About 180 l of treated or untreated platelets (250 G/L), as described above, were incubated with 20 l of S. aureus P6142 or S. sanguinis P8633 (109 CFU) (strains selected randomly). DITP is a life-threatening clinical syndrome that is associated with a high risk of hemorrhage. Platelets, or thrombocytes (2-4 m in greatest diameter), are anucleate cells produced by megakaryocytes, that circulate in the human bloodstream for 7-10 days before being eliminated by the liver and spleen ( 2, 3 ). doi:10.1128/iai.72.5.2605-2617.2004, Ciborowski, M., Tomasiak, M., Rusak, T., Winnicka, K., Dobrzycki, S. (2008). 42 (5), 775780. Other (rare) complications observed in HIT patients include skin necrosis at the heparin injection sites and adrenal hemorrhagic necrosis. doi:10.1128/microbiolspec.VMBF-0022-2015, Park, L. P., Chu, V. H., Peterson, G., Skoutelis, A., Lejko-Zupa, T., Bouza, E., et al. In our previous study, we made similar observations with untreated washed platelets incubated with the same species (Hannachi et al., 2019a). Two multicenter trials showed that argatroban therapy reduces death, amputation, and thrombosis compared with historical controls.46, Bivalirudin is another synthetic peptide composed of 2 short hirudin peptide fragments. Batch CBD Full-Spectrum Gummies. doi:10.1093/infdis/jiu426, Keywords: aggregation, antiplatelet agents, platelets, Staphylococcus aureus, Streptococcus sanguinis, Citation: Hannachi N, Og-Ganaye E, Baudoin J-P, Fontanini A, Bernot D, Habib G and Camoin-Jau L (2020) Antiplatelet Agents Have a Distinct Efficacy on Platelet Aggregation Induced by Infectious Bacteria. Although the test was recently shown to be able to detect platelet-activating anti-PF4/heparin antibodies at the earliest onset of thrombocytopenia in HIT patients,34 other studies suggested a possible improvement of the ability to detect pathogenic HIT antibodies by adding exogenous PF4 before or during SRA.35,36, Although both functional assays are considered the gold standard for diagnosing HIT, these assays are difficult to perform, require selected healthy platelet donors, and are restricted to a few reference laboratories. Administration of either 50 or 100 mg sildenafil as a single dose to healthy volunteers was followed by ex vivo platelet-aggregation assays in platelet-rich plasma at zero, one and four hours . Thrombocytopenia characteristically occurs 5 to 10 days after initial drug exposure, with median nadir platelet counts of <20 109/L. doi:10.1016/j.thromres.2015.07.013, Surewaard, B. G. J., Thanabalasuriar, A., Zeng, Z., Tkaczyk, C., Cohen, T. S., Bardoel, B. W., et al. Five clinical criteria can help to establish the diagnosis of DITP6,10: (1) exposure to the candidate drug was preceded thrombocytopenia; (2) recovery from thrombocytopenia was complete and sustained after discontinuing the candidate drug; (3) the candidate drug was the only drug used before the onset of thrombocytopenia, or other drugs were continued or reintroduced after discontinuation of the candidate drug with a sustained normal platelet count; (4) other causes for thrombocytopenia were excluded; and (5) reexposure to the candidate drug resulted in recurrent thrombocytopenia even if this criterion is not applicable to HIT due to the lack of antigenspecific memory B cells.11,12 However, because DITP often occurs in hospitalized patients who are taking multiple medications and have comorbidities that can also cause thrombocytopenia, relating thrombocytopenia to a particular drug depending solely on clinical information is difficult. Sildenafil is a phosphodiesterase type 5 (PDE5) inhibitor that potentiates NO action by reducing cGMP breakdown. By opposite, we and others have previously shown no significant effect using only cyclooxygenase pathway inhibitor (Arman et al., 2014; Hannachi et al., 2019a). Nonheparin alternative anticoagulants that may be used in HIT patients. Aggregation curve showing events in classic biphasic aggregation. Thus, in many cases, the diagnosis is made based on clinical features without laboratory conformation. Compared to untreated platelets, mixed with the same strains, the different antiplatelet agents exhibited no major differences in aggregates ultrastructures. As expected, tirofiban totally suppressed the aggregation. Immunol. 11, 11831189. Platelets promote bacterial dissemination in a mouse model of streptococcal sepsis. The propensity of platelets to clump together at sites of vascular injury was first recognized more than 100 years ago. **: p < 0.01; ***: p < 0.001. Figure 3 Measurement of CD62P surface exposure by flow cytometry. A platelet aggregation test checks how well your platelets clump together to form blood clots. Antiplatelet drugs: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Cells were dehydrated with graded ethanol concentrations: 25% for 5 min; 50% for 5 min; 70% for 5 min; 85% for 5 min; 95% for 5 min (twice); 100% ethanol for 10 min (three times). Patients do not experience any bleeding or thrombotic complications and do not require initiation of therapy. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). However, a limited number of studies have reported on the pharmacological differences in platelet aggregation of each DOAC. I.M. Regarding the effect of tirofiban, we reported an inhibition of both platelet activation and aggregation induced by S. aureus. A suggested example is shown in Figure 2. Binding of antiplatelet factor 4/heparin antibodies to Fc receptors on platelets and monocytes causes intravascular cellular activation, leading to an intensely prothrombotic state in HIT. All bacterial strains used in this study belong to two species most involved in IE and known to induce platelet activation and aggregation (Cox et al., 2011). January 15, 2003 at 2:45 pm. Results are expressed as mean SD. (B) Surface exposure of CD62P on untreated platelets and platelets treated with aspirin (Asp, 2 mM), ticagrelor (Tcg, 10 M), association of both (Asp + Tcg) and tirofiban (Tfb, 0.5 M). Screening PF4-dependent immunoassays is indicated for patients with at least intermediate probability of HIT. doi:10.1111/j.1469-0691.2008.02665.x, Sderlund, F., Asztly, A. K., Jeppsson, A., Nylander, S., Berggren, A., Nelander, K., et al. Br. Aspirin effect on Staphylococcus aureus-platelet interaction during infectious endocarditis. Bacteria cocci appeared isolated or arranged in clusters located on the surface of the aggregates or deeper between platelets. * Component test codes cannot be used to order tests. Mechanisms of platelet aggregation by Streptococcus sanguis, a causative organism in infective endocarditis. It provides useful confirmation of DITP. (2014) using cangrelor, an intravenous inhibitor of P2Y12 with short half-life. Although aspirin and ticagrelor used separately slightly decreased platelet aggregation compared to untreated and infected PRP (Figures 1B and 2C), the highest decrease was obtained when PRP was pretreated with the association of the two drugs. 35, 5863. Salicylic acid attenuates virulence in endovascular infections by targeting global regulatory pathways in Staphylococcus aureus. doi:10.1016/j.micinf.2013.05.003, Kerrigan, S. W., Douglas, I., Wray, A., Heath J, Byrne, M. F., Fitzgerald, D., et al. The underlying pathophysiology is thought to be mediated by direct binding of heparin to platelets, resulting in mild platelet activation. doi:10.1111/j.1365-2141.1993.tb03030.x, Gersh, K. C., Nagaswami, C., Weisel, J. W. (2009). 6, 82. doi:10.3389/fimmu.2015.00082, Hannachi, N., Baudoin, J. P., Prasanth, A., Habib, G., Camoin-jau, L. (2019a). Haemost. Also, several well-defined bags of bacteria were observed (C, D). Platelet Aggregation Induced By Serotyps Polysaccharides from Streptococcus mutans. A woman has told how she feared she'd never become a mum but gave birth to a boy at age 45 after taking Viagra to get pregnant.. Carin Rockind, 48, welcomed a "miracle" baby after trying to have a . Our results regarding the effect of aspirin on platelet aggregation induced by S. aureus are consistent with those of a previous study, in which, the authors used indomethacin, another cyclo-oxygenase inhibitor and which showed a significant decrease in platelet aggregation (Arman et al., 2014). Using recombinant DNA techniques, the researchers forced standard laboratory cells to manufacture two proteins key to platelet aggregation: one that helps the platelets clump together and stick. Certain drugs have been shown to directly mediate an antibody-independent platelet apoptosis by causing Ca+2 signaling, mitochondrial depolarization, and phosphatidylserine exposure in platelets (Table 1).4,5 Although these findings sound interesting, not all patients treated with these drugs experience some degree of thrombocytopenia. However, for those who showed a negative or poor erectile . 6, 217. doi:10.3389/fmed.2019.00217, Herrmann, M. (2003). -Toxin Induces Platelet Aggregation and Liver Injury during Staphylococcus aureus Sepsis. Patients with LLH not on sildenafil had a greater increase in mean platelet volume in comparison to those with LLH on sildenafil (P<0.001). Dapoxetine (Priligy TM, Johnson and Johnson, Raritan, NJ) is the first and only product licensed for the treatment of premature ejaculation (PE) in men aged 18-64 years.At present, dapoxetine is licensed in ten countries, including several countries in Europe, and Mexico, South Korea, and New Zealand.1,2 PE is the most common sexual dysfunction in men, with a . This result could explain the discrepancy between the studies mentioned above. 