Reticulated platelets are immature platelets circulating in blood; they reflect the activity of megakaryopoiesis in the bone marrow. Therefore, they can be used as a non-invasive test in patients with thrombocytopenia in various clinical conditions. The preferred method of analysis is by flow cytometry. However, there is an evident lack of analytical standardization, making it difficult to compare results obtained in different laboratories. Currently, two types of hematology analyzers are on the market offering fully automated measurement of reticulated or immature platelets: the high end analyzers manufactured by Sysmex (XE- and XN-series) and Abbott (CELL-DYN Sapphire). Although the methods are essentially different and cannot be used interchangeably, both have been proven to have clinical utility. Reticulated or immature platelet assays are useful for the differential diagnosis of thrombocytopenia and for monitoring bone marrow recovery after chemotherapy or stem cell transplantation. These assays may aid clinicians in platelet transfusion decisions when recovery from thrombocytopenia is imminent. In addition, preliminary findings indicate that there is a rationale for reticulated or immature platelets for risk stratification in acute coronary syndromes and for monitoring the effect of treatment with antiplatelet drugs in patients with coronary artery diseases. The aim of this paper is to present the present technology available for measuring reticulated platelets as well as an overview of the current status of clinical application. This overview also indicates that more research is needed before reticulated or immature platelet assays can be applied in other clinical conditions than thrombocytopenia and after transplantation.
Formation and maturation of megakaryocytes
The study of blood platelets or thrombocytes started in the late 19th century, when Wright had developed his variant of the Romanovsky stain that allowed detailed observations of the smallest blood elements . Platelets represent the terminal stage of megakaryopoiesis, a highly complex sequence of events that can be traced back to the generation of the pluripotent hematopoietic stem cell in bone marrow. This pluripotent stem cell proliferates and differentiates via several intermediates into a megakaryoblast and eventually into a megakaryocyte (Figure 1). Megakaryopoiesis is regulated by various growth factors and cytokines, of which thrombopoietin (TPO) is the most important. TPO stimulates the number, the size and the ploidy of megakaryocytic cells and is the key regulator of platelet concentration in the circulation . Once the megakaryoblast stage is reached, the cell loses its proliferative capacity and starts the maturation process. Megakaryopoiesis has a unique way of maturation that does not occur in other cell lines: endomitosis. This is nuclear division without cell division; the cell is multiplying its nuclear material and increases its cytoplasm, all within the same cell. Finally, maturation results in a megakaryocyte that possesses multiple nuclear copies and abundant cytoplasm. The nuclear ploidy of a megakaryocyte is normally between 8N and 64N (median 16N), whereas higher and lower ploidy may occur in various pathological conditions. Depending on the organism’s need of new platelets, endomitosis stops and the formation of platelets commences (Figure 1). First, there is intracytoplasmic formation of channel-like structures composed of lipids, called the membrane demarcation system . These lipids later assemble into membrane bilayers and eventually form the cell membranes of platelets when the megakaryocyte cytoplasm starts to disintegrate. In this phase there is also active protein synthesis and cytoskeletal assembly.
Platelet production by megakaryocytes
Eventually, megakaryocytes form pseudopodia-like extensions protruding into sinuses and release platelets into the extracellular space. How this exactly takes place is not fully elucidated [4–6]. A healthy human produces approximately 1–2 million platelets per second. In response to thrombocytopenia, platelet production can be accelerated by up to a 10-fold increase .
Megakaryocyte cytoplasmic volume expands synchronized with nuclear ploidy and this eventually determines the number of platelets that a megakaryocyte will produce. A single megakaryocyte can generate up to 5000 platelets [1, 2]. In steady-state conditions, the platelet production rate is aimed at keeping the total circulating platelet mass (platelet number×mean platelet volume, also called plateletcrit) constant . In conditions of stress, platelets are released from megakaryocytes at an earlier stage, which results in platelets that are larger than normal.
Each individual has its own personal setpoint for platelet count and platelet volume; these are largely under genetic control . As a consequence, intra-individual variations in platelet count are quite small in comparison with the population reference ranges. In the normal population, platelet count is inversely correlated with mean platelet volume (MPV), and consequently the total circulating platelet mass is less variable between individuals than platelet count.
Physiology of reticulated platelets
When platelets are released from the megakaryocyte cytoplasm, they still contain a small amount of RNA. For long it has been thought that this RNA was a vestigial remnant of megakaryocytic RNA, but there are recent indications that platelets are able using this RNA for protein synthesis . Anyway, they represent the youngest platelets in the circulation and are named reticulated platelets (retPLT), in analogy with reticulocytes in erythropoiesis . The concentration of retPLT in bone marrow is on the average 2–3 times higher than in peripheral blood, where they correlate with megakaryocyte numbers . And whereas platelets persist in the circulation for 7–10 days, retPLT have a much shorter lifespan (<1 day). Therefore they can act as a marker of megakaryopoietic activity in the bone marrow [12, 13], which gives retPLT clinical and diagnostic utility.
Reticulated platelet methods – flow cytometry
The initial description of retPLT dates back to 1969, when Ingram and Coopersmith studied a canine model of acute blood loss and observed coarsely punctuated reticulum in platelets after supravital staining of blood with new methylene blue . This technique was initially also used in human blood, but it is obviously not well suited for routine applications.
Kienast and Schmitz initiated a breakthrough in the field when they described a flow cytometric technique for analyzing retPLT, based on RNA staining by thiazole orange . In subsequent years, several research groups published their findings in a wide variety of conditions like thrombocytopenia [16–21], thrombocytosis [22, 23], after stem cell transplantation [24–27], hereditary platelet diseases [28, 29], thrombo-embolic disorders [30, 31], kidney disease [32–34], preeclampsia , hyperthyroidism  and in healthy and thrombocytopenic neonates [37, 38]. The overall conclusion from these studies is that retPLT in blood represent a useful non-invasive marker of megakaryopoietic activity in the bone marrow. However, it also became evident that the flow cytometric assay was prone to methodological variation, which made it difficult to compare results obtained with different assays. For example, the normal reference range was reported to range between 1% and 15% [23, 39]. This wide range can be explained by lack of standardization of the methods. Many factors have been identified that contribute to this analytical issue: the type and concentration of fluorescent dye, incubation time and temperature, fixation, RNAse treatment and the flow cytometric data analysis, including gating and threshold settings [17, 18, 39–41]. One of the major problems is that platelets show non-RNA-specific binding of fluorescent dye, resulting in background staining, which is size-dependent [39, 42, 43]. This issue can be solved by optimizing the assay conditions and, in particular, by applying a two-dimensional gating process . Nevertheless, standardization attempts for improving concordance between laboratories were unsuccessful, even when using the same protocol . Recently, new initiatives were undertaken that are aimed at developing a method with the potential to become a future international reference method [44, 45]. However, even if a standardized method would be available, it would carry the disadvantage of not being well suited for routine clinical applications, since flow cytometry requires a great deal of expertise and is hardly available for patient care on a 24/7 basis. For the time being, a surrogate level of standardization is possible, since two manufacturers offer hematology analyzers that are capable of measuring reticulated or immature platelets (Table 1).
