Platelets最新文献

{"title":"Effect of avatrombopag in the management of severe and refractory chemotherapy-induced thrombocytopenia (CIT) in patients with solid tumors.","authors":"Yanting Gao,&nbsp;Qi Liu,&nbsp;Yingying Shen,&nbsp;Yuzhu Li,&nbsp;Keding Shao,&nbsp;Baodong Ye,&nbsp;Yiping Shen,&nbsp;Yuhong Zhou,&nbsp;Dijiong Wu","doi":"10.1080/09537104.2022.2026910","DOIUrl":"https://doi.org/10.1080/09537104.2022.2026910","url":null,"abstract":"<p><p>Chemotherapy-induced thrombocytopenia (CIT) is a common complication in cancer patients, especially after multiple cycles of chemotherapy, which leads to the delayed treatment or reduced dosage. The treatment of CIT is limited for refractory and severe cases. Herein we reported a single-center study of avatrombopag, a type of thrombopoietin receptor agonist (TPO-RA), for the treatment of severe and refractory (S/R) CIT who failed from multi-line treatments. A total of 13 cancer patients with S/R CIT were enrolled at the First Affiliated Hospital of Zhejiang Chinese Medical University from September 2020 to February 2021. All the patients were administered oral avatrombopag at an initial dose of 60 mg/day, which could be decreased as needed, over a period of 8 weeks. Eight (8/13, 61.5%) patients responded to avatrombopag (with a platelet count ≥50 × 10⁹/L and transfusion independent), with a median response time of 27.5 (11-50) days, and the median cumulative day of platelet response was 79 (20-167). Ten of 13 patients (76.9%) no longer required platelet transfusion at the study endpoint. The predictor of response was the level of hemoglobin (HB) at study entry, patients with an HB over 90 g/L achieved a response rate of 88.9%. In addition, platelet count showed 87.5% sensitivity and 100% specificity to predict the treatment response at a cutoff value of 25.5× 10⁹/L at the end of the third week management. No drug-related side effects were noticed during administration. Our study showed that avatrombopag could be a novel and effective drug for the treatment of severe and refractory CIT, especially for those with hemoglobin above 90 g/L. This study was registered at <i>chictr.org.cn</i> as # ChiCTR2100050646.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9227520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-GPVI (HY101) activates platelets in a multicolor flow cytometry panel.","authors":"Marie-Astrid van Dievoet,&nbsp;Davide Brusa,&nbsp;Marie Octave,&nbsp;Sandrine Horman,&nbsp;Xavier Stephenne","doi":"10.1080/09537104.2022.2027359","DOIUrl":"https://doi.org/10.1080/09537104.2022.2027359","url":null,"abstract":"<p><p>The platelet transmembrane receptor GPVI can be assessed together with other platelet membrane markers in a whole blood multicolor flow cytometry panel. The advantage of combining multiple antibodies in a single tube is the possibility of distinguishing multiple platelet subgroups. In this short communication, we describe an activation problem encountered with anti-GPVI, clone HY101. Activation of platelets was seen after the addition of anti-GPVI in a flow cytometry panel, highlighted by the expression of the activation markers CD62P, PAC-1, CD63, and CD107a. This was also confirmed by platelet aggregation studies.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39826646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thrombosis and hemorrhage in myeloproliferative neoplasms: The platelet perspective.","authors":"Yiming Feng,&nbsp;Yue Zhang,&nbsp;Jialan Shi","doi":"10.1080/09537104.2021.2019210","DOIUrl":"https://doi.org/10.1080/09537104.2021.2019210","url":null,"abstract":"<p><p>Classical myeloproliferative neoplasm (MPN), also known as BCR-ABL-negative MPN, is a clonal disease characterized by abnormal expansion of hematopoietic stem cells. It has been demonstrated that MPN patients are more susceptible to thrombotic events compared to the general population. Therefore, researchers have been exploring the treatment for MPN thrombosis. However, antithrombotic therapies have brought another concern for the clinical management