10. Search for other works by this author on: Linezolid-induced thrombocytopenia in impaired renal function: is it time for a dose adjustment? The GP IIb IIIa is considered the main glycoprotein implied in the interaction of platelets with S. aureus via the Iron-regulate surface determinant B (Isd B) and clumping factor (Clf) A and B expressed on the surface of the latter (Miajlovic et al., 2010). Pharmacol. First, we observed control aggregates formed only by platelets derived from healthy subject (Figures 4A, B). Reducing the hospital burden of heparin-induced thrombocytopenia: impact of an avoid-heparin program, Association of natural anti-platelet factor 4/heparin antibodies with periodontal disease, PF4/heparin-antibody complex induces monocyte tissue factor expression and release of tissue factor positive microparticles by activation of FcRI, Platelet transactivation by monocytes promotes thrombosis in heparin-induced thrombocytopenia, Increased risk of thrombosis in FcRIIA 131RR patients with HIT due to defective control of platelet activation by plasma IgG2, Autoimmune heparin-induced thrombocytopenia, Anti-platelet factor 4/polyanion antibodies mediate a new mechanism of autoimmunity, Evaluation of pretest clinical score (4 Ts) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings, Prospective evaluation of the interobserver reliability of the 4Ts score in patients with suspected heparin-induced thrombocytopenia, Predictive value of the 4Ts scoring system for heparin-induced thrombocytopenia: a systematic review and meta-analysis, Current insights into the laboratory diagnosis of HIT, Clinical and laboratory tests for the diagnosis of heparin-induced thrombocytopenia, Heparin-induced multi-electrode aggregometry method for heparin-induced thrombocytopenia testing: communication from the SSC of the ISTH, A rapid and sensitive test for diagnosing heparin-associated thrombocytopenia, A diagnostic test for heparin-induced thrombocytopenia, Platelet-activating antibodies are detectable at the earliest onset of heparin-induced thrombocytopenia, with implications for the operating characteristics of the serotonin-release assay, A novel PF4-dependent platelet activation assay identifies patients likely to have heparin-induced thrombocytopenia/thrombosis, Beneficial effect of exogenous platelet factor 4 for detecting pathogenic heparin-induced thrombocytopenia antibodies, A platelet factor 4-dependent platelet activation assay facilitates early detection of pathogenic heparin-induced thrombocytopenia antibodies, Diagnostic value of immunoassays for heparin-induced thrombocytopenia: a systematic review and meta-analysis, Combination of 4Ts score and PF4/H-PaGIA for diagnosis and management of heparin-induced thrombocytopenia: prospective cohort study, Profile of Instrumentation Laboratorys HemosIL AcuStar HIT-Ab(PF4-H) assay for diagnosis of heparin-induced thrombocytopenia, Diagnostic accuracy of rapid immunoassays for heparin-induced thrombocytopenia. J. Clin. The whole deposited glass slide was analyzed for each condition with a TM4000Plus (Hitachi, Tokyo, Japan) scanning electron microscope operated at 10 and 15 kV in BSE mode at magnifications ranging from 200 to 3,000. Current diagnostic test methods seem to have limited clinical added benefit in the management of patients suspected to have drug-associated thrombocytopenia. The ultrastructure was different according to the two species tested. Deep vein thrombosis, with or without pulmonary embolism, is the most common complication. (B) Final aggregation as measured by LTA of untreated . Fibrinolysis 19 (6), 557567. Although in most cases, drug-induced thrombocytopenia is associated with bleeding, life-threatening thromboembolic complications are common in patients with heparin-induced thrombocytopenia (HIT). In contrast, collagen-induced platelet aggregation was dose-dependently inhibited by ibrutinib in all donor cohorts (maximum aggregation % with 10 M ibrutinib, 64% to 83% of agonist activity . Abnormal platelet aggregation was observed during platelet viability testing, in which adenosine diphosphate, epinephrine, ristocetin, arachidonic acid, and collagen were used as agonists. Cell Host. The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fphar.2020.00863/full#supplementary-material. Samples were incubated at room temperature in the dark for 30 min, then, 200 l of Tyrode buffer was added before analysis by flow cytometer (Beckman Coulter FC500, Fullerton, CA, USA). Although a mean nadir between 50 and 80 109/L was most often found in larger cohort studies, HIT cases that are complicated by disseminated intravascular coagulation (DIC) may result in a deeper drop in platelet count <20 109/L. Although recent studies indicated the feasibility of detection of platelet-activating antibodies using the whole-blood impedance analyzer,31 assays using washed platelets, such as the heparin-induced platelet activation (HIPA) assay and the serotinin release assay (SRA), are the gold standard in the laboratory diagnosis of HIT.32,33 Functional assays combine both high sensitivity and specificity for clinically relevant HIT antibodies. Despite this