Immature Platelet Fraction In Patients Research Articles

Early prediction of platelet recovery with immature platelet fraction in patients receiving hematopoietic stem cell transplantation.

Hematopoietic stem cell transplantation (HSCT) is pivotal in treating hematologic disorders, yet it poses the risk of post-transplantation pancytopenia. Prophylactic platelet transfusions are often administered to mitigate this risk. Utilizing practical markers, such as immature platelet fraction (IPF), to predict hematopoietic recovery in advance could reduce unnecessary prophylactic transfusions. Our prospective study, involving 53 HSCT patients at Taipei Veterans General Hospital between September 2022 and May 2023, utilized the Sysmex XN analyzer to assess peripheral blood cell parameters. We investigated whether IPF could predict platelet recovery early, determined the optimal cut-off value, and compared platelet usage. Neutrophil and platelet engraftment occurred 10 (median; range: 10-12) and 15 (median; range: 15-18) days post-HSCT. Notably, 71.7% of patients exhibited an IPF increase exceeding 2% before platelet recovery. The optimal cut-off IPF on day 10 for predicting platelet recovery within five days was 2.15% (specificity 0.89, sensitivity 0.65). On average, patients received 3.89 units of post-transplantation platelet transfusion. Our results indicate that IPF serves as a predictive marker for platelet engraftment, peaking before the increase in platelet count. This insight aids clinicians in assessing the need for prophylactic platelet transfusions. Integrating reference IPF values alongside platelet counts enhances the accuracy of evaluating a patient's hematopoietic recovery status. Anticipating the timing of platelet recovery optimizes blood product usage and mitigates transfusion reaction risks.

Immature platelet fraction in patients diagnosed with COVID-19.

The recent pandemic caused by the newly identified virus, SARS-Cov-2 is associated with thromboembolic events. Patients infected with COVID-19 have been found to have thrombocytopenia. A decrease in platelet count may be caused by increased destruction and consumption of platelets or by decreased production of platelets in the bone marrow. Immature platelet fraction (IPF) is a new platelet parameter that is an indicator for peripheral destruction and consumption of platelets. To assess the immature platelet fraction (IPF) in patients infected with COVID-19. The present study is a retrospective study where secondary data obtained from previous laboratory records of COVID-positive patients admitted at a tertiary care hospital in Delhi from 4 January to 4 February 2022 was analyzed. Sixty-eight COVID-positive patients were included. Platelet parameters included from the automated hematology analyzer Mindray were platelet count, mean platelet volume (MPV), immature platelet fraction (IPF), and platelet large cell ratio (P-LCR). Data was analyzed using SPSS Version 25. A P value less than 0.05 was considered statistically significant. In the present study mild thrombocytopenia was noted in 40% of the patients infected with COVID-19 admitted to the hospital. The median platelet count in these patients was found to be 91,000/mm3 (64,000-1,31,000). Low platelet count was associated with a significantly higher IPF, MPV, PDW, P-LCR, and a significantly lower PCT as compared to patients infected with COVID-19 with normal platelet count. There was a significant increase in IPF with a decrease in platelet count (P value < 0.05). A significant increase in IPF was noted with an increase in MPV and P-LCR (P value < 0.05). The present study suggests that thrombocytopenia in patients infected with COVID-19 may probably be due to peripheral destruction and consumption of platelets.

Immature Platelet Fraction Predicts Adverse Events in Patients With Acute Coronary Syndrome: the ISAR-REACT 5 Reticulated Platelet Substudy.

Immature or reticulated platelets are associated with impaired efficacy of antiplatelet drugs and adverse events in cardiovascular patients. Their role as a predictive biomarker in patients with acute coronary syndrome treated with potent P2Y12 receptor inhibitors is not fully understood. We aimed to prospectively evaluate reticulated platelets as a predictor of the primary end point of the ISAR-REACT 5 trial consisting of death, myocardial infarction, or stroke at 1 year in patients with acute coronary syndrome randomized to prasugrel or ticagrelor. Immature platelet fraction (IPF) was assessed within 48 hours after randomization. Patients were divided based on the IPF median values: the IPFhigh group included patients with IPF>median and the IPFlow group included patients with IPF≤median. Platelet aggregation was assessed using the Multiplate Analyzer and was correlated to IPF. Five hundred seventy-seven patients were included in the study. IPF values in % (median [interquartile range]) within the first 48 hours did not differ between the two study groups: 3.6 (2.5-5.2)% in the prasugrel group and 3.6 (2.5-5.4)% in the ticagrelor group (P=0.882). The incidence of the primary end point was significantly higher in the IPFhigh (IPF>3.6%) group compared with the IPFlow (IPF≤3.6%) group: 13.0% versus 7.2% (HRadj, 1.74 [1.02-3.00]; P=0.044), independently from the assigned drug (Pint=0.159). No significant association between IPF and BARC 3 to 5 bleeding was observed. ADP-induced platelet aggregation correlated significantly with IPF in patients treated with prasugrel (r=0.22; P=0.005) while no correlation was detected in patients treated with ticagrelor (r=0.09; P=0.257). Independently from drug treatment, IPF was associated with the primary end point and therefore is a promising biomarker for the prediction of adverse cardiovascular events in patients with acute coronary syndrome treated with prasugrel or ticagrelor. https://www. gov; Unique identifier: NCT01944800.

