OBJECTIVE: Primary immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by isolated thrombocytopenia that is often misdiagnosed due to the lack of a gold standard for diagnosis and currently relies on exclusionary approaches. This project combines several laboratory parameters to construct a clinical prediction model for adult ITP patients.
METHODS: A total of 428 patients with thrombocytopenia who visited the West China Hospital of Sichuan University between January 2021 and March 2023 were enrolled. Based on the diagnostic criteria, we divided those patients into an ITP group and a non-ITP group. A total of 34 laboratory parameters were analyzed via univariate analysis and correlation analysis, and the least absolute shrinkage and selection operator regression analysis was used to establish the model. The training and validation sets were divided at a ratio of 7:3, and we used a fivefold cross-validation method to construct the model.
RESULTS: The model included the following variables: red blood cell, mean corpuscular hemoglobin concentration, red blood cell distribution width-standard deviation, platelet variability index score, immature platelet fraction, lymphocyte absolute value. The prediction model exhibited good performance, with a sensitivity of 0.89 and a specificity of 0.83 in the training set and a sensitivity of 0.90 and a specificity of 0.87 in the validation set.
CONCLUSIONS: The clinical prediction model can assess the probability of ITP in thrombocytopenic patients and has good predictive accuracy for the diagnosis of ITP.

Prolonged thrombocytopenia (PT) is a serious complication after haematopoietic stem cell transplantation (HSCT). PT has been suggested to be associated with an increased platelet transfusion requirement and poor outcomes after transplantation. Due to the complex mechanism of PT development, it is difficult to diagnose in the early post-transplant period. Our study aimed to identify an early predictive marker for PT after HSCT. Previous studies showed that the clinical utility of immature platelet fraction (IPF) predicts platelet recovery after chemotherapy and successful engraftment. However, the relationship between IPF and PT after HSCT remains unclear. Fifty-two patients with malignant haematological diseases who underwent HSCT were included in the study. We observed the kinetics of recovery of haematological parameters after transplantation and performed receiver operating characteristics (ROC) curve analysis using data from the 52 HSCT patients. The days to rise and peak of IPF, absolute IPF count (A-IPF) and highly fluorescent IPF (H-IPF) were almost synchronised in all patients, at day 10 and day 15, respectively. The begin to rise levels of IPF, H-IPF and A-IPF were all significantly lower in the PT group than in the good engraftment (GE) group (p=0.0016, p=0.0094, p=0.0086, respectively). The peak levels of IPF were significantly lower in the PT group than the GE group (p=0.0036). However, the peaks of H-IPF and A-IPF were not statistically significant between the two groups (p=0.3383, p=0.0887, respectively). The area under the ROC curve (AUC) of IPF rise was 0.739 (95% CI 0.583-0.896; p<0.05) and the cut-off value was 3.5%, while the AUC of IPF peak was 0.800 (95% CI 0.637-0.962; p<0.01) and the cut-off value was 8.0%. In conclusion, early low levels of IPF predict the development of PT after HSCT. These findings may help improve the management and treatment strategies for PT after HSCT.

Reliable indicators that can predict drug responsiveness in primary immune thrombocytopenia (ITP) patients are urgent. We aimed to establish a reference interval of percentage of immature platelet fraction (IPF%) and absolute immature platelet count (A-IPC), and assess their efficacy in discriminating ITP patients from controls, especially their predictive value for responsiveness to drug treatment. We retrospectively studied 72 treatment-naive adult patients with ITP who received Dexamethasone monotherapy or combination therapy. Baseline (pretreatment) information was collected from medical records. Reference intervals for A-IPC and IPF% were established based on controls and their effectiveness in discriminating ITP patients from controls was assessed. Predictive value of pretreatment IPF% and A-IPC at four co-primary endpoints of treatment response in patients were investigated. The 95% reference intervals for A-IPC and IPF% were (2.7-15.6) × 109/L and 1.2%-7.3%, respectively. Both A-IPC and IPF% had excellent discrimination ability for ITP patients from controls. It showed highly statistically significant differences in pretreatment A-IPC for predicting treatment response at day 7 between responders and non-responders, but not at days 14, 21 and 28. Pretreatment A-IPC had the higher area under the ROC curve with a cut-off of 0.86 than that of IPF% with a cut-off of 14.5% in predicting the treatment response in ITP patients at day 7. Pretreatment A-IPC exhibited acceptable predictive power and could be a promising predictor of response to short-term Dexamethasone monotherapy or combination therapy at day 7 in ITP patients.