of MPN because they may cause bleeding events. When thrombosis and bleeding, two seemingly contradictory complications, occur in MPN patients at the same time, they will lead to more serious consequences. Therefore, it is a major challenge to achieving the best antithrombotic effect and minimizing bleeding events simultaneously. To date, there has yet been a perfect strategy to meet this challenge and therefore a new treatment method needs to be established. In this article, we describe the mechanism of thrombosis and bleeding events in MPN from the perspective of platelets for the first time. Based on the double-sided role of platelets in MPN, optimal antithrombotic treatment strategies that can simultaneously control thrombosis and bleeding at the same time may be formulated by adjusting the administration time and dosage of antiplatelet drugs. We argue that more attention should be paid to the critical role of platelets in MPN thrombosis and MPN bleeding in the future, so as to better manage adverse vascular events in MPN.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39862392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New oral protease-activated receptor 4 antagonist BMS-986120: tolerability, pharmacokinetics, pharmacodynamics, and gene variant effects in humans.","authors":"Samira Merali,&nbsp;Zhaoqing Wang,&nbsp;Charles Frost,&nbsp;Mario Callejo,&nbsp;Michael Hedrick,&nbsp;Lester Hui,&nbsp;Stephanie Meadows Shropshire,&nbsp;Ke Xu,&nbsp;Michel Bouvier,&nbsp;Mary M DeSouza,&nbsp;Jing Yang","doi":"10.1080/09537104.2022.2088719","DOIUrl":"https://doi.org/10.1080/09537104.2022.2088719","url":null,"abstract":"<p><p>BMS-986120 is a novel first-in-class oral protease-activated receptor 4 (PAR4) antagonist exhibiting robust antithrombotic activity that has shown low bleeding risk in monkeys. We sought to assess pharmacokinetics, pharmacodynamics, and tolerability of BMS-986120 in healthy participants and platelet responses to BMS-986120 in participants carrying PAR4 A120T variants. Phase I, randomized, double-blind, placebo-controlled single-ascending-dose (SAD; N = 56) and multiple-ascending-dose (MAD; N = 32) studies were conducted. Exposure was approximately dose-proportional: maximum concentrations 27.3 and 1536 ng/mL, areas under the curve (AUC) to infinity of 164 and 15,603 h*ng/mL, and half-lives of 44.7 and 84.1 hours for 3.0 and 180 mg, respectively. The accumulation index suggested an ~2-fold AUC increase at steady state. Single doses of 75 and 180 mg BMS-986120 produced ≥80% inhibition of 12.5 μM PAR4 agonist peptide (AP)-induced platelet aggregation through at least 24 hours postdose, and doses ≥10 mg for ~7 days inhibited aggregation completely through 24 hours. No differences in PAR4-mediated platelet response were seen between AA120 versus TT120 PAR4 variants. In cells expressing A120 or T120 PAR4 proteins, no differences in half-maximal effective concentration in receptor activation by PAR4-AP were observed. BMS-986120 was well tolerated with dose-proportional pharmacokinetics and concentration-dependent pharmacodynamics in healthy participants over a wide dose range.<b>ClinicalTrials.gov ID</b>: NCT02208882.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40404146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bleeding and mortality risk in patients implanted with mechanical prosthetic heart valves with and without thrombocytopenia. Insights from the nationwide PLECTRUM registry.","authors":"Danilo Menichelli,&nbsp;Daniela Poli,&nbsp;Emilia Antonucci,&nbsp;Flavio Giuseppe Biccirè,&nbsp;Gualtiero Palareti,&nbsp;Pasquale Pignatelli,&nbsp;Daniele Pastori","doi":"10.1080/09537104.2022.2026909","DOIUrl":"https://doi.org/10.1080/09537104.2022.2026909","url":null,"abstract":"<p><p>Previous studies showed that mechanical prosthetic heart valve (MPHV) patients may develop thrombocytopenia, but its association with clinical outcomes has not been investigated. We enrolled 1,663 patients with available platelet count from the multicenter nationwide retrospective