|Flow cytometry||Sysmex IPF||Abbott retPLT|
|Sample preparation||Variable: none, fixation or isolation of platelets||None||None|
|Fluorescent dye||Thiazole orange, acridin orange||Polymethine (XE-series); oxazine (XN-series)||CD4K530|
|Incubation time||Variable 15 min–2.5 h||Not specified||47 s|
|Precision at normal platelet count, CV||Not specified||7%–11%||<12%|
|Precision in thrombocytopenia, CV||Not specified||9%–36%||11%–32%|
|Reference range,%||Highly variable 1%–15%||1.1–6.6||0.5–6.0|
|Reference range, 109/L||Mean 3.2||2–17||1–18|
Immature platelet methods – Sysmex hematology analyzers
The first available fully automated method for measuring reticulated platelets was in the R-3000, a dedicated reticulocyte analyzer developed by Toa Medical (later Sysmex) [46, 47]. The method used auramine O as a fluorescent RNA dye and a 488 nm Argon laser. By plotting forward light scatter (representing cell size) against fluorescence (RNA content), reticulated platelets could be distinguished from mature platelets. In normal healthy individuals the mean retPLT count was 0.98%–1.27% and thrombocytopenic patients with a variety of diseases had increased concentrations, in accordance with the flow cytometric results mentioned above [18, 47, 48]. Notably, a strong positive correlation existed between percentage retPLT and the fraction of large platelets, except in patients with aplastic anemia . Furthermore, the large platelet fraction highly correlated with MPV; data on the correlation between retPLT and MPV were not provided, but one can reasonably assume that such correlation was present.
Automated measurement was later integrated into the Sysmex XE-2100 and XE-5000 hematology analyzers, as a part of the reticulocyte determination. This enabled automated quantification of what from then on was called immature platelet fraction (IPF) . As these instruments employ a 633 nm diode laser as the light source, other dyes were needed and a mixture of polymethine and oxazine was selected. As before, a forward scatter versus fluorescence scatterplot defined platelets with the highest fluorescence intensity as immature platelets (Figure 2A). The reference values in a healthy population were clearly higher than with the previous R-3000 method: mean 3.4% (range 1.1%–6.1%) . These reference values were later confirmed by others [50–54]. In all studies, patients with idiopathic thrombocytopenia (ITP) had increased IPF; in some patients IPF was even strongly increased, up to 50%–60% [49, 54, 55]. Such extreme values were later recognized to be artifacts due to interference by white blood cell fragments .
With the introduction of the XN-series hematology analyzers, Sysmex changed the IPF method. It is now part of the fluorescent platelet assay, which uses a proprietary oxazine-based dye for staining RNA. Still, IPF is derived from the forward scatter (cell size) versus sideward fluorescence (RNA content) scatterplot [56, 57], as shown in Figure 2B. The moderate correlation in IPF between XE-2100 and XN is explained, at least partially, by reduced interference in the XN system . Preliminary data suggest that the XN reference values of IPF are comparable with the XE-2100 method .
Reticulated platelet methods – Abbott CELL-DYN Sapphire
Apart from the Sysmex method discussed above, the Abbott CELL-DYN Sapphire is currently the only hematology analyzer capable of measuring retPLT. The assay is an integral part of the reticulocyte assay, which is based on the fluorescent dye CD4K530  that is excited by a 488 nm solid state laser. Three angles of scattered light plus fluorescence are recorded, which allows multi-dimensional separation of platelets and red blood cells. The embedded algorithm defines retPLT in an FL1 versus 7° scatterplot (Figure 2C). This approach enables correcting for the size-dependent background fluorescence of platelets . In healthy individuals, mean retPLT are between 1.4% and 2.2%, and reported reference ranges are 0.4%–2.8% , 0.4% to 4.45%–6.0% [60–62] and 1.0%–3.8% .
In the CELL-DYN Sapphire, the correlation between retPLT and MPV was investigated in relatively small groups and was described as not significant  or only weak . However, in a large group of subjects with normal platelet counts, we found a significant negative correlation between retPLT and MPV .
Comparison of reticulated and immature platelet methods
Due to the lack of a standardized reference method for retPLT, assessing the performance of the automated methods is difficult; only a few side-by-side comparisons are available.
Studies where Sysmex XE-2100 IPF was compared with reference flow cytometric retPLT indicated low or moderate correlations [65, 66]. Remarkably, the coefficients of correlation differed between patients groups, from no correlation in healthy individuals to relatively high correlations in patients with thrombocytopenia due to peripheral destruction [66, 67]. One study using the Sysmex XT-2000iV, which uses an identical method as XE-2100, demonstrated reasonable correlation between IPF and reference flow cytometry, albeit with a significant systematic bias .
Direct comparison between Sysmex XE-2100 or XE-5000 IPF and CELL-DYN Sapphire retPLT resulted in weak or modest correlations [63, 64]. Sapphire was found to have a distinctively narrower reference range than XE-5000, enabling higher sensitivity for separating normal and abnormal patients .
These weak correlations and the different relationships between IPF/retPLT and MPV mentioned previously, lead to the conclusion that although both parameters harbor information of platelet turnover, they do reflect different aspects of thrombopoiesis. As a consequence, the two parameters cannot be used interchangeably .
Obviously, immature or reticulated platelets are normally measured in blood samples collected into K2-EDTA, as for other hematologic parameters. One single study advised that citrate-theophylline-adenosine-dipyridamole solution (CTAD) was to be preferred over EDTA, as IPF measured using a Sysmex XE-5000 remained more stable in blood from patients with chronic ITP .
Regarding storage temperature before analysis, most authors agree that XE-2100 IPF is stable for 24–48 h after blood collection, provided the samples are kept at ambient temperature [49, 70, 71]. Others, however, reported stability for 3–8 h only [50, 51]. When blood samples are kept at 4 °C, IPF is rather unstable [69, 72], but the increase in IPF is apparently so predictable that it can be corrected for by a simple algorithm .
Stability data on retPLT as measured with CELL-DYN Sapphire range between <6 h  and at least 26 h .