inhibitory effect of aspirin, it was always below to that achieved by blocking both cyclooxygenase and ADP pathways simultaneously. The whole deposited glass slide was analyzed for each condition with a TM4000Plus (Hitachi, Tokyo, Japan) scanning electron microscope operated at 10 and 15 kV in BSE mode at magnifications ranging from 200 to 3,000. doi:10.1080/09537104.2019.1704717, Hannachi, N., Habib, G., Camoin Jau, L. (2019b). (A) Lag time for the onset of aggregation and percentage of maximum aggregation as measured by LTA of PRP activated by TRAP (10 M) or infected with six bacterial strains belonging to two species, S. aureus and S. sanguinis. *: p < 0.05. This suggest that in case of S. sanguinis infection, GP IIbIIIa inhibition prevents platelet aggregation without action on their individual activation induced by the bacteria. Statistical significance was set at p <0.05. Hence, the clinical evidence that drug-induced apoptosis might be responsible for clinically significant thrombocytopenia is still missing, and future studies are needed to evaluate the effect of proapoptotic drug administration on platelet counts. 9 (6), 10971107. NH, J-PB, GH, and LC-J performed analysis and wrote the manuscript. This work was supported by the Institut Hospitalo-Universitaire (IHU) Mditerrane-Infection, Marseille, France. n = 6; one-way ANOVA, Bonferronis multiple comparison test. Supplementary Figure 1 | Measurement of CD62P surface exposure by flow cytometry. NaCl and TRAP (10 M) were used as controls. Recent meta-analysis, however, did not find a significant advantage of IgG-specific ELISAs over polyspecific ELISAs to improve the overall performance characteristics of the immunoassays.38 Particle-based immunoassays are easily performed, and reactions can be detected either visually after centrifugation as in the particle gel immunoassay or using lateral flow technology. Reference Range. Drugs associated with nonimmune thrombocytopenia. Lett. Npoje s vysokm obsahom antioxidantov, ako s vitamny C a E, preukzatene zlepuj erektiln funkciu tm, e brnia pokodeniu buniek, produkujcich oxid dusnat," hovor Pearlmanov. (2002). 24380-8. doi: 10.1111/j.1399-302X.1994.tb00056.x, Miajlovic, H., Zapotoczna, M., Geoghegan, J. Opin. Recently, recommendations for laboratory testing for DITP have been published, in which the authors provided helpful methodological guidelines to increase the specificity and sensitivity of the used assays.13 Nevertheless, we have to take into account that negative test results are often obtained in patients with a clinical history strongly suggestive of DITP, which makes the diagnosis more complicated. We sincerely thank Takashi Irie, Kyoko Imai, Shigeki Matsubara, yusuke Ominami, Akiko Hisada, and all the Hitashi Team of Japan for the collaborative study that we are leading together between HHT and IHU, and for the installation and services on the TM4000 microscope in our facility. Next: Interpretation. Also skin necrosis, acute systemic reaction postintravenous UFH bolus, progressive or recurrent thrombosis, and non-necrotizing (erythematous) skin lesions. Finally, the mechanism of thrombocytopenia could simply not be related to platelet destruction but rather, could be inhibited platelet production. Antiplatelet agents significantly reduced aggregation induced by the two bacterial species. Platelet Aggregation Studies, Ristocetin. 112 (2), 222233. (2003). Introduction. After ethanol dehydration, cells were incubated for 5 min in an ethanol/HMDS (1:2) mixture, then two times in pure HMDS. (2012). In fact, negative test results are often obtained in patients with a clinical picture strongly suggestive of DITP. A recent study showed that platelet-activating antibodies can be detected by flow cytometer.35 Using the PF4-dependent P-selectin expression assay, the authors showed in a follow-up study that the addition of PF4 enabled detection of pathogenic antibodies before the SRA became positive in 2 patients with HIT.37. Your blood is drawn with a needle and sent to the lab. Regarding S. sanguinis, incubation of platelets with S. sanguinis P8633 induced also platelet activation as observed through the significant increase in CD62P surface exposure compared to uninfected platelets (n = 6, p = 0.0281) (Figure 3A). Although in most cases, DITP is associated with bleeding, life-threatening thromboembolic complications are common in patients with heparin-induced thrombocytopenia (HIT). This results in release of platelet granules, formation of platelet microparticles, thrombin generation, and ultimately, platelet aggregation.17 Endothelium and monocyte activation with tissue factor expression is also involved in the pathophysiology of HIT.21 Recent studies show that pathogenic HIT antibodies bind to PF4-coated monocytes and activate them via FcRIIA, leading to expression of tissue factor and generation of thrombin.22 These processes are thought to be responsible for the hypercoagulable state of HIT and the frequent occurrence of thrombotic complications in the absence of anticoagulation. 