PLECTRUM registry to investigate the association of thrombocytopenia with all-cause mortality and major bleeding (MB) in patients implanted with MPHV. Thrombocytopenia was defined by platelet count <150 × 10⁹/L. Overall, 44.9% of patients were women and the mean age was 56.7 years. At baseline, 184 (11.1%) patients had thrombocytopenia. Patients with thrombocytopenia were more frequently men and elderly. Platelet count showed an age-dependent decline in men but not in women. We found an increased risk of death in patients with age ≥ 65 years, with a low anticoagulation quality, concomitant arterial hypertension, heart failure, a higher INR range, or with thrombocytopenia (OR 1.739, 95%CI 1.048-2.886, p = .032). At multivariable logistic regression, patients with age ≥65 years, concomitant AF and thrombocytopenia (OR 1.907, 95%CI 1.219-2.983, p = .005) had an increased risk of MBs. In MPHV patients, thrombocytopenia is associated with an increased risk of death and MB. There is a growing need for a sex- and age-specific threshold to define platelet count in adult patients.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39691754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Akt pathway activation reduces platelet apoptosis and contributes to the increase of platelet counts in solid tumor patients.","authors":"Huan Tian,&nbsp;Songyin Huang,&nbsp;Qing Luo,&nbsp;Zhuochen Lin,&nbsp;Huanhuan Liu,&nbsp;Zhixian Zhang,&nbsp;Wengcheng Fong,&nbsp;Jinghua Zhao,&nbsp;Fengyan Yu","doi":"10.1080/09537104.2022.2026908","DOIUrl":"https://doi.org/10.1080/09537104.2022.2026908","url":null,"abstract":"<p><p>Platelets counts increase in various cancer patients, which is associated with poor prognosis. However, the cause of high platelet counts in cancer patients is still not fully understood. Here we demonstrated that compared with healthy controls, there were significant differences in platelet parameters, mean platelet volume (MPV), platelet distribution width (PDW), platelet larger cell ratio (P-LCR), and platelet crit (PCT), reflecting platelet volume in breast cancer patients by clinical retrospective analysis. The mitochondrial transmembrane potential (ΔΨm) depolarization and phosphatidylserine (PS) externalization declined, accompanied by reduced expression of pro-apoptotic factors Bak, Bax and apoptotic executor caspase-3, and elevated of anti-apoptotic factor Bcl-xl in various cancer patients' platelets. Notably, the phosphorylation level of Akt and its downstream target Bad increased in platelets from cancer patients. MK2206, the inhibitor of Akt, reduced the phosphorylation level of Akt and Bad, and induced apoptosis of platelets. When platelets from healthy controls cocultured with the cultural supernatant of cancer cells, the phosphorylation level of Akt and Bad in the platelets was elevated and the cultural supernatant of cancer cells could rescue the apoptosis of platelet induced by MK2206. Therefore, in our study the apoptosis of platelets in cancer patients was declined, which exerted an influence on the rise of platelet counts in breast cancer patients. The cross-talking between tumor and platelets could affect platelet apoptosis by regulating Akt signaling pathway in platelets.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39962560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does hsa-miR-223-3p from platelet-derived extracellular vesicles regulate tissue factor expression in monocytic cells?","authors":"Mary E W Collier,&nbsp;Ashley R Ambrose,&nbsp;Alison H Goodall","doi":"10.1080/09537104.2022.2027903","DOIUrl":"https://doi.org/10.1080/09537104.2022.2027903","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) released from activated platelets contain microRNAs, the most abundant of which is hsa-miR-223-3p. Endogenous hsa-miR-223-3p suppresses the expression of tissue factor (TF), the initiator of the extrinsic coagulation pathway, in endothelial cells. Monocytes can be induced to express TF to enhance coagulation, but the role of hsa-miR-223-3p in regulating monocyte TF