Correlation between Immature Platetet Fraction Value and SOFA Score in Sepsis Patient

Sepsis is a medical emergency that describes systemic inflammation reaction to infectious process that can lead to organ dysfunction and death. Sequential Organ Failure Assesment (SOFA) score is used to assess severity of organ dysfunction in septic patients. Immature platelet fraction (IPF) value can be used to evaluate thrombopoiesis. Research shows IPF can provide information regarding inflammatory activity and disease prognosis. A high IPF value in septic patient indicates the formation and recruitment of immature platelets that are triggered by infection. The aim of this study was to determine correlation between IPF value and SOFA score in sepsis patients. This was an analytical study with a cross-sectional design in 28 patients with sepsis who met the inclusion and exclusion criteria and conducted IPF tests at Central Laboratory of Dr M. Djamil Padang Hospital. The study was conducted from February 2020 to March 2021. Value of IPF was performed using automated hematology analyzer with flow cytometry method and SOFA scores are assessed by clinicians and obtained from medical records. Data were analyzed by Pearson correlation test, significant if p &lt;0.05. Median value of IPF in patients with sepsis was 4.8 (1.4-15.7) %. Median of SOFA score in patients with sepsis was 5,5 (2-12). Correlation test showed a strong positive correlation between IPF values and SOFA score with r= 0.684 and p &lt;0.05. There was a strong positive correlation between IPF values and SOFA score in sepsis.

Evaluation of Immature Platelet Fraction in Patients with Fever and Thrombocytopenia and its Clinical Utility

Introduction: Thrombocytopenia is very common in dengue and other haematological disorders and the aetiology is multifactorial. Immature Platelet Fraction (IPF) is a novel parameter which is a measure of reticulated platelets and it reflects the rate of regeneration of platelets. Aim: To evaluate the relationship between the IPF and platelet recovery and the consistency of its expression. Materials and Methods: The present study was a retrospective observational study done at Institute of Pathology, Madras Medical College between November 2018 to December 2018. Total 37 patients having fever with thrombocytopenia in dengue and other haematological causes were included for analysis. The platelet count, IPF, Mean Platelet Volume (MPV), Platelet Distribution Width (PDW) and Plateletcrit (PCT) was evaluated at the time of admission and once in every 24 hours and plotted in excel spread sheet. Results: About 86.4% were recovered in 24 hours after attaining the peak, 89.1% showed recovery in 24-48 hours of the rise of the IPF compared to the previous value and 94.5% recovered within 24 hours after the fall in the IPF value. It was observed that 81.8% were recovered when the IPF value ≥10% within 24- 48 hours. IPF readings are able to appreciate even in low platelet count levels but the other platelet recovery parameters did not. Conclusion: IPF is a consistent and reliable marker which can be measured even when the platelet count is low and it also predicts the platelets recovery. It is a promising marker that helps in guiding the decision towards platelet transfusion.

Immature Platelet Fraction in Patients with Chronic Liver Disease, A Marker for Evaluating Cirrhotic Changes.

