No abstract available.
Blood Platelets* ; Platelet Factor 4*

OBJECTIVE: To investigate the bacteriostatic effect of platelet-rich plasma (PRP) and its derivative platelet gel (PG) supernatant on Escherichia coli in vitro and its relationship with platelet factor 4 (PF4). METHODS: Apheresis platelets donated by healthy volunteers were obtained from the Blood station of Lu an Blood Center as the source of PRP. The counts of platelet, white blood cell and red blood cell in PRP and its derivative PG supernatant were detected by automatic hematology analyzer. Bacterial growth of PRP and PG supernatants co-cultured with bacteria for different time was observed by plate coating culture method, and the contents of PF4 in PRP and PG supernatants were detected by ELISA. RESULTS: Apheresis platelets were collected from 28 healthy volunteers with a median age of 33 (21-56) years old. PRP can inhibit the growth of escherichia coli, but there were individual differences in antibacterial effect within 24 hours. PRP of 13 healthy volunteers had strong antibacterial effect at 24 hours, 7 cases had weak antibacterial effect at 24 hours, and 8 cases had no antibacterial effect at 24 hours. PG supernatant showed no significant individual difference, and all of them had bacteriostatic effect within 12 hours, but no bacteriostatic effect after 12 hours. There was no statistical difference in the bacteriostatic effect of PRP at 24 hours between healthy volunteers aged ≤30 years and >30 years (P>0.05), and there was no statistical difference between the white blood cell count ≤0.1×10⁹/L and (0.1-1) ×10⁹/L groups (P>0.05). There was significant difference in the bacteriostatic effect of PRP between the two groups with platelet content ≤1 000×10⁹/L and >1 000×10⁹/L (P<0.05). The platelet count in PRP was higher than that in PG supernatant ［(911.57±160.52) ×10⁹/L vs 0］. The PF4 level in PRP was higher than that in PG supernatant (23623.34±9822.14 vs 6664.74±4065.83, P<0.05). CONCLUSION Both PRP and PG supernatant have antibacterial effects in Escherichia coli. The bacteriostatic effect of PRP was better than that of PG supernatant, and the platelet and PF4 contents in PRP were higher than those in PG supernatant, suggesting that the platelet and PF4 levels play an important role in bacteriostasis.
Adult ; Humans ; Middle Aged ; Escherichia coli ; Platelet Factor 4 ; Platelet-Rich Plasma

BACKGROUND: Dual antiplatelet therapy (aspirin and clopidogrel) is used to prevent adverse cardiac events in patients undergoing percutaneous coronary intervention (PCI). Some patients do not respond adequately to clopidogrel. Beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) can act as markers to detect platelet activation. We investigated the relationship between clopidogrel response and the dynamics of beta-TG and PF4 concentrations. METHODS: This study included 36 myocardial infarction (MI) patients, who underwent PCI and was indicated for dual antiplatelet therapy. Platelet reactivity, using the VerifyNow P2Y12 assay, was measured on the 3rd day of PCI. At the time of admission, and on the 3rd and 10th day of PCI, the plasma beta-TG and PF4 concentrations were quantified. RESULTS: Ten patients (27.8%) were clopidogrel non-responders displaying >208 P2Y12 reaction units. At the time of admission, levels of beta-TG in patients were elevated than that in the healthy controls (P<0.001). A similar trend was observed on the 3rd and 10th day of PCI (P<0.001). The beta-TG levels on the 10th day were reduced than those at the time of admission and on the 3rd day of PCI. PF4 levels were not different between patients and controls, and were not significantly reduced after PCI. Higher beta-TG levels were observed in clopidogrel non-responders on the 10th day, but not significant. CONCLUSIONS: Clopidogrel therapy in MI reduce beta-TG concentration, but the beta-TG and PF4 levels before and after therapy are not associated with the response to clopidogrel. Platelet-derived markers may not be suitable for distinguishing clopidogrel non-responders.
beta-Thromboglobulin ; Blood Platelets* ; Humans ; Infarction* ; Myocardial Infarction ; Percutaneous Coronary Intervention ; Plasma ; Platelet Activation* ; Platelet Factor 4