remains unknown. This study examined whether hsa-miR-223-3p from platelet-derived EVs (pdEVs) affects TF expression in monocytes. THP-1 cells, differentiated into a monocyte-like phenotype with 1α,25-dihydroxyvitaminD3, were transfected with hsa-miR-223-3p mimic or control microRNA. Alternatively, THP-1 cells were incubated with pdEVs from PAR1-agonist peptide activated-platelets, as platelet releasate, or pdEVs isolated by ultracentrifugation. Transfection with hsa-miR-223-3p mimic resulted in significant reductions in TF protein, determined by western blotting and flow cytometry and reduced procoagulant activity, measured by a TF-specific factor Xa generation assay, compared to cells transfected with control microRNA. This reduction was reversed by co-transfection with hsa-miR-223-3p inhibitor, AntagomiR-223. Incubation of THP-1 cells with pdEVs also decreased TF expression; however, this was not reversed by AntagomiR-223. Taken together, monocyte TF expression is downregulated by hsa-miR-223-3p, but when transferred via pdEVs the effect was not reversed with Antagomir-223, suggesting other pdEV components may contribute to TF regulation.<b>Abbreviations:</b> Tissue factor (TF), Factor VII (FVII), activated Factor VII (FVIIa), Factor X (FX), activated Factor X (FXa), extracellular vesicles (EVs), microvesicles (MVs), platelet-derived extracellular vesicles (pdEVs), protease-activated receptor 1 agonist peptide (PAR1-AP), lipopolysaccharide (LPS), P-selectin glycoprotein ligand-1 (PSGL-1), Tris-Buffered Saline Tween (TBST), room temperature (RT)[Figure: see text].</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39775077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TSST-1 protein exerts indirect effect on platelet activation and apoptosis.","authors":"Min Guo,&nbsp;Tiantian Yi,&nbsp;Qian Wang,&nbsp;Daqing Wang,&nbsp;Ping Feng,&nbsp;Dai Kesheng,&nbsp;He Chunyan","doi":"10.1080/09537104.2022.2026907","DOIUrl":"https://doi.org/10.1080/09537104.2022.2026907","url":null,"abstract":"<p><p>Thrombocytopenia or platelet dysfunction is a risk factor for severe infection. <i>Staphylococcus aureus</i> (<i>S. aureus</i>) releases a variety of virulence factors especially toxic shock syndrome toxin 1 (TSST-1), which may cause toxic shock syndrome. <i>S. aureus</i>, when carrying the <i>tst</i> gene, is more prone to cause toxic shock syndrome and is responsible for an especially high rate of mortality. However, the effect of TSST-1 protein on platelets is unknown. Patients with the <i>tst</i> gene positive <i>S. aureus</i> bacteremia showed more serious infection, higher mortality and lower platelet count. The <i>tst</i> gene positive <i>S. aureus</i> strains induce more platelet apoptosis and activation and corresponding up-regulation of Bak and down-regulation of Bcl-XL in addition to the activation of Caspase-3. C57BL/6 mice infected with the <i>tst</i> gene positive strains resulted in both a decrease in platelet count and an increase in platelet apoptosis and/or activation events and mortality. Moreover, TSST-1 protein, encoded by <i>tst</i> gene, caused the decrease of platelet count, the increase of platelet apoptosis and activation events and the level of inflammatory cytokines <i>in vivo</i>. However, TSST-1 protein was unable to induce traditional activation and apoptosis on human platelets <i>in vitro</i>. These results suggested that TSST-1 protein may exert indirect effects on platelet activation and apoptosis <i>in vivo</i>.