Objective: To evaluate the role of Immature platelet fraction in patients with chronic liver disease, a marker for evaluating cirrhotic changes.&#x0D; Methodology: This case control study was conducted at department of Pathology, Aziz Fatima Medical and Dental College, Faisalabad, over a period of Seven months from June 2020 to January 2021. A total of 126 participants were included in the study consisting of 63 patients with chronic liver disease in group A and 63 participants without any known disease in group B as control. The IPF master program in combination with XE-2100 multiparameter automatic hematology analyzer was used to measure the immature platelet fraction. Ethylene diamine tetraacetic acid was used to collect the blood sample for IPF measurement and was maintained till analysis on room temperature. Ten repeated analyses, immediately and after 24 hours were done for reproducibility of IPF%.&#x0D; Results: The mean age of liver disease patients was 52.35 ± 13.64 years and in control group the mean age was 51.62 ± 11.27 years. There was no significant (p-value &gt; 0.05) difference between both groups based on age and gender. The hemoglobin level and red cell count was found to be significantly (p-value &lt; 0.05) reduced in cases group. While white blood cells count was comparable in both groups. The mean platelet count was significantly (p-value &lt; 0.05) less in cases group (163.5 ± 90.4 vs 233.4 ± 54.5 (x10*3/µl). The mean value of immature platelet fraction (IPF%) was significantly (p-value &lt; 0.05) raised in cases group (5.62 ± 2.92 vs 3.06 ± 1.87). The multivariate discriminant analysis (MDA) score showed a significant (p-value &lt; 0.05) association with chronic hepatis as compared to other liver related diseases.&#x0D; Conclusions: In chronic liver disease patients, there is an inverse relationship between platelet count and IPF% with decreased platelet count and increased IPF%. The proposed MDA function can be used to identify the cirrhotic changes in liver disease patients.

Immature platelet fraction over time and clinical outcomes in patients with acute myocardial infarction.

Immature platelets in the circulation can be measured as immature platelet fraction (IPF). Limited data exist regarding IPF during the course of an acute myocardial infarction (AMI), the association between IPF and extent of cardiac damage, and the long-term prognostic implications of IPF in patients with AMI. To examine the temporal course of IPF during the first month after AMI, the association between IPF and extent of cardiac damage, and the long-term prognostic effect of IPF in AMI patients. Patients with AMI treated with percutaneous coronary intervention (PCI) were examined. IPF was evaluated by a Sysmex XN-3000 autoanalyzer, at 4 time points: baseline; one day post-PCI; 3days post-PCI, and 30days post-PCI. The association between peak troponin-T levels and IPF was evaluated. One-year clinical outcomes (cardiac hospitalization, urgent revascularization, or death) were assessed. One hundred patients were included, mean age was 59.5±11.3years, 82 were men, 27 had diabetes, and 54 were hospitalized with ST-segment elevation myocardial infarction (STEMI) and 46 with non-ST segment elevation myocardial infarction (NSTEMI). The levels of IPF modestly decreased a day after PCI but did not change in subsequent measurements. Peak troponin-T level was significantly associated with the levels of IPF at all 4 time points. IPF levels three days post-PCI were associated with the composite clinical outcome at 1year. The levels of IPF following AMI remain relatively stable over a one-month period. Higher levels of IPF during the acute phase of AMI appear to be associated with worse cardiac outcomes at 1year.

Impact of uric acid on immature platelet fraction in patients undergoing percutaneous coronary intervention

IntroductionReticulated platelets have been involved in the pathophysiology of coronary artery disease (CAD). Immature platelet fraction (IPF) allows their measurement in daily clinical practice, although the factors conditioning their elevation are still largely unexplored. Serum uric acid (SUA) is the end product of purine metabolism, displaying a pro-oxidant and pro-inflammatory action and increasing the cardiovascular risk. The aim of our study was to investigate the impact of SUA on IPF levels in patients undergoing percutaneous coronary intervention (PCI), and their relationship with CAD. MethodsWe enrolled a cohort of consecutive patients undergoing coronary angiography in a single center. Hyperuricemia was defined by SUA ≥ 6.5 mg/dl. Significant CAD was defined as at least 1 vessel stenosis >50%, while severe CAD was defined as left main and/or three-vessel disease. IPF was measured at admission by routine blood cells count (A Sysmex XE-2100). ResultsWe included in our study 2217 patients, of whom 544 had high levels of SUA, while 1673 had normal levels. Hyperuricemics were older, with higher percentage of renal failure, hypertension, dilated cardiomyopathy or valvular disease as indication to angiography, higher levels of creatinine and C-reactive protein (p < 0.001, respectively) when compared to normouricemics. Immature platelet fraction (IPF) was significant higher in hyperuricemic patients (3.96% vs 3.59%, p = 0.004). A progressive direct increase in the IPF values was observed in relation to SUA levels (r = 0.101, p < 0.001), although at multivariate analysis, hyperuricemia did not result as an independent predictor of IPC in 3rd tertile (adjusted OR [95%CI] = 1.21 [0.85–1.71] P = 0.288). When stratifying hyperuricemics and normouricemics according to IPF tertiles (<2.3%; 2.3–3.9%; ≥ 4%), reticulated platelets were not associated to the prevalence of CAD (SUA ≥6.5:80.9 vs 79.3% vs 78.6%, p = 0.60; SUA < 6.5: 79.3% vs 81.3% vs 78.9%, p = 0.878) or severe CAD (SUA ≥6.5: 34.9% vs 38.9% vs 35.2%, p = 0.99; SUA < 6.5: 30.4% vs 33.5% vs 34%, p = 0.192), and the results were confirmed at multivariate analysis for CAD (SUA ≥6.5: adjusted OR [95%CI] = 1.11 [0.81–1.51] P = 0.524, SUA < 6.5: adjusted OR [95%CI] = 0.89 [0.75–1.05] P = 0.170) or severe CAD (SUA ≥6.5: adjusted OR [95%CI] = 1.03 [0.81–1.31] P = 0.795; SUA < 6.5: adjusted OR [95%CI] = 1.10 [0.96–1.26] P = 0.192). ConclusionsIn the present study we found a direct relationship between SUA levels and IPF values; however, hyperuricemia did not result as an independent predictor of higher IPF tertile values. Neither in hyperuricemics nor in normouricemics higher IPF were independently associated to the prevalence of CAD or severe CAD.

Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease.

Smoking represents a major cardiovascular risk factor, due to the induction of oxidative stress and low-grade, continuous, inflammation that contribute to promote atherothrombosis. However, the mechanisms leading to increased platelet aggregability associated with smoking are only partially defined. A potential role has been hypothesized for immature platelets, a younger and potentially more reactive fraction, previously associated with the main determinants of coronary artery disease (CAD). Therefore, the aim of our study was to define the impact of smoking on the immature platelet fraction (IPF) and its relationship with prevalence and extent of coronary artery disease. We enrolled a cohort of consecutive patients undergoing coronary angiography in a single centre. Significant CAD was defined as at least 1 vessel stenosis >50%, while severe CAD was defined as left main and/or three-vessel disease. IPF was measured at admission by routine blood cell count (Sysmex XE-2100). We included in our study 2553 patients who were divided according to smoking status (active smokers: 512; nonactive smokers: 2041). Smokers were younger, more frequent males, with lower rate of diabetes mellitus, previous PCI and previous CABG (P<.001, respectively) and were in treatment less often with ARB, BB, nitrates, statins, ASA, clopidogrel, CCB and diuretics (P<.001, respectively) as compared to nonactive smokers. Higher percentage of smokers was observed in patients with higher IPF values, and at multivariate analysis, active smoking resulted as an independent predictor of higher IPF (adjusted OR [95% CI]=1.59[1.03-2.45], P=.035). Among smokers, higher IPF was associated with lower ejection fraction (P=.034), percentage of acute coronary syndrome (P=.002) and platelet count (P<.001) compared to ones with lower IPF. However, the IPF (according to quartiles values) was not associated with the prevalence and extent of CAD (82.5%, 80.4%, 86.1% and 80.9%, from 1st to 4th quartile, respectively, adjusted OR[95% CI]=0.98[0.79-1.23], P=.89) and severe CAD (31%, 31.1%, 39.1% and 35.2%, from 1st to 4th quartile, respectively, adjusted OR[95% CI]=1.03[0.86-1.23], P=.76). The present study shows an independent association between active smoking and the levels of immature platelet fraction in patients undergoing coronary angiography. However, among active smokers, IPF did not result as an independent predictor of CAD or severe CAD.

Influence of antiretroviral therapy and cardiovascular disease on the immature platelet fraction in patients living with HIV

Cardiovascular disease is an important contributor to morbidity and mortality in people living with HIV . The immature platelet fraction (IPF) is increased in HIV-negative patients with cardiovascular disease and evidence suggests that an enlarged IPF is associated with adverse cardiovascular events. In this multi-center observational study, we aimed to investigate how the IPF in people living with HIV is influenced by antiretroviral therapy and cardiovascular disease. Subjects without cardiovascular disease that received antiretroviral therapy showed a smaller IPF accompanied by lower D-dimer and C-reactive protein (CRP) levels compared to therapy-naïve subjects (mean IPF: 2.9% vs. 3.9%, p = .016; median D-dimer: 252 µg/L vs. 623 µg/L, p < .001; median CRP: 0.2 mg/dL vs. 0.5 mg/dL, p = .004). No significant differences for the IPF, D-dimer or CRP were found between subjects on antiretroviral therapy with documented cardiovascular disease and therapy-naïve subjects. In conclusion, we observed a reduction in the IPF among subjects on therapy only in the absence of cardiovascular disease. In contrast, subjects receiving therapy that had documented cardiovascular disease showed an IPF comparable to therapy-naïve subjects. Future studies are needed to investigate if an enlarged IPF may serve as a biomarker in predicting adverse cardiovascular events in people living with HIV.