Heparin-induced thrombocytopenia (HIT) is a prothrombotic, immune-mediated adverse reaction to heparin therapy. It is caused by antibodies binding to a complex of heparin and platelet factor 4, and this leads to platelet activation, excessive thrombin generation and often thrombosis. HIT with thrombosis (HITT) can lead to limb amputation, stroke, myocardial infarction and death. We report here on a case of a HITT patient who was successfully managed with argatroban therapy. Further knowledge is need about the ideal medical management for HITT.
Amputation ; Antibodies ; Extremities ; Heart ; Heparin ; Humans ; Myocardial Infarction ; Pipecolic Acids ; Platelet Activation ; Platelet Factor 4 ; Stroke ; Thrombin ; Thrombocytopenia ; Thrombosis

platelet factor 4 forms a PF4/heparin-immunoglobulin G immune complex on platelet surfaces. This complex activates platelets, which leads to multiple coagulation in venous and arterial blood. We report here on a rare occurrence of HIT type II following fibula free flap surgery.]]>
Antigen-Antibody Complex ; Blood Platelets ; Fibula ; Free Tissue Flaps ; Heparin ; Platelet Factor 4 ; Thrombocytopenia ; Venous Thrombosis

Objectives: To assess the diagnostic values of latex immunoturbidimetric assay (LIA) and particle immunofiltration assay (PIFA) for heparin-induced thrombocytopenia (HIT) . Methods: Samples from 94 patients with suspected HIT from May 2016 to July 2018 in our hospital were prospectively analyzed by the two immunoassays. Their medical records and further follow-up data were also collected and analyzed by our hematologists to make the 4Ts scores and confirm the diagnosis of HIT, respectively. Performance characteristics of the two immunoassays were assessed, including sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) . Their post-test probabilities (PTP) were also calculated based on the 4Ts score. Results: Among 94 cases, 15 (16.0%) had a positive HIT, including 6 of 37 (16.2%) with an intermediate, and 9 of 15 (60.0%) with a high 4Ts score. PIFA operating characteristics were: sensitivity 100.0% (15/15) , specificity 51.9% (41/80) , PPV 28.3% (15/53) , NPV 100.0% (41/41) . The positive PTP in intermediate and high 4Ts score group were 28.7% and 75.7%, respectively, while negative PTP were all 0. At manufacturers' cutoffs, LIA operating characteristics were: sensitivity 66.7% (10/15) , specificity 94.9% (75/79) , PPV 71.4% (10/14) and NPV 93.8% (75/80) . The positive and negative PTP in intermediate 4Ts score group were 71.8% and 6.3%, while 95.2% and 34.4% in high 4Ts score group, respectively. Receiver operating characteristic (ROC) analysis manifested that LIA was preferable than PIFA, and combining the 2 assays together was significantly better than single test. Conclusions: 4Ts score is still an important tool for the diagnosis of HIT. Combining clinical score with heparin/PF4 antibody assay can increase the accuracy of confirming or excluding HIT. Although PIFA is inferior to LIA in the diagnostic value, its user friendliness and 100% NPV have major advantages. Combining the 2 assays together can achieve a higher diagnostic value.
Antibodies ; Anticoagulants ; Enzyme-Linked Immunosorbent Assay ; Heparin/adverse effects* ; Humans ; Immunoassay ; Platelet Factor 4 ; Thrombocytopenia/chemically induced*

A 78-year-old man presented with an eight-hour history of chest distress. Electrocardiograph and serum cardiac enzymes were suggestive of acute inferior myocardial infarction with right ventricular infarction. The patient, who underwent emergency percutaneous coronary intervention, suffered from thrombocytopenia presenting with cerebral infarction and myocadial reinfarction during haparin exposure. The laboratory test for heparin-induced thrombocytopenia (HIT) specific antibodies (heparin-platelet factor, PF4) was positive. The case was diagnosed as arteries thrombosis due to heparin-induced thrombocytopenia; the patient died after cessation of heparin.
Aged ; Coronary Thrombosis ; diagnosis ; etiology ; metabolism ; Heparin ; adverse effects ; Humans ; Male ; Platelet Factor 4 ; metabolism ; Thrombocytopenia ; chemically induced ; complications