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39856558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances on GPIb-IX-V complex.","authors":"Renhao Li","doi":"10.1080/09537104.2022.2075146","DOIUrl":"https://doi.org/10.1080/09537104.2022.2075146","url":null,"abstract":"An abundant receptor complex exclusively expressed on the surface of platelets and megakaryocytes, glycoprotein (GP)Ib-IX-V complex plays a major role in hemostasis and thrombosis. Its importance is corroborated by the bleeding symptoms in patients with congenital defects in this complex [1]. GPIbα, the main subunit in this receptor complex, contains the binding domain for plasma protein von Willebrand factor (VWF) and thrombin [2–4]. Recent studies, utilizing genetically altered animal models as well as new cutting-edge biomechanical, molecular, and cellular techniques, produced exciting insights on the inner workings of this receptor complex and expanded its involvement into platelet clearance, cancer metastasis, and inflammatory complications. Some studies have also identified potential new ligands of GPIbα, such as the SARS-CoV-2 spike protein [5], although the underlying mechanisms await verification and further elucidation [6]. Thus, it is appropriate time to review recent advances on GPIb-IX -V and related pathways. Dr Jerry Ware led the development of the first genetically altered murine model for GPIbα, which validates the applicability of mice to study GPIb-IX-V and to model related diseases [7]. In his review, Dr Ware describes various knockout and transgenic murine models that alter either receptor expression or an aspect of GPIb-IX functions. Their characterization has firmly established critical involvement of GPIb-IX in platelet generation, activation, and clearance and also generated valuable insights on the underlying mechanisms. Critical features associated with each murine model, along with important caveats, are noted and compared, which would be important in data interpretation as these animal models are increasingly applied to assess the involvement of GPIb-IX in a variety of physiological or pathophysiological processes. Dr Edward Quach is a young investigator who reported key evidence for the defining mechanical feature of GPIb-IX activation [8]. His review focuses on recent exciting advances in understanding how GPIb-IX activation critically drives platelet clearance in several common thrombocytopenic conditions. A common feature in the form of a conformational change in GPIb-IX appears in these disease settings, which may be potentially applicable to other more complications involving thrombocytopenia. Dr Xiaoping Du first demonstrated the association of GPIX with GPIbα and GPIbβ to form a highly integrated GPIb-IX complex [9]. Here, he and his coworkers review the intracellular signaling events that are induced by GPIb-IX ligands and lead up to the activation of integrin αIIbβ3 in platelets. Intracellular molecules associated with cytoplasmic domains of GPIb-IX, such as 14-3-3ζ and filamin, are required for these signaling pathways. Additional downstream kinases and related molecules, connecting extensively with other signaling pathways, are also delineated. Finally, although GPV is associated with GPIb-IX and highly ex","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9378636/pdf/nihms-1812396.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10023382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Successful treatment of acquired amegakaryocytic thrombocytopenia with eltrombopag and immunosuppressant.","authors":"Hong Tian,&nbsp;Danqing Kong,&nbsp;Yun Li,&nbsp;Chengyuan Gu,&nbsp;Ziqiang Yu,&nbsp;Zhaoyue Wang,&nbsp;Depei Wu,&nbsp;Jie Yin","doi":"10.1080/09537104.2021.2012140","DOIUrl":"https://doi.org/10.1080/09537104.2021.2012140","url":null,"abstract":"<p><p>Acquired amegakaryocytic thrombocypenia (AAMT) is an extremely rare hematologic disorder and standard treatment strategy has not been established. We described herein two cases of AAMT who were fully responded to eltrombopag and immunosuppressant. Patient 1 was refractory to steroid, IVIG and recombinant human thrombopoietin (rhTPO). Patient 2 did not respond to high dosage of steroid, IVIG, rhTPO and rituximab. Moreover, his AAMT progressed to aplastic anemia in 5 months. Both patients took eltrombopag and immunosuppressant, then they achieved long-term remission without obvious side effects. Our findings suggest that this combination can be a valuable alternative in AAMT.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39820280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}