Traditionally, IPF is expressed in relation to the PLT count, as a percentage. The absolute IPF (IPF#), the concentration of immature platelets (in 109/L), might better reflect real-time platelet production in analogy with what absolute reticulocyte count does for erythropoietic activity . There are indeed some reports indicating the usefulness of IPF# in neonatal infections , in chronic liver disease  and in differentiating acute ITP and from thrombocytopenia due to acute leukemia . It has been reported that IPF#, but not relative IPF predicts imminent platelet recovery in chemotherapy-induced thrombocytopenia in children . Importantly, IPF# seems not to be influenced by platelet transfusions, whereas IPF% decreases, most likely due to dilution . Other authors found IPF# not helpful for assessing platelet turnover . More studies are needed in order to fully appreciate whether the absolute IPF or absolute retPLT count have additional value to relative counts.
It is well accepted that accelerated megakaryopoiesis is associated with increased MPV. As also IPF is often increased in this condition, this has led to the widespread belief that immature platelets are synonymous with large platelets [47, 78]. This notion seems to be reinforced by high correlations between IPF and MPV [64, 66, 79–81]. This correlation is only present in Sysmex analyzers, most likely as a result of how IPF is derived: the scatterplots indeed suggest that immature platelets are the largest platelets [49, 54, 82]. In contrast, no significant correlation was found between retPLT and MPV in flow cytometry  and neither in CELL-DYN Sapphire [63, 83]. It is true that platelets produced in response to stress megakaryopoiesis are on the average larger, but there is no evidence that this can be extrapolated to normal megakaryopoiesis. In healthy individuals with steady-state platelet production, we found a significant negative association between retPLT and MPV . This is more in keeping with the concept of a constant circulating platelet mass, which would require more small platelets or fewer larger platelets . So, reticulated platelets are not necessarily large platelets.
Clinical utility of reticulated/immature platelets
In the earlier years, retPLT research focused on a possible differential diagnostic aid in patients with thrombocytopenia. Since megakaryopoietic activity is low in patients with bone marrow failure, the assumption was that consequently retPLT would be low, too. In contrast, conditions with peripheral platelet destruction like ITP are characterized by accelerated megakaryopoiesis and hence the retPLT count would be increased. Many studies have now confirmed that retPLT or IPF are valuable in establishing the cause of thrombocytopenia: decreased production can reliably be distinguished from peripheral destruction (see Table 2).
|Condition||Intended goal||References retPLT||References IPF|
|Low platelet count|
|Thrombocytopenia of unknown etiology||Differentiating hypoproduction from accelerated destruction||[15, 63, 66, 84, 85]||[49, 55, 63, 66, 75]|
|Chemotherapy||Predicting platelet recovery||[86, 87]|||
|Bone marrow or peripheral stem cell transplantation||Predicting platelet recovery||[17, 88–90]||[91–95]|
|Normal or high platelet count|
|Thrombocytosis||Estimating platelet turnover||[22, 23, 96]|
Another well-documented application of retPLT is monitoring the thrombocytopenic phase after chemotherapy and transplantation for hematological malignancies (Table 2). Generally, an increase in retPLT precedes the recovery of platelet count by 2–3 days. This creates the opportunity to defer platelet transfusions that would be given when transfusion decisions are based on platelet counts only. Until present, limited clinical evidence supporting this concept has been reported and there is an evident need for randomized, controlled clinical studies in this field [82, 97, 98]. A highly interesting observation that also needs to be confirmed is that prophylactic transfusions with high IPF platelet concentrates seem to be more effective than low IPF platelets .
Researchers in the field of cardiovascular diseases have recently gained interest in retPLT (Table 3). The current literature seems to provide preliminary support for the clinical utility of retPLT or IPF determinations, for risk assessment in acute coronary syndrome [100–104] as well as for monitoring drug treatment of coronary artery disease [78, 79, 105–107]. However, larger and randomized studies are necessary for proving that these concepts are effective and safe in clinical practice. There are also indications that it is preferentially immature platelets that are recruited into arterial thrombi  and if confirmed, this finding may have consequences for treatment with anti-platelet drugs .
|Condition||Possible application||References retPLT||References IPF|
|Low platelet count without marrow dysfunction|
|ITP||Predicting treatment response|||
|Disseminated intravascular coagulation||Assessing prognosis|||
|Thrombotic thrombocytopenic purpura||Assessing disease activity and adjusting therapy||[49, 109]|
|Cyclic thrombocytopenia||Predicting next thrombocytopenia phase|||||
|Myelodysplastic syndrome||Assessing prognosis in cases with aberrant karyotype||[98, 112]|
|Normal or high platelet count|
|Essential thrombocytemia and polycythemia vera||Investigate possible linkage with Jak2 mutation|||
|Therapy with thrombopoietic drugs||Assessing treatment effect|||
|Altered platelet function|
|Acute coronary syndrome||Assessing role of platelet activation in prognosis||[100, 104]||[101–104]|
|Drug treatment of coronary artery disease||Predicting treatment response||[78, 106, 107]||[79, 105]|
|Chronic uremia||Assessing effect of hemodialysis on platelet kinetics|||||
|Chronic liver disease||Differentiating between hepatitis and cirrhosis|||
|ICU patients||Predicting development of sepsis|||
|Neonates||Predicting degree of thrombocytopenia||[116, 117]|
|Diabetes mellitus||Predicting cardiovascular complications|||
|Platelet transfusions||Supporting transfusion decisions||||[82, 98, 99]|
Apart from the above disease states, there are several other conditions where retPLT are supposed to play a role (Table 3). Most of these associations are only described in a single paper or are based on small patient numbers, thus the scientific evidence is still weak. Therefore, additional research studies are absolutely required for obtaining independent confirmation on the utility retPLT or IPF in these settings.