Heparin-induced thrombocytopenia (HIT) is an antibody-mediated complication of heparin treatment that can lead to thrombosis and thromboembolism. HIT is mainly caused by immunoglobulin G (IgG) class among anti-heparin/platelet factor 4 antibodies that bind to epitopes on platelet factor 4 (PF4) released from activated platelets that developed when it forms complexes with heparin. Platelet aggregation and hypercoagulation status result from this process. Besides, the reactions between antibodies and vascular endothelial cells and monocytes are involved in HIT. Laboratory detection of anti-heparin/platelet factor 4 antibodies after heparin administration may help diagnose HIT early. Tests for detecting antibodies to the heparin/PF4 complex can be classified into functional platelet assays (which rely on the demonstration of platelet activation) and immunoassays (which detect the presence of an antibody without regard for its functional ability). But there is no simple and effective test available currently. In this article the anti-heparin/platelet factor 4 antibodies, pathogenesis of HIT, clinical laboratory assays and immunoassays are reviewed.
Antigen-Antibody Complex ; immunology ; Heparin ; adverse effects ; immunology ; Humans ; Immunoglobulin G ; immunology ; Platelet Aggregation ; Platelet Factor 4 ; immunology ; Thrombocytopenia ; chemically induced ; immunology

BACKGROUND: It is critical to differentiate heparin-induced thrombocytopenia (HIT) from disseminated intravascular coagulation (DIC) in heparinized intensive care unit (ICU) patients with thrombocytopenia because the therapeutic approach differs based on the cause. We investigated the usefulness of PF4/heparin antibody tests in these patients. METHODS: A total of 127 heparinized ICU patients whose platelet counts were <150x10(9)/L or reduced by >50% after 5-10 days of heparin therapy were enrolled. PF4/heparin antibodies were measured using 2 immunoassays. We assessed the probability of HIT by using Warkentin's 4T's scoring system for antibody positive patients and compared routinely performed coagulation test results between patients with and without antibodies to evaluate the ability of these tests to discriminate between HIT and DIC. RESULTS: Positive results were obtained for 14 (11.0%) and 11 (8.7%) patients in the 2 assays. The analysis performed using the 4T's scoring system revealed that 11 of 20 (15.7%) patients with antibodies in at least 1 assay had intermediate or greater probability of HIT. Patients without antibodies had significantly higher levels of D-dimer than those with antibodies. However, there were no intergroup differences in platelet counts, PT, aPTT, fibrinogen, DIC score, and rate of overt DIC. CONCLUSION: Seropositivity for PF4/heparin antibody was 8.7-11.0% in the patients with thrombocytopenia, and more than a half of them had an increased probability of HIT. Among the routine coagulation tests, only D-dimer was informative for differentiating HIT from DIC. PF4/heparin antibody test is useful to ensure appropriate treatment for thrombocytopenic heparinized ICU patients.
Antibodies ; Dacarbazine ; Dietary Sucrose ; Disseminated Intravascular Coagulation ; Fibrin Fibrinogen Degradation Products ; Fibrinogen ; Heparin ; Humans ; Immunoassay ; Critical Care ; Intensive Care Units ; Platelet Count ; Platelet Factor 4 ; Thrombocytopenia

This study was aimed to investigate the abnormal expression of PDGFRA gene in eosinophilia by FISH. Translocations of PDGFRA gene in 13 patients with eosinophilia were detected by using 4q12 three-color probe and FISH technology. Fifteen people were used as control to establish the normal cut-off value of fluorescence signal of PDGFRA. The results indicated that 1 out of 13 patients with eosinophilia was corrected and was diagnosed as CML. The fusion gene of FIP1L1-PDGFRA (F/P) was found in 2 patients and the positive rate of F/P fusion gene detected by probe 4q12 was 17% in the 12 patients with eosinophilia. Other translocation forms involving PDGFRA gene were not found. It is concluded that a variety of translocation forms of PDGFRA gene can be detected in patients with eosinophilia by using 4q12 three-color probe and FISH technology, which can provide important information for assessing diagnosis and treatment.
Chromosomes, Human, Pair 4 ; Eosinophilia ; metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Oncogene Proteins, Fusion ; Receptor, Platelet-Derived Growth Factor alpha ; genetics ; Translocation, Genetic