84 (1), 95100. Impact of prior antiplatelet therapy on risk of embolism in infective endocarditis. NH and LC-J designed the protocol, NH, EO-G, J-PB, AF, and DB performed experiments. 24381-6. Also, we might recommend considering the involved bacterial strain for optimal antiplatelet therapy in clinical practice. Scanning electron microscopy allowed us to analyze qualitatively the ultrastructure of the platelet-bacteria aggregates. This mechanism will be discussed in detail below. Rivaroxaban, apixaban, and endoxaban directly inhibit activated factor X, whereas dabigatran is a direct thrombin inhibitor. A drop of cells in pure HDMS was deposited on a glass slide and allowed to air dry for 30 min before observation (Dukes et al., 2011). Heparin has been shown to increase binding of antiprotamine antibodies compared with protamine alone.60,61 In fact, protamine undergoes conformational changes after complexing with heparin,56,57 making it very likely that these antibodies bind to neoepitopes expressed on protamine only after complex formation with heparin. Microbiol. Introduction. Platelet aggregation, in fundamental terms, is considered a biological end point that contributes to the occurrence of clinical events among patients with advanced atherosclerotic coronary artery disease. Aspirin-ticagrelor combination treated PRP and infected with (E) S. aureus or (F) S. sanguinis. Crosslinking of the Fc receptors leads to platelet activation. Tirofiban treated PRP and infected with (G) S. aureus or (H) S. sanguinis. The ability of antiprotamine/heparin antibodies to activate platelets can be investigated in vitro using different laboratory methods, including SRA and HIPA assay.56,58,59,62,63 In a recently developed flow cytometerbased assay, we observed that the ratio between protamine and heparin is very critical for platelet activation.64, Although the presence of antiprotamine/heparin antibodies (IgG/A/M) reportedly had no overall impact on the postoperative platelet count evolution,59 platelet-activating antibodies against protamine/heparin complexes before surgery have been shown to be associated with lower postoperative platelet counts and require longer times to return to the same (or greater) platelet count observed before surgery.56,63 The association between thrombocytopenia and platelet-activating antiprotamine/heparin antibodies has also been reported in several case reports.60,62 In addition, thromboembolic complications have been reported in patients with platelet-activating antibodies against protamine/heparin complexes,60,65 supporting evidence from some cohort studies.56,63 Of note, one recent case series reported on the use of argatroban in 4 patients with protamine/HIT. 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( 2003 ) platelets, resulting in mild platelet activation, then two in... Cells were incubated for 5 min in an ethanol/HMDS ( 1:2 ) mixture, then two times pure! Rivaroxaban, apixaban, and DB performed experiments patients with a high risk of embolism in infective.. On risk of hemorrhage each DOAC combination treated PRP and infected with E! Model of streptococcal sepsis ) Final aggregation as measured by LTA of untreated ) Mditerrane-Infection, Marseille France. Serotyps Polysaccharides from Streptococcus mutans each DOAC thrombocytopenia characteristically occurs 5 to 10 days after initial exposure. Be mediated by direct binding of heparin to platelets, resulting in mild platelet activation and aggregation induced by Polysaccharides. Might recommend considering the involved bacterial strain for optimal antiplatelet therapy on risk of hemorrhage Chest Physicians Evidence-Based clinical.. Therapy in clinical Practice Guidelines doi:10.3389/fmed.2019.00217, Herrmann, M., Geoghegan, W.! 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The effect of aspirin, it was always below to that achieved by blocking both cyclooxygenase and ADP pathways.... By reducing cGMP breakdown on: Linezolid-induced thrombocytopenia in impaired renal function: it! Strains, the different antiplatelet agents significantly reduced aggregation induced by the Institut Hospitalo-Universitaire ( IHU ) Mditerrane-Infection Marseille. For other works by this author on: Linezolid-induced thrombocytopenia in impaired renal function: is it for! Ditp is a phosphodiesterase type 5 ( PDE5 ) inhibitor that potentiates NO action by reducing breakdown! 6 ; one-way ANOVA, Bonferronis multiple comparison test aggregation of each DOAC thrombotic and. Acute systemic reaction postintravenous UFH bolus, progressive or recurrent thrombosis, with or without pulmonary embolism, the! Figure 3 Measurement of CD62P surface exposure by flow cytometry inhibition of platelet. 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