Highlights and conclusions
Summarizing the literature reviewed above, it can be concluded that:
Reticulated platelets are the most immature platelets in the circulation and they reflect the megakaryopoietic activity in bone marrow
Reticulated platelets are not necessarily large platelets
The two commercially available methods (Sysmex IPF and Abbott reticulated platelets) are not interchangeable and each require their own reference values and clinical decision limits
There is an urgent need for a standardized method that can serve as an international reference for assessing the performance of reticulated/immature platelet methods
Measuring reticulated/immature platelets is of proven clinically usefulness in patients with thrombocytopenia of unknown etiology and for monitoring bone marrow recovery after chemotherapy and stem cell transplantation
Reticulated platelets seem to play a role in the etiology of coronary arterial diseases. If confirmed in large-scale trials, measurement of reticulated platelets or IPF may be useful for risk assessment as well as therapy monitoring
Some other indications look promising, but need further investigation before routine use of reticulated platelet assays is warranted
About the author
Johannes (Hans) Hoffmann started his career in clinical chemistry in 1976 as a trainee. Once certified as a specialist he became the head of the hematology laboratory in a large tertiary-care teaching hospital in the Netherlands, where he later was also appointed director of the Department of Clinical Laboratories. In 1992 he obtained his PhD in medical sciences at Leiden University, the Netherlands, on a thesis in the field of fibrinolysis. Since 2008 he is responsible for scientific affairs in hematology with Abbott Diagnostics in Europe. His scientific work comprises over 100 papers in peer-reviewed journals, mainly focused on general hematology, flow cytometry, coagulation and fibrinolysis. He is also author and co-author of several books on laboratory medicine and hematology. He gave numerous oral and poster presentations in congresses and other scientific events. He acts as a reviewer for various journals, including Clinical Chemistry and Laboratory Medicine, where he currently serves his last term as an Editorial Board member. He is a member of several international committees and working groups on standardization in laboratory hematology.
I thank my colleagues Ting Yu and Nigel Llewellyn-Smith for their valuable comments and advice.
Conflict of interest statement
Author’s conflict of interest disclosure: The author stated that there are no conflicts of interest regarding the publication of this article. Employment and leadership played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.
Research funding: None declared.
Employment or leadership: The author is a scientific employee of Abbott Diagnostics.
Honorarium: None declared.
3. Schulze H, Korpal M, Hurov J, Kim S-W, Zhang J, Cantley LC, et al. Characterization of the megakaryocyte demarcation membrane system and its role in thrombopoiesis. Blood 2006;107:3868–75.10.1182/blood-2005-07-2755Search in Google Scholar PubMed PubMed Central
4. Kosaki G. Platelet production by megakaryocytes: protoplatelet theory justifies cytoplasmic fragmentation model. Int J Hematol 2008;88:255–67.10.1007/s12185-008-0147-7Search in Google Scholar PubMed
6. Machlus KR, Thon JN, Italiano JE. Interpreting the developmental dance of the megakaryocyte: a review of the cellular and molecular processes mediating platelet formation. Br J Haematol 2014:165:227–36.10.1111/bjh.12758Search in Google Scholar PubMed
8. Shameer K, Denny JC, Ding K, Jouni H, Crosslin DR, de Andrade M, et al. A genome- and phenome-wide association study to identify genetic variants influencing platelet count and volume and their pleiotropic effects. Hum Genet 2014;133:95–109.10.1007/s00439-013-1355-7Search in Google Scholar PubMed PubMed Central
10. Ault KA, Rinder HM, Mitchell J, Carmody MB, Vary CP, Hillman RS. The significance of platelets with increased RNA content (reticulated platelets). A measure of the rate of thrombopoiesis. Am J Clin Pathol 1992;98:637–46.10.1093/ajcp/98.6.637Search in Google Scholar PubMed
11. Stohlawetz P, Schulenburg A, Stiegler G, Panzer S, Höcker P, Kalhs P, et al. The proportion of reticulated platelets is higher in bone marrow than in peripheral blood in haematological patients. Eur J Haematol 1999;63:239–44.10.1111/j.1600-0609.1999.tb01884.xSearch in Google Scholar PubMed
12. Ault KA, Knowles C. In vivo biotinylation demonstrates that reticulated platelets are the youngest platelets in circulation. Exp Hematol 1995;23:996–1001.Search in Google Scholar
13. Dale GL, Friese P, Hynes LA, Burstein SA. Demonstration that thiazole-orange-positive platelets in the dog are less than 24 hours old. Blood 1995;85:1822–5.10.1182/blood.V85.7.1822.bloodjournal8571822Search in Google Scholar
15. Kienast J, Schmitz G. Flow cytometric analysis of thiazole orange uptake by platelets: a diagnostic aid in the evaluation of thrombocytopenic disorders. Blood 1990;75:116–21.10.1182/blood.V220.127.116.11Search in Google Scholar
16. Rinder HM, Munz UJ, Ault KA, Bonan JL, Smith BR. Reticulated platelets in the evaluation of thrombopoietic disorders. Arch Pathol Lab Med 1993;117:606–10.Search in Google Scholar
18. Watanabe K, Takeuchi K, Kawai Y, Ikeda Y, Kubota F, Nakamoto H. Automated measurement of reticulated platelets in estimating thrombopoiesis. Eur J Haematol 1995;54:163–71.10.1111/j.1600-0609.1995.tb00209.xSearch in Google Scholar PubMed
19. Koike Y, Yoneyama A, Shirai J, Ishida T, Shoda E, Miyazaki K, et al. Evaluation of thrombopoiesis in thrombocytopenic disorders by simultaneous measurement of reticulated platelets of whole blood and serum thrombopoietin concentrations. Thromb Haemost 1998;79:1106–10.10.1055/s-0037-1615024Search in Google Scholar