Can Immature Platelet Fraction (IPF) be Used to Assess Bleeding Risk in Pediatric Immune Thrombocytopenia (ITP) and to Differentiate ITP from Bone Marrow Failure/Aplastic Anemia? A Retrospective Analysis

Immune Thrombocytopenia (ITP) usually presents with isolated, severe thrombocytopenia with very low platelet count (generally less than <30 x 109/L) in the absence of other hematologic abnormalities. However, ITP is a diagnosis of exclusion without any definite diagnostic test that can confirm the diagnosis at the time of presentation and clinicians occasionally worry at the time of presentation about other bone marrow processes that may present with thrombocytopenia, which would require considerably different therapy. In light of current guidelines suggesting that observation is likely to be safe in pediatric patients with low platelet counts without significant bleeding, identifying patients at risk for severe hemorrhage is even more important to help guide therapy. In addition, appropriately differentiating ITP from other diagnoses may also prevent inappropriate administration of ineffective therapies. The immature platelet fraction (IPF) is a measure of platelet turnover measuring RNA containing, large platelets by fluorescently labeling the platelets and utilizing flow cytometric gates programmed into the Sysmex XN-3000 hematology analyzer. We examined the medical laboratory records of 134 patients who had an IPF performed over the past 4 months for correlation between IPF and bleeding manifestations. In ITP patients who presented with significant bleeding symptoms (defined as epistaxis which was more than brief, oral bleeding more than palatal petechiae or GI or intracranial hemorrhage), the IPF was significantly lower than in those who presented with no bleeding or cutaneous bleeding only (bruising and petechiae): IPF=4.3%±1.6 SEM in bleeding patients versus 21.8%±1.8 SEM in not bleeding patients; p<0.0001. In two patients with life threatening hemorrhage and ITP (GI bleeding with drop in hemoglobin requiring both PRBC transfusion and treatment to raise the platelet count; ICH resulting in mortality), the IPF was low at the time of initial hemorrhage, but increased after ITP therapy (GI Bleed: plt 1K, IPF 5.3% increased to 20.3% after IVIG; ICH plt 6K, IPF 1.8% increased to 12.8% after IVIG and prednisone). We also examined first platelet count and IPF in 127 patients with ITP and 21 patients with BMF/AA who presented to our institution since October 2013. In this cohort of patients, the IPF in patients with ITP was significantly higher than in the BMF/AA patients and an IPF of >5.3 was associated with a negative predictive value of 80% for BMF/AA (IPF 16.6%±1.2 SEM in ITP vs. 2.9%±1.4 SEM in BMF/AA). In summary, we demonstrate that the IPF is a useful and simple adjunct in diagnosis of ITP which can help differentiate the patients most likely to have ITP from those who may need further diagnostic evaluation and require treatment to prevent bleeding complications. Further studies will focus on the ability of the IPF to prospectively predict the bleeding risk of patients and categorize patients. DisclosuresLambert:GSK: Consultancy; NovoNordisk: Honoraria; Hardin Kundla McKeon & Poletto: Consultancy.