The pathogenesis of thrombocytopenia can be divided into increased destruction (ID) of platelets in the peripheral blood and decreased production (DP) of platelets in the bone marrow. This study aimed to analyze the efficacy of immature platelet fraction (IPF) related parameters, including the IPF count (IPF#), IPF percentage (IPF%) and highly fluorescence IPF percentage (H-IPF%), measured by XN-9000, in the differential diagnosis of thrombocytopenia. One hundred and twenty healthy volunteers were enrolled in the healthy control (HC) group, and 180 thrombocytopenia patients were grouped into either the increased destruction (ID) group or the decreased production (DP) group according to their final diagnosis. IPF# was significantly lower in the DP group than in the ID and HC groups (P < .01). Among the three groups, the ID group had the highest IPF% and H-IPF%, and the HC group had the lowest IPF% and H-IPF%. The differences between the three groups were all statistically significant (P < .01). In differentiating the ID patients from the DP patients, the areas under the operating characteristics curve of IPF#, IPF% and H-IPF% were 0.859, 0.944 and 0.930, respectively. False positive rates were below 0.04 when IPF#, IPF% and H-IPF% were above 2.65, 7.55 and 2.35, respectively. IPF related parameters showed high efficacy in the differential diagnosis of thrombocytopenia. However, due to the small numerical values of the IPF related parameters in some thrombocytopenia patients, the fluctuations of IPF% and H-IPF% should also be taken into consideration. Though H-IPF% is a new parameter, its effectiveness in the differential diagnosis of thrombocytopenia is not better than IPF%\'s.

OBJECTIVE: An increased rate of platelet production is a possible cause of reduced antithrombotic response to once-daily aspirin. Markers of immature platelets (IPs), such as immature platelet count (IPC), immature platelet fraction (IPF), and mean platelet volume (MPV) might be useful for identifying patients who have an increase in their rate of platelet production. However, their potential as markers of platelet production has not been rigorously evaluated. We aimed to investigate the utility of the IPC, IPF, and MPV as surrogates for increased platelet production using coronary artery bypass grafting (CABG) as a model of enhanced thrombopoiesis.
METHODS: Daily changes in platelet count, IPC, IPF, and MPV were followed in 45 patients undergoing CABG.
RESULTS: The rise in IP markers preceded that in the platelet count. IPC (16% per day increase from nadir) but not IPF or MPV showed a significant and sustained rise, which paralleled the pattern observed with platelet count (18% per day increase from nadir).
CONCLUSIONS: Of the 3 markers, IPC was the most promising as surrogates for platelet production. Future studies should evaluate the utility of the IPC to identify patients with cardiovascular disease with reduced response to aspirin who might benefit from twice-daily aspirin.