20. Saxon BR, Blanchette VS, Butchart S, Lim-Yin J, Poon AO. Reticulated platelet counts in the diagnosis of acute immune thrombocytopenic purpura. J Pediatr Hematol Oncol 1998;20:44–8.10.1097/00043426-199801000-00007Search in Google Scholar PubMed
21. Saxon BR, Mody M, Blanchette VS, Freedman J. Reticulated platelet counts in the assessment of thrombocytopenic disorders. Acta Paediatr 1998;424(Suppl):65–70.10.1111/j.1651-2227.1998.tb01238.xSearch in Google Scholar PubMed
22. Rinder HM, Schuster JE, Rinder CS, Wang C, Schweidler HJ, Smith BR. Correlation of thrombosis with increased platelet turnover in thrombocytosis. Blood 1998;91:1288–94.10.1182/blood.V91.4.1288Search in Google Scholar
23. Robinson MS, Harrison C, Mackie IJ, Machin SJ, Harrison P. Reticulated platelets in primary and reactive thrombocytosis. Br J Haematol 1998;101:388–9.10.1046/j.1365-2141.1998.00738.xSearch in Google Scholar
24. Romp KG, Peters WP, Hoffman M. Reticulated platelet counts in patients undergoing autologous bone marrow transplantation: an aid in assessing marrow recovery. Am J Hematol 1994;46:319–24.10.1002/ajh.2830460411Search in Google Scholar
25. Richards EM, Jestice HK, Mahendra P, Scott MA, Marcus RE, Baglin TP. Measurement of reticulated platelets following peripheral blood progenitor cell and bone marrow transplantation: implications for marrow reconstitution and the use of thrombopoietin. Bone Marrow Transplant 1996;17:1029–33.Search in Google Scholar
26. Catani L, Vianelli N, Luatti S, Rizzi S, Castellani S, Valdrè L, et al. Characterization of autotransplant-related thrombocytopenia by evaluation of glycocalicin and reticulated platelets. Bone Marrow Transplant 1999;24:1191–4.10.1038/sj.bmt.1702062Search in Google Scholar
27. Stohlawetz P, Stiegler G, Knöbl P, Höcker P, Panzer S. The rise of reticulated platelets after intensive chemotherapy for AML reduces the need for platelet transfusions. Ann Hematol 1999;78:271–3.10.1007/s002770050513Search in Google Scholar
28. Semple JW, Siminovitch KA, Mody M, Milev Y, Lazarus AH, Wright JF, et al. Flow cytometric analysis of platelets from children with the Wiskott-Aldrich syndrome reveals defects in platelet development, activation and structure. Br J Haematol 1997;97:747–54.10.1046/j.1365-2141.1997.1132938.xSearch in Google Scholar
29. Fabris F, Cordiano I, Steffan A, Ramon R, Scandellari R, Nichol JL, et al. Indirect study of thrombopoiesis (TPO, reticulated platelets, glycocalicin) in patients with hereditary macrothrombocytopenia. Eur J Haematol 2000;64:151–6.10.1034/j.1600-0609.2000.90072.xSearch in Google Scholar
30. Joseph JE, Donohoe S, Harrison P, Mackie IJ, Machin SJ. Platelet activation and turnover in the primary antiphospholipid syndrome. Lupus 1998;7:333–40.10.1191/096120398678920163Search in Google Scholar
31. Harrison P. Platelet function and turnover in acute coronary syndromes. Blood 2000;96:256A.Search in Google Scholar
32. Tassies D, Reverter JC, Cases A, Escolar G, Villamor N, Lopez-Pedret J, et al. Reticulated platelets in uremic patients: effect of hemodialysis and continuous ambulatory peritoneal dialysis. Am J Hematol 1995;50:161–6.10.1002/ajh.2830500303Search in Google Scholar
34. Tassies D, Reverter JC, Cases A, Calls J, Escolar G, Ordinas A. Effect of recombinant human erythropoietin treatment on circulating reticulated platelets in uremic patients: association with early improvement in platelet function. Am J Hematol 1998;59:105–9.10.1002/(SICI)1096-8652(199810)59:2<105::AID-AJH1>3.0.CO;2-1Search in Google Scholar
35. Rinder HM, Bonan JL, Anandan S, Rinder CS, Rodrigues PA, Smith BR. Noninvasive measurement of platelet kinetics in normal and hypertensive pregnancies. Am J Obstet Gynecol 1994;170:117–22.10.1016/S0002-9378(13)70291-6Search in Google Scholar
36. Stiegler G, Stohlawetz P, Brugger S, Jilma B, Vierhapper H, Höcker P, et al. Elevated numbers of reticulated platelets in hyperthyroidism: direct evidence for an increase of thrombopoiesis. Br J Haematol 1998;101:656–8.10.1046/j.1365-2141.1998.00765.xSearch in Google Scholar
38. Peterec SM, Brennan SA, Rinder HM, Wnek JL, Beardsley DS. Reticulated platelet values in normal and thrombocytopenic neonates. J Pediatr 1996;129:269–74.10.1016/S0022-3476(96)70253-6Search in Google Scholar
39. Matic GB, Chapman ES, Zaiss M, Rothe G, Schmitz G. Whole blood analysis of reticulated platelets: improvements of detection and assay stability. Cytometry 1998;34:229–34.10.1002/(SICI)1097-0320(19981015)34:5<229::AID-CYTO4>3.0.CO;2-2Search in Google Scholar
40. Bonan JL, Rinder HM, Smith BR. Determination of the percentage of thiazole orange (TO)-positive, “reticulated” platelets using autologous erythrocyte TO fluorescence as an internal standard. Cytometry 1993;14:690–4.10.1002/cyto.990140615Search in Google Scholar
41. Rapi S, Ermini A, Bartolini L, Caldini A, Del GA, Miele AR, et al. Reticulocytes and reticulated platelets: simultaneous measurement in whole blood by flow cytometry. Clin Chem Lab Med 1998;36:211–4.10.1515/CCLM.1998.036Search in Google Scholar
42. Robinson MS, Mackie IJ, Khair K, Liesner R, Goodall AH, Savidge GF, et al. Flow cytometric analysis of reticulated platelets: evidence for a large proportion of non-specific labelling of dense granules by fluorescent dyes. Br J Haematol 1998;100:351–7.10.1046/j.1365-2141.1998.00563.xSearch in Google Scholar
43. Balduini CL, Noris P, Spedini P, Belletti S, Zambelli A, Da PG. Relationship between size and thiazole orange fluorescence of platelets in patients undergoing high-dose chemotherapy. Br J Haematol 1999;106:202–7.10.1046/j.1365-2141.1999.01475.xSearch in Google Scholar
44. Hedley B, Llewellyn-Smith N, Lang S, Hsia C, Keeney M. Enumerating reticulated platelets: technical challenges in developing a standardized, validated diagnostic test. Int J Lab Hematol 2013;35:22–3.Search in Google Scholar
45. Machin SJ. Development of a consensus standard reference method for immature platelets. Int J Lab Hematol 2013;35:26.Search in Google Scholar
46. Watanabe K, Kawai Y, Takeuchi K. Reticulated platelets – automated measurement and clinical utility. Rinsho Ketsueki 1995;36:267–72.Search in Google Scholar