Immature platelet fraction in hypertensive pregnancy

Background: Imbalance in hemostatic mechanisms can occur during pregnancy with a tendency for hypercoagulability and increased thrombosis risk. Pregnant women with hypertensive disorder, especially preeclampsia, show alterations in platelet indexes. Immature platelet fraction (IPF) has been suggested as a sensitive index for monitoring changes in platelet production and destruction. Objectives: To evaluate the IPF in patients diagnosed with a gestational hypertensive disorder (GHD). Patients and methods: A cross-sectional study was conducted at an University Hospital to estimate maternal blood IPF index in 99 pregnant women, divided into three groups: normotensive pregnancy (NP), preeclampsia syndrome (PES), and non-proteinuric hypertensive pregnancy (nPHP). Following ethical approval and written informed consent, samples were collected from 33 NP, 34 PES, and 32 nPHP women. Platelet indexes were measured by fluorescent flow cytometry. Results: IPF and mean platelet volume (MPV) counts in GHD were significantly higher than in NP (IPF: 3.8, 2.4–5.1%; 8.6, 5.8–10.6%; 7.3, 4.2–10.2%; p < 0.001 and MPV: 10.6 ± 0.9 fL; 12.1 ± 1.0 fL; 11.6 ± 1.0 fL; p < 0.001 for NP, PES, and nPHP, respectively). No difference was detected between PES and nPHP groups. The distribution of patients with an IPF above 6.1%for NP, PES, and nPHP was 9%, 65%, and 43.8%, respectively (p < 0.001). IPF as a test to differentiate GHD from the controls achieved an area under the curve of 0.83 on a receiver operating characteristics curve. Conclusion: A distinct profile in platelet indexes was detected in hypertensive pregnancies. It suggests that these markers could be used in daily routine as an additional tool in the management of pregnant women.

Impact of immature platelets on platelet response to ticagrelor and prasugrel in patients with acute coronary syndrome.

The influence of reticulated platelets (RPs) on platelet inhibition by ticagrelor when compared with prasugrel is unknown. We aimed to determine the influence of RPs on adenosine diphosphate- (ADP-) induced platelet aggregation in patients with acute coronary syndrome who were randomly assigned to receive either ticagrelor or prasugrel for P2Y12 receptor inhibition. One hundred and twenty-four patients were prospectively enrolled. The immature platelet fraction (IPF) was measured by an automated haematoanalyzer and platelet aggregation was assessed by multiple electrode aggregometry. In a subgroup of patients (n = 28) ADP-induced P-selectin expression was measured in dependence of the time point of study drug intake in RPs that were discriminated from mature platelets by thiazole-orange (TO) staining. The primary endpoint was the correlation of platelet aggregation and IPF in ticagrelor- vs. prasugrel-treated patients. Platelet aggregation significantly correlated with IPF in patients who received prasugrel (r = 0.41, P < 0.001). In contrast, no correlation between IPF and platelet aggregation was observed in ticagrelor-treated patients (r = 0.08, P = 0.51, P for difference of correlation coefficients P = 0.05). Within the TO-positive RP fraction, P-selectin expression was significantly higher in prasugrel when compared with ticagrelor-treated individuals (prasugrel 18.6 ± 16.0% vs. ticagrelor 11.5 ± 6.0%, P = 0.047). A time-dependent P-selectin expression was observed in prasugrel but not in ticagrelor-treated patients (prasugrel early 11.9 ± 9.4% vs. late 26.3 ± 19.0%, P = 0.031, ticagrelor early 9.6 ± 4.9% vs. late 13.5 ± 6.6%, P = 0.127). Reticulated platelets show a greater impact on platelet reactivity in response to prasugrel when compared with ticagrelor.

Increased Levels of Thrombopoietin and IPF in Patients with Iron Deficiency Anemia

BackgroundThrombocytosis has been reported in about 50% of patients with iron deficiency anemia (IDA). However, the mechanism of the increase in the number of platelets is unknown. To investigate the relationship of endogenous thrombopoietin (TPO) and circulating platelet counts, we measured the plasma levels of TPO, immature platelet fraction (IPF) and erythropoietin ( EPO ) in 25 patients with IDA.Patients and methodsPatients with IDA (newly diagnosed) were recruited from February 2013 through March 2014 in Teikyo University School of Medicine. TPO (Immuno-Biological Laboratory, Japan), was determined by an EILSA. IPF was measured on the Sysmex XE2100. EPO (Roch Diagnostic Japan) was determined by an EILSA.Results and ConclusionsThe number of platelets was increasing in the half patients with IDA in this study. Peripheral blood samples for measuring IPF were obtained from 300 healthy adult controls (160 women and 140 men) and 20 patients with IDA, consisting of 19 women and 6 men with age ranging from 16 to 75 years. The etiology of iron deficiency was gastrointestinal (GI) blood loss, menometrorrhagia, previous GI surgery, and low dietary iron intake. The mean absolute-IPF was significantly higher for IDA patients than for healthy control (8193±571 vs. 4254±193 p＜0.05). The endogenous levels of TPO were significantly elevated in patients with IDA (216.4±41 pg/ ml) as compared with normal controls (116.5±23 pg/ml). Also, The endogenous levels of EPO were significantly elevated in patients with IDA as compared with normal controls. There was a significant inverse correlation between serum Fe levels and platelet counts (r=0.551, p＜0.05). Also, a positive correlation (r=0.311, p＜0.05) between platelet counts and endogenous level of TPO was found. Moreover, there was a significant inverse correlation (r=-0.458, p＜0.05) between Hb and TPO. These results suggest that TPO is active regulator, in thrombopoiesis and megakaryocytopoiesis in patients with IDA. Also, it appears there is relationship between erythropoiesis and TPO. DisclosuresNo relevant conflicts of interest to declare.