UNASSIGNED: Kawasaki disease is a kind of systemic vasculitis that mainly damages moderate and small-sized blood vessels, and is a leading cause of coronary artery lesions (CAL). Antiplatelet therapy is a routine component of Kawasaki disease treatment strategies. So it is important to evaluate the antiplatelet effect of aspirin because of the individual biological variability of antiplatelet effect of aspirin. The immature platelet fraction (IPF) has attracted particular attention as it may influence the antiplatelet effect of aspirin. This study investigated the prognostic factors for evaluating the degree of vasculitis and the effect of antiplatelet therapy in children with Kawasaki disease.
UNASSIGNED: Blood samples were collected from 44 patients with Kawasaki disease before aspirin treatment and 7 to 10 days after treatment. The IPF counts, percentage of the IPF, and highly fluorescent IPF were detected by a Sysmex XE-5000 instrument. The levels of 11-dehydrothromboxane B2 (11-DH-TXB2), soluble CD40 ligand (sCD40L), and soluble P-selectin (sP-selectin) were measured by ELISA. The correlation between the measured factors and the degree of coronary artery damage in Kawasaki disease was analyzed.
UNASSIGNED: We found that 11-DH-TXB2, sP-selectin, and sCD40L levels were much more elevated in the CAL group than in the non-coronary artery lesions (NCAL) group before aspirin treatment. The concentrations of 11-DH-TXB2, sCD40L, sP-selectin, and IPF were reduced after aspirin treatment in the NCAL group but not the CAL group. This is related to the degree of coronary artery damage in Kawasaki disease patients. Additionally, 11-DH-TXB2, sCD40L, sP-selectin, and IPF were positively correlated with the degree of coronary artery damage in Kawasaki disease patients.
UNASSIGNED: The current study suggests that the presence of high plasma concentrations of 11-DH-TXB2, sCD40L, sP-selectin, and IPF can be considered a risk factor and experimental biomarker for CAL in Kawasaki disease patients.

Stromal cell-derived factor-1 (SDF-1), signaling through CXCR4, is implicated in megakaryopoiesis and platelet production. SDF-1 rs2297630 is a functional polymorphism in linkage disequilibrium with other functional variants in SDF-1. This study aimed to investigate the role of SDF-1 rs2297630 in chronic ITP. The genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism and confirmed by direct sequencing. Immature platelet fraction (IPF) was performed using Sysmex XE-2100. Anti-platelet autoantibodies were assayed by enzyme-linked immunosorbent assay. The main characteristics at diagnosis and the outcome of chronic ITP in 201 Chinese patients were retrospectively reviewed. There was no significant difference in either genotype or allelic distribution between ITP patients and the controls (p = 0.114; p = 0.787). However, both heterozygote (GA) and homozygote minor allele (AA) patients had significantly increased megakaryocyte quantity compared to homozygote genotype (GG) patients at diagnosis (p = 0.011). The mean IPF values of GA and AA genotype patients were higher than those observed in the GG genotype patients when platelet counts ≤50 × 10(9)/L at diagnosis (p = 0.007). Patients with GA and AA genotype showed a higher response rate to standard treatments than patients with GG genotype (p < 0.001). In particular, GA and AA genotype patients had a significantly increased chance of responding to steroids, intravenous immunoglobulin (IVIG), and thrombopoietin analogs (p = 0.007; p = 0.029; p = 0.034, respectively). No significant difference was found between anti-platelet antibodies and genotypes (p = 0.296). In summary, the SDF-1 rs2297630 was associated with platelet production and treatment response in Chinese patients with chronic ITP.

The immature platelet fraction (IPF) measures the number of reticulated platelets in peripheral blood, and can be used to help determine if thrombocytopenia is secondary to low-platelet production or increased platelet turnover. The aim of this study was to determine whether abnormalities in the IPF were associated with thrombocytopenia in patients with hepatitis B virus-related chronic hepatitis (CHB). One hundred fifty-six patients with chronic hepatitis B, including 80 thrombocytopenia, 76 without thrombocytopenia, and 48 healthy controls were enrolled in the study. The IPF percentages (IPF%) were measured using a XE-2100 multiparameter automatic hematology analyzer. We demonstrated that in the thrombocytopenic group, the IPF% was significantly increased compared with that in healthy controls and the non-thrombocytopenic group (both p < 0.001). Multivariate analysis demonstrated that IPF%, splenomegaly, and the model for end-stage liver disease score were independent predictors for thrombocytopenia (both p < 0.001). High IPF% during the course of thrombocytopenia suggests that platelet destruction/sequestration due to hypersplenism is a major factor contributing to thrombocytopenia in patients with CHB.