47. Koh KR, Yamane T, Ohta K, Hino M, Takubo T, Tatsumi N. Pathophysiological significance of simultaneous measurement of reticulated platelets, large platelets and serum thrombopoietin in non-neoplastic thrombocytopenic disorders. Eur J Haematol 1999;63:295–301.10.1111/j.1600-0609.1999.tb01131.xSearch in Google Scholar
48. Takubo T, Yamane T, Hino M, Tsuda I, Tatsumi N. Usefulness of determining reticulated and large platelets in idiopathic thrombocytopenic purpura. Acta Haematol 1998;99:109–10.10.1159/000040823Search in Google Scholar PubMed
49. Briggs C, Kunka S, Hart D, Oguni S, Machin SJ. Assessment of an immature platelet fraction IPF in peripheral thrombocytopenia. Br J Haematol 2004;126:93–9.10.1111/j.1365-2141.2004.04987.xSearch in Google Scholar PubMed
50. Jung H, Jeon HK, Kim HJ, Kim SH. Immature platelet fraction: establishment of a reference interval and diagnostic measure for thrombocytopenia. Korean J Lab Med 2010;30:451–9.10.3343/kjlm.2010.30.5.451Search in Google Scholar PubMed
51. Nomura T, Kubota Y, Kitanaka A, Kurokouchi K, Inage T, Saigo K, et al. Immature platelet fraction measurement in patients with chronic liver disease: a convenient marker for evaluating cirrhotic change. Int J Lab Hematol 2010;32:299–306.10.1111/j.1751-553X.2009.01184.xSearch in Google Scholar PubMed
52. Sinclair L. The immature platelet fraction: an assessment of its application to a routine clinical laboratory. Aust J Med Sci 2012;33:48–57.Search in Google Scholar
53. Ko YJ, Kim H, Hur M, Choi SG, Moon HW, Yun YM, et al. Establishment of reference interval for immature platelet fraction. Int J Lab Hematol 2013;35:528–33.10.1111/ijlh.12049Search in Google Scholar PubMed
54. Abe Y, Wada H, Tomatsu H, Sakaguchi A, Nishioka J, Yabu Y, et al. A simple technique to determine thrombopoiesis level using immature platelet fraction (IPF). Thromb Res 2006;118:463–9.10.1016/j.thromres.2005.09.007Search in Google Scholar PubMed
55. Cannavo I, Ferrero VC, Sudaka I, Aquaronne D, Berthier F, Raynaud S. Valeur du pourcentage de plaquettes réticulées dans le diagnostic étiologique d’une thrombopénie. Ann Biol Clin 2010;68:415–20.10.1684/abc.2010.0449Search in Google Scholar PubMed
56. Briggs C, Longair I, Kumar P, Singh D, Machin SJ. Performance evaluation of the Sysmex haematology XN modular system. J Clin Pathol 2012;65:1024–30.10.1136/jclinpath-2012-200930Search in Google Scholar PubMed
57. Schoorl M, Schoorl M, Oomes J, van Pelt J. New fluorescent method (PLT-F) on Sysmex XN2000 hematology analyzer achieved higher accuracy in low platelet counting. Am J Clin Pathol 2013;140:495–9.10.1309/AJCPUAGGB4URL5XOSearch in Google Scholar PubMed
58. Kim YR, Kantor J, Landayan M, Kihara J, Bearden J, Sheehan E. A rapid and sensitive reticulocyte method on a high-throughput hematology instrument. Lab Hematol 1997;3:19–26.Search in Google Scholar
59. Costa O, van Moer G, Jochmans K, Jonckheer J, Damiaens S, De Waele M. Reference values for new red blood cell and platelet parameters on the Abbott Diagnostics Cell-Dyn Sapphire. Clin Chem Lab Med 2012;50:967–9.10.1515/cclm-2011-0789Search in Google Scholar PubMed
60. Gordillo M, de la Iglesia S, Lemes A, Lopez Brito J, Garcia Bello M, Molero T. Reticulated platelets (RP) counts by Cell-Dyn Sapphire (Abbott) method. Preliminary data. Int J Lab Hematol 2011;33(Suppl 1):118.Search in Google Scholar
61. Lang S, David R, Cohen J. Reticulated platelet normal ranges on CELL-DYN Sapphire. Int J Lab Hematol 2013;35(Suppl 1):112.Search in Google Scholar
62. Hoffmann JJ, van den Broek NM, Curvers J. Reference intervals of reticulated platelets and other platelet parameters and their associations. Arch Pathol Lab Med 2013;137:1635–40.10.5858/arpa.2012-0624-OASearch in Google Scholar PubMed
63. Meintker L, Haimerl M, Ringwald J, Krause SW. Measurement of immature platelets with Abbott CD-Sapphire and Sysmex XE-5000 in haematology and oncology patients. Clin Chem Lab Med 2013;51:2125–32.10.1515/cclm-2013-0252Search in Google Scholar PubMed
64. de Wit N, Oosting J, Hoffmann J, Krockenberger M, van Dun L. Comparative evaluation of the Abbott Cell-Dyn Sapphire reticulated platelets fraction and the Sysmex XE-2100 IPF. Int J Lab Hematol 2009;31(Suppl 1):98.Search in Google Scholar
65. Kim HR, Park BR, Lee MK, Park AJ, Ahn JY. Comparison of an immature platelet fraction and reticulated platelet in liver cirrhosis. Korean J Lab Med 2007;27:7–12.10.3343/kjlm.2007.27.1.7Search in Google Scholar PubMed
66. Pons I, Monteagudo M, Lucchetti G, Muñoz L, Perea G, Colomina I, et al. Correlation between immature platelet fraction and reticulated platelets. Usefulness in the aetiology diagnosis of thrombocytopenia. Eur J Haematol 2010;85:158–63.Search in Google Scholar
67. Barsam SJ, Psaila B, Forestier M, Page LK, Sloane PA, Geyer JT, et al. Platelet production and platelet destruction: assessing mechanisms of treatment effect in immune thrombocytopenia. Blood 2011;117:5723–32.10.1182/blood-2010-11-321398Search in Google Scholar PubMed PubMed Central
68. Pankraz A, Bauer N, Moritz A. Comparison of flow cytometry with the Sysmex XT2000iV automated analyzer for the detection of reticulated platelets in dogs. Vet Clin Pathol 2009;38:30–8.10.1111/j.1939-165X.2008.00086.xSearch in Google Scholar PubMed
69. Nishiyama M, Hayashi S, Kabutomori O, Yamanishi H, Suehisa E, Kurata Y, et al. Effects of anticoagulants and storage temperature on immature platelet fraction% (IPF%) values in stored samples measured by the automated hematology analyzer, XE-5000 – utility of CTAD-anticoagulation and room temperature storage. Rinsho Byori 2011;59:452–8.Search in Google Scholar
70. Kickler TS, Oguni S, Borowitz MJ. A clinical evaluation of high fluorescent platelet fraction percentage in thrombocytopenia. Am J Clin Pathol 2006;125:282–7.10.1309/50H8JYHN9JWCKAM7Search in Google Scholar