Patients With Previous Definite Stent Thrombosis Have a Reduced Antiplatelet Effect of Aspirin and a Larger Fraction of Immature Platelets

This study sought to evaluate the platelet response to aspirin and the immature platelet fraction in patients with previous stent thrombosis (ST). ST is a potentially fatal complication of coronary stenting. A reduced platelet response to aspirin increases the risk of cardiovascular events. We included 117 patients previously undergoing percutaneous coronary intervention. A total of 39 patients had suffered ST and 78 patients served as controls matched at a 1:2 ratio with respect to age, sex, stent type, and percutaneous coronary intervention indication. All patients were treated with aspirin 75 mg once daily. Platelet function was assessed by multiple electrode aggregometry in citrated and hirudinized blood and by VerifyNow Aspirin Assay (Accumetrics, San Diego, California). Flow cytometric determination of the immature platelet fraction was performed to evaluate platelet turnover. Platelet activation was evaluated by soluble serum P-selectin. Compliance was confirmed by serum thromboxane B(2). All patients were fully compliant, which was confirmed by suppressed levels of serum thromboxane B(2). Platelet aggregation was increased in patients with previous ST when assessed by multiple electrode aggregometry induced by collagen (p(citrated blood) = 0.003; p(hirudinized blood) < 0.0001) and by arachidonic acid (p(citrated blood) = 0.16; p(hirudinized blood) = 0.04), respectively. Similarly, platelet aggregation assessed by VerifyNow was higher in ST cases (p = 0.12). A trend toward an increased immature platelet fraction among cases was seen (p = 0.13), whereas P-selectin levels (p = 0.56) did not differ between groups. Overall, patients with previous ST had a reduced antiplatelet effect of aspirin, which might be explained by an increased platelet turnover.

Correlation between immature platelet fraction and reticulated platelets. Usefulness in the etiology diagnosis of thrombocytopenia

Reticulated platelets (RP) are a surrogate marker for megakaryocytic activity, but the limitation of this determination is the lack of standardization of methodology. The determination of the immature platelet fraction (IPF) is performed in a simple, automated, and reproducible way between laboratories. We analyzed the correlation between IPF and RP, and usefulness of IPF in patients with thrombocytopenia. RP were determined by flow cytometry using double staining with thiazole orange and CD61 PerCP. IPF was performed with Sysmex XE2100 analyzer. We used a control group with normal platelets, and thrombocytopenic patients were classified into three groups: Group 1. Central thrombocytopenia, Group 2. Thrombocytopenia as a result of enhanced peripheral platelet destruction, and Group 3. Peripheral non-immune thrombocytopenia by abnormal distribution. Fourteen controls and 66 patients were analyzed. Group 1: 25 patients, they had mean and confidence interval 95% (95% CI) for IPF 8.67% (6.49-10.46%) and RP 4.08% (2.86-5.30%). Group 2: 20 patients, they had mean and 95%CI for IPF 16.80% (12.20-21.39%) and RP 16.14% (9.89-22.40%). Group 3: 21 patients, they had mean and 95% CI for IPF 9.04% (6.95-11.14%) and RP 5.23% (3.41-7.05%). The overall Pearson linear correlation between IPF and RP was r: 0.65. There were statistically significant differences in values of IPF and RP between Group 2 and the other two groups (P < 0.01). There is a good correlation between IPF and RP mainly in thrombocytopenia by peripheral destruction. Determination of IPF is an easy technique in their implementation, standardized and reproducible, so it could be a useful screening technique in patients with thrombocytopenia.

Assessment of Immature Platelet Fraction in Patients with Ph-Negative Myeloproliferative Disorders and Thrombocytosis.

