITP and 113 with IT in six different centres. The Platelet count and MPV was each measured by the instrument routinely used in each institution. In some centres, Platelet count was also measured by optical microscopy. MPD was evaluated centrally by image analysis of peripheral blood films. The previously identified cut-off value for MPV had 91% specificity in distinguishing ITP from inherited macrothrombocytopenias (mono and biallelic Bernard-Soulier, MYH9-related disease), while its sensitivity was greatly variable depending on the instrument used. With an appropriate instrument, specificity was 83%. The diagnostic accuracy of MPD was lower than that obtained with MPV. We concluded that MPV is a useful parameter for differentiating ITP from IT provided that it is measured by appropriate cell counters.
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Platelet Size distinguishes between inherited macrothrombocytopenias and immune thrombocytopenia
Journal of Thrombosis and Haemostasis, 2009Co-Authors: Patrizia Noris, Federica Melazzini, Valeria Bozzi, Catherine Klersy, Marco Zecca, Luca Arcaini, Alessandro Pecci, V Terulla, Chiara Ambaglio, Francesco PassamontiAbstract:Summary. Background: Distinguishing inherited thrombocytopenias from immune thrombocytopenia (ITP) can be difficult, and patients are therefore at risk of misdiagnosis and inappropriate treatments. Although it is known that the most common inherited forms of thrombocytopenia are characterized by increased Platelet Size, the diagnostic power of this feature has never been investigated. Objectives: The aim of this study was to test the hypothesis that Platelet Size can be used to differentiate ITP from inherited macrothrombocytopenias. Patients/methods: We measured mean Platelet volume (MPV) and mean Platelet diameter (MPD), within 2 h of blood sampling, in 35 patients with inherited macrothrombocytopenias [15 MYH9-related disease (MYH9-RD), three biallelic and 17 monoallelic Bernard–Soulier syndrome (BSS)], and 56 with ITP. Using receiving operating characteristic analysis, we searched for the best cut-off values to differentiate between these conditions. Results: As expected, Platelets were larger in inherited macrothrombocytopenias than in ITP. An MPD larger than 3.3 μm differentiated MYH9-RD and BSS from ITP with 0.89 sensitivity and 0.88 specificity, and an MPV larger than 12.4 fL had 0.83 sensitivity and 0.89 specificity. Combining MPD with MPV increased sensitivity and specificity to 0.97 and 0.89, respectively. Conclusion: Platelet Size evaluation by both an appropriate cell counter and blood film examination is useful for differentiating inherited macrothrombocytopenias from ITP.
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von Willebrand disease type 2B must be always considered in the differential diagnosis of genetic thrombocytopenias with giant Platelets
'Informa UK Limited', 2006Co-Authors: G. Loffredo, Patrizia Noris, L. Baronciani, F. Menna, A.b. Federici, Carlo L BalduiniAbstract:Type 2B von Willebrand's disease (VWD) is an inherited bleeding disorder characterized by spontaneous binding of large von Willebrand factor (VWF) multimers to Platelets in vivo. This phenomenon induces the clearance of both large multimers and Platelets, usually resulting in thrombocytopenia with slightly increased Platelet Size. We describe a newborn with a VWD type 2B due to the heterozygous missense mutation V1316M who presented the atypical feature of giant Platelets in peripheral blood. Based on this observation and literature review, we suggest that the diagnosis of VWD 2B should be always considered in patients with chronic thrombocytopenia and giant Platelets
L Pizzulli - One of the best experts on this subject based on the ideXlab platform.
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mean Platelet volume as marker of restenosis after percutaneous transluminal coronary angioplasty in patients with stable and unstable angina pectoris
Thrombosis Research, 2006Co-Authors: Alexander Yang, L Pizzulli, B LuderitzAbstract:Abstract Introduction Several experimental and clinical studies have demonstrated that Platelet Size and function correlate since large Platelets are hemostatically more reactive than Platelets of normal Size. Since Platelets play a crucial role in vascular remodeling after percutaneous transluminal coronary angioplasty (PTCA), we investigated the influence of the mean Platelet volume (MPV), a parameter of Platelet Size, on restenosis after PTCA. Methods The retrospective study comprised 174 patients who underwent elective PTCA and follow-up angiography within 6 months thereafter. According to the follow-up angiograms, the patients were assigned to group A (“restenosis”, n = 74) or group B (“no restenosis”, n = 100). Both groups were compared in regard to pre-procedural hematological routine parameters including MPV, Platelet count, hematocrit, white blood cell count and fibrinogen. Results MPV was significantly increased in group A, compared with that in group B (8.75 ± 0.99 fl vs. 8.04 ± 0.74 fl, p Conclusions The MPV seems to be a marker of coronary restenosis in patients undergoing PTCA. Patients with high pre-procedural MPV values might benefit from an intensified antiPlatelet therapy after coronary interventions.
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changes in Platelet Size and count in unstable angina compared to stable angina or non cardiac chest pain
European Heart Journal, 1998Co-Authors: L Pizzulli, A Yang, J F Martin, B LuderitzAbstract:Aims An increase in Platelet aggregability is associated with unstable angina and myocardial infarction. Platelet Size and activity correlate and mean Platelet volume was found to be increased before acute myocardial infarction. We measured the mean Platelet volume and Platelet count in patients with stable angina, unstable angina and non-cardiac chest pain. Methods and results We studied 981 patients (734 men; 247 women) defined clinically as stable angina (n=688), unstable angina (n=108) and unstable angina requiring immediate angioplasty (n=52). After coronary angiography the patients were subdivided into single (n=269), double (n=304) and triple-vessel disease (n=311) and the control group of non-cardiac chest pain (n=97). There was no significant difference in Platelet count between the control group and patients with 1, 2, or 3-vessel disease. However, the Platelet Size in patients with coronary artery disease was significantly larger (single: 8·7±1·19fl; double: 8·7±1·12fl; triple-vessel disease: 8·8±1·18fl) than the control group (8·2±0·95fl) ( P <0·01). Patients with stable angina similarly had no significant difference in Platelet count compared to the control group but did have a significantly increased mean Platelet volume (8·7±1·13; P <0·01). In contrast, patients with unstable angina had a decreased Platelet count (245±56×10/l) compared to either stable angina (262±62×10/l; P <0·05) or the control group (261±58×10/l; P <0·05); furthermore, the mean Platelet volume (9·4±1·23fl) was significantly greater than for stable angina ( P <0·01). Patients with unstable angina requiring immediate PTCA had an even lower Platelet count (231±55×10/l) and higher mean Platelet volume (10·4±1·03fl) ( P <0·01) than the rest of the population with unstable angina. Conclusions In stable angina the Platelet count is unchanged compared to patients with normal coronary arteries but the Platelet Size is increased. However, in unstable angina there is a decrease in Platelet count and an even larger increase in Platelet Size. We interpret this as meaning that unstable angina might be associated or preceded by an increase in Platelet destruction rate that is not completely compensated for by an increase in Platelet production rate. The large, more reactive Platelets might be causally related to an ongoing coronary artery obstruction in unstable angina.