73. Osei-Bimpong A, Saleh M, Sola-Visner M, Widness J, Veng-Pedersen P. Correction for effect of cold storage on immature platelet fraction. J Clin Lab Anal 2010;24:431–3.10.1002/jcla.20426Search in Google Scholar PubMed PubMed Central
74. Cremer M, Weimann A, Schmalisch G, Hammer H, Bührer C, Dame C. Immature platelet values indicate impaired megakaryopoietic activity in neonatal early-onset thrombocytopenia. Thromb Haemost 2010;103:1016–21.10.1160/TH09-03-0148Search in Google Scholar PubMed
75. Strauß G, Vollert C, von Stackelberg A, Weimann A, Gaedicke G, Schulze H. Immature platelet count: a simple parameter for distinguishing thrombocytopenia in pediatric acute lymphocytic leukemia from immune thrombocytopenia. Pediatr Blood Cancer 2011;57:641–7.10.1002/pbc.22907Search in Google Scholar PubMed
76. Have LW, Hasle H, Vestergaard EM, Kjaersgaard M. Absolute immature platelet count may predict imminent platelet recovery in thrombocytopenic children following chemotherapy. Pediatr Blood Cancer 2013;60:1198–203.10.1002/pbc.24484Search in Google Scholar PubMed
77. Bat T, Leitman SF, Calvo KR, Chauvet D, Dunbar CE. Measurement of the absolute immature platelet number reflects marrow production and is not impacted by platelet transfusion. Transfusion 2013;53:1201–4.10.1111/j.1537-2995.2012.03918.xSearch in Google Scholar PubMed PubMed Central
78. Guthikonda S, Alviar CL, Vaduganathan M, Arikan M, Tellez A, DeLao T, et al. 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. J Am Coll Cardiol 2008;52:743–9.10.1016/j.jacc.2008.05.031Search in Google Scholar PubMed
79. Cesari F, Marcucci R, Caporale R, Paniccia R, Romano E, Gensini GF, et al. Relationship between high platelet turnover and platelet function in high-risk patients with coronary artery disease on dual antiplatelet therapy. Thromb Haemost 2008;99:930–5.10.1160/TH08-01-0002Search in Google Scholar PubMed
80. Koike Y, Miyazaki K, Higashihara M, Kimura E, Jona M, Uchihashi K, et al. Clinical significance of detection of immature platelets: comparison between percentage of reticulated platelets as detected by flow cytometry and immature platelet fraction as detected by automated measurement. Eur J Haematol 2010;84:183–4.10.1111/j.1600-0609.2009.01364.xSearch in Google Scholar PubMed
81. Lee EY, Kim SJ, Song YJ, Choi SJ, Song J. Immature platelet fraction in diabetes mellitus and metabolic syndrome. Thromb Res 2013;132:692–5.10.1016/j.thromres.2013.09.035Search in Google Scholar PubMed
82. Briggs C, Hart D, Kunka S, Oguni S, Machin SJ. Immature platelet fraction measurement: a future guide to platelet transfusion requirement after haematopoietic stem cell transplantation. Transfus Med 2006;16:101–9.10.1111/j.1365-3148.2006.00654.xSearch in Google Scholar PubMed
83. de Wit N, Oosting J, Hoffmann J, Krockenberger M, van Dun L. Novel method for measuring reticulated platelets using the Abbott CELL-DYN Sapphire. Int J Lab Hematol 2009;31(Suppl 1):98.Search in Google Scholar
84. Thomas-Kaskel A-K, Mattern D, Köhler G, Finke J, Behringer D. Reticulated platelet counts correlate with treatment response in patients with idiopathic thrombocytopenic purpura and help identify the complex causes of thrombocytopenia in patients after allogeneic hematopoietic stem cell transplantation. Cytometry 2007;72B:241–8.10.1002/cyto.b.20163Search in Google Scholar PubMed
85. Monteagudo M, Amengual MJ, Munoz L, Soler JA, Roig I, Tolosa C. Reticulated platelets as a screening test to identify thrombocytopenia aetiology. Quart J Med 2008;101:549–55.10.1093/qjmed/hcn047Search in Google Scholar PubMed
86. Macchi I, Chamlian V, Sadoun A, Le Dirach A, Guilhot J, Guilhot F, et al. Comparison of reticulated platelet count and mean platelet volume determination in the evaluation of bone marrow recovery after aplastic chemotherapy. Eur J Haematol 2002;69:152–7.10.1034/j.1600-0609.2002.02702.xSearch in Google Scholar PubMed
87. Wang C, Smith BR, Ault KA, Rinder HM. Reticulated platelets predict platelet count recovery following chemotherapy. Transfusion 2002;42:368–74.10.1046/j.1537-2995.2002.00040.xSearch in Google Scholar PubMed
88. Michur H, Maslanka K, Szczepinski A, Marianska B. Reticulated platelets as a marker of platelet recovery after allogeneic stem cell transplantation. Int J Lab Hematol 2008;30:519–25.Search in Google Scholar
89. Martinelli G, Merlo P, Fantasia R, Gioia F, Crovetti G. Reticulated platelet monitoring after autologous peripheral haematopoietic progenitor cell transplantation. Transfus Apher Sci 2009;40:175–81.10.1016/j.transci.2009.03.018Search in Google Scholar PubMed
90. Lang S, Rosenfeld D, Cohen J, Kariotis M. Reticulated platelet levels as an indicator of PBSC harvest and engraftment. Int J Lab Hematol 2013;35:113.Search in Google Scholar
91. Yamaoka G, Kubota Y, Nomura T, Inage T, Arai T, Kitanaka A, et al. The immature platelet fraction is a useful marker for predicting the timing of platelet recovery in patients with cancer after chemotherapy and hematopoietic stem cell transplantation. Int J Lab Hematol 2010;32:e208–16.10.1111/j.1751-553X.2010.01232.xSearch in Google Scholar PubMed
92. Hennel E, Kentouche K, Beck J, Kiehntopf M, Boër K. Immature platelet fraction as marker for platelet recovery after stem cell transplantation in children. Clin Biochem 2012;45:749–52.10.1016/j.clinbiochem.2012.03.022Search in Google Scholar PubMed
93. Zucker ML, Murphy CA, Rachel JM, Martinez GA, Abhyankar S, McGuirk JP, et al. Immature platelet fraction as a predictor of platelet recovery following hematopoietic progenitor cell transplantation. Lab Hematol 2006;12:125–30.10.1532/LH96.06012Search in Google Scholar PubMed
94. Takami A, Shibayama M, Orito M, Omote M, Okumura H, Yamashita T, et al. Immature platelet fraction for prediction of platelet engraftment after allogeneic stem cell transplantation. Bone Marrow Transplant 2007;39:501–7.10.1038/sj.bmt.1705623Search in Google Scholar PubMed