Abstract 4980 BackgroundMyeloproliferative disorders (MPD) in general result from proliferation of a clone of myeloid cells derived from a neoplastic pluripotent precursor or from connective tissue elements in bone marrow. This leads to increased numbers in one or more blood cell lines in peripheral blood. Some MPDs can be associated with thrombocytosis (MPD-T): essential thrombocythaemia (ET), polycythaemia vera (PV) and early stages of chronic idiopathic myelofibrosis (CIMF). Usually in MPD-T the thrombocytosis is caused by increased platelet production from proliferating mature megakaryocytes, especially in ET. Elevated platelet counts in these patients are often associated with both thromboembolic events and bleeding. One of the goals of MPD treatment is the control of platelet count. Immature platelets mirror the platelet production in bone marrow. In certain automated blood count analyzers it is possible to measure Immature platelet fraction (IPF) from the routine CBC samples sent to haematology lab. Reference range for IPF parameter for method used in this study is 1,1-6,1%. ObjectiveMeasurement of IPF parameter by fully automated analyzer (XE-2100, Sysmex, Kobe, Japan) in optical channel and analyzing it ( software IPF Master) in patients treated for Ph-negative MPD. We enrolled 85 pts- 67 ET (79%), 10PV(12%) and 8 CIMF (9%) patients; 57 were women and 28 men; median age 56 years ranging from 20 up to 83 years. We analyzed and evaluated IPF in whole group as well as in subgroups depending on diagnosis, gender, age, JAK-2 mutation and platelet count. ResultsAt the time of assessment the majority of our pts were already commenced on treatment for their MPD. Platelet counts (plt) in whole cohort ranged from 164 up to 2148 ×109/l, with median 374 ×109/l. Thirty eight pts (45%) had plt < 350 ×109/l. Plt <450 ×109/l (WHO 2008 recommended cut off level for thrombocytosis) were found in 59 pts (69%). IPF median in whole cohort was 5,9% (0,7-14,4%). When comparing IPF in subgroups mentioned above statistically significant differences (p<0,05) was found only between subgroups with normal and abnormal plt counts: IPF median 7,45% (0,8-14,4%) resp. 4,6% (0,7-11,9%), (p=0,002) and between subgroups with less and more than 450×109/l plt (IPF median 6,6% (0,8-14,4%) resp. 3,85% (0,7-9,6%), (p<0,001). Fact, that patients with higher plt had lower IPF and vice versa, was confirmed also by Spearman correlation coefficient. When correlating results of plt a IPF in the whole cohort, we found the trend to indirect dependence (rs= –0,386). ConclusionsMPD-T patients in our cohort did not have marked elevation of IPF parameter, neither those with high platelet counts (so far untreated pts). Thus we can speculate, that increased number of Plts in peripheral blood is caused by increased number of mature megacaryocytes in bone marrow which produce adequate numbers of platelets without increase of immature fraction rather than increased number of immature platelets released from megacaryocytes appearing in normal numbers in bone marrow Thus it seems that negative feedback of increased Plt counts on releasing of Plts from megacaryocytes is maintained also in patients with MPD-T. Further assessment is needed and should further determine, what is the clinical relevance (if any) of measurement of IPF in patients treated for MPD-T. DisclosuresBlatny:Sysmex, Czech Republic: Consultancy.

Aberrant increase in the immature platelet fraction in patients with myelodysplastic syndrome: a marker of karyotypic abnormalities associated with poor prognosis

Some patients with myelodysplastic syndrome (MDS) show a marked increase in the percentage of immature platelet fraction (IPF%) despite the absence of severe thrombocytopenia. To determine the significance of such an unbalanced increase in the IPF%, we investigated the IPF% and other laboratory findings of 51 patients recently diagnosed with MDS. Subjects consisted of 80 healthy males, 90 healthy females, and 51 patients with MDS and 20 patients with idiopathic thrombocytopenic purpura (ITP). The IPF and IPF% were determined using a Sysmex XE-2100 system loaded with IPF Master software (XE IPF Master, Sysmex). Platelet counts were measured simultaneously. IPF% and platelet counts of these patients ranged from 1.1% to 25.1% (median, 5.3%) and from 6 to 260 x 10(9)/L (median, 71 x 10(9)/L), respectively. Twelve patients showed platelet counts more than 50 x 10(9)/L with 10% or more IPF%. All of the 12 patients had chromosome abnormalities including monosomy 7 and complex abnormalities involving 7 or 5q. In the other 39 patients who did not show the aberrant IPF% increase, chromosomal abnormalities were seen only in seven patients and none of them had chromosome 7 abnormalities. The IPF% of two patients increased to more than 10% in association with the appearance of monosomy 7. These findings suggest that a high IPF% in MDS patient may be a marker for karyotypic abnormalities with a poor prognosis, including chromosome 7 abnormalities.