95. Linden van der N, Klinkenberg LJ, Meex SJ, Beckers EA, de Wit NC, Prinzen L. Immature platelet fraction (IPF) measured on the Sysmex XN haemocytometer predicts thrombopoietic recovery after autologous stem cell transplantation. Eur J Haematol 2014. doi: 10.1111/ejh.12319. [Epub ahead of print 25 Apr 2014].10.1111/ejh.12319Search in Google Scholar PubMed PubMed Central
96. Ryningen A, Apelseth T, Hausken T, Bruserud Ø. Reticulated platelets are increased in chronic myeloproliferative disorders, pure erythrocytosis, reactive thrombocytosis and prior to hematopoietic reconstitution after intensive chemotherapy. Platelets 2006;17:296–302.10.1080/09537100600746508Search in Google Scholar PubMed
97. Chaoui D, Chakroun T, Robert F, Rio B, Belhocine R, Legrand O, et al. Reticulated platelets: a reliable measure to reduce prophylactic platelet transfusions after intensive chemotherapy. Transfusion 2005;45:766–72.10.1111/j.1537-2995.2005.04286.xSearch in Google Scholar PubMed
98. Saigo K, Sakota Y, Masuda Y, Matsunaga K, Takenokuchi M, Nishimura K, et al. Automatic detection of immature platelets for decision making regarding platelet transfusion indications for pediatric patients. Transfus Apher Sci 2008;38:127–32.10.1016/j.transci.2008.01.003Search in Google Scholar PubMed
99. Parco S, Vascotto F. Application of reticulated platelets to transfusion management during autologous stem cell transplantation. Onco Targets Ther 2012;5:1–5.10.2147/OTT.S27883Search in Google Scholar PubMed PubMed Central
100. Lakkis N, Dokainish H, Abuzahra M, Tsyboulev V, Jorgensen J, De LA, et al. Reticulated platelets in acute coronary syndrome: a marker of platelet activity. J Am Coll Cardiol 2004;44:2091–3.10.1016/j.jacc.2004.05.033Search in Google Scholar PubMed
102. Gonzalez-Porras JR, Martin-Herrero F, Gonzalez-Lopez TJ, Olazabal J, María D-C, Pabon P, et al. The role of immature platelet fraction in acute coronary syndrome. Thromb Haemost 2010;103:247–9.10.1160/TH09-02-0124Search in Google Scholar PubMed
103. Cesari F, Marcucci R, Gori AM, Caporale R, Fanelli A, Casola G, et al. Reticulated platelets predict cardiovascular death in acute coronary syndrome patients: insights from the AMI-florence 2 study. Thromb Haemost 2013;109:846–53.10.1160/TH12-09-0709Search in Google Scholar PubMed
104. Ibrahim H, Nadipalli S, Delao T, Paranilam J, Barker C, Kleiman N. Immature platelets for prediction of clinical events: a possible future target for antiplatelet therapy. Cathet Cardiovasc Intervent 2013;81:S108–9.Search in Google Scholar
105. Ibrahim H, Nadipalli S, DeLao T, Guthikonda S, Kleiman N. Immature platelet fraction (IPF) determined with an automated method predicts clopidogrel hyporesponsiveness. J Thromb Thrombolysis 2012;33:137–42 (erratum 33: 299).10.1007/s11239-011-0665-7Search in Google Scholar PubMed
106. McBane RD, Gonzalez C, Hodge DO, Wysokinski WE. Propensity for young reticulated platelet recruitment into arterial thrombi. J Thromb Thrombolysis 2014;37:148–54.10.1007/s11239-013-0932-xSearch in Google Scholar PubMed
107. Perl L, Lerman-Shivek H, Rechavia E, Vaduganathan M, Leshem-Lev D, Zemer-Wassercug N, et al. Response to prasugrel and levels of circulating reticulated platelets in patients with ST-elevation myocardial infarction. J Am Coll Cardiol 2014;63:513–7.10.1016/j.jacc.2013.07.110Search in Google Scholar PubMed
108. Hong KH, Kim HK, Kim JE, Jung JS, Han KS, Cho HI. Prognostic value of immature platelet fraction and plasma thrombopoietin in disseminated intravascular coagulation. Blood Coagul Fibrinol 2009;20:409–14.10.1097/MBC.0b013e32832b1866Search in Google Scholar PubMed
109. Kier YE, Stempak LM, Maitta RW. Immature platelet fraction can help adjust therapy in refractory thrombotic microangiopathic hemolytic anemia cases. Transfus Apher Sci 2013;49:644–6.10.1016/j.transci.2013.07.005Search in Google Scholar PubMed
110. Connor DE, Joseph JE. Cyclic thrombocytopenia associated with marked rebound thrombocytosis and fluctuating levels of endogenous thrombopoietin and reticulated platelets: a case report. Am J Hematol 2012;87:120–2.10.1002/ajh.22186Search in Google Scholar PubMed
111. Yujiri T, Tanaka Y, Tanaka M, Tanizawa Y. Fluctuations in thrombopoietin, immature platelet fraction, and glycocalicin levels in a patient with cyclic thrombocytopenia. Int J Hematol 2009;90:429–30.10.1007/s12185-009-0415-1Search in Google Scholar PubMed
112. Sugimori N, Kondo Y, Shibayama M, Omote M, Takami A, Sugimori C, et al. Aberrant increase in the immature platelet fraction in patients with myelodysplastic syndrome: a marker of karyotypic abnormalities associated with poor prognosis. Eur J Haematol 2009;82:54–60.10.1111/j.1600-0609.2008.01156.xSearch in Google Scholar PubMed
113. Panova-Noeva M, Marchetti M, Buoro S, Russo L, Leuzzi A, Finazzi G, et al. JAK2V617F mutation and hydroxyurea treatment as determinants of immature platelet parameters in essential thrombocythemia and polycythemia vera patients. Blood 2011;118:2599–601.10.1182/blood-2011-02-339655Search in Google Scholar PubMed
114. Schoorl M, Bartels PC. Changes in platelet volume, morphology and RNA content in subjects treated with haemodialysis. Scand J Clin Lab Invest 2008;68:335–42.10.1080/00365510701744481Search in Google Scholar PubMed
115. De Blasi RA, Cardelli P, Costante A, Sandri M, Mercieri M, Arcioni R. Immature platelet fraction in predicting sepsis in critically ill patients. Intens Care Med 2013;39:636–43.10.1007/s00134-012-2725-7Search in Google Scholar PubMed
116. Cremer M, Paetzold J, Schmalisch G, Hammer H, Loui A, Dame C, et al. Immature platelet fraction as novel laboratory parameter predicting the course of neonatal thrombocytopenia. Br J Haematol 2009;144:619–21.10.1111/j.1365-2141.2008.07485.xSearch in Google Scholar PubMed
117. Kihara H, Ohno N, Karakawa S, Mizoguchi Y, Fukuhara R, Hayashidani M, et al. Significance of immature platelet fraction and CD41-positive cells at birth in early onset neonatal thrombocytopenia. Int J Hematol 2010;91:245–51.10.1007/s12185-009-0482-3Search in Google Scholar PubMed
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