Platelets最新文献

{"title":"Branched endovascular aortic aneurysm repair decreases platelet reactivity and platelet-rich thrombus formation - a prospective, cohort study.","authors":"Aleksandra Gąsecka, Ewelina Błażejowska, Agata Konieczka, Mateusz Leśniewski, Magdalena Ostaszewska, Michał Łomiak, Magdalena Gajewska, Sylwester Rogula, Łukasz Szarpak, Krzysztof J Filipiak, Mateusz Zawadka, Katarzyna Jama, Paweł Andruszkiewicz, Marcin Grabowski, Tomasz Jakimowicz","doi":"10.1080/09537104.2025.2458622","DOIUrl":"https://doi.org/10.1080/09537104.2025.2458622","url":null,"abstract":"<p><p>Appropriate platelet function determines both the perioperative haemostasis and the risk of postoperative thrombotic complications in patients undergoing branched endovascular repair (bEVAR) of thoracoabdominal aortic aneurysm (TAAA). We aimed to assess the effect of bEVAR on platelet function and the predictive value of preoperative platelet function for postoperative bleeding. We measured platelet function using impedance aggregometry and total thrombus-formation analysis system in 50 consecutive patients, with TAAA undergoing elective bEVAR. After bEVAR, platelet reactivity was assessed using ASPI test, ADP test and TRAP test and thrombus size decreased, whereas time to clot formation increased, compared to baseline (<i>p</i> ≤ .042 for all). Preoperative platelet reactivity in the TRAP test was lower in patients who experienced post-operative bleeding, defined as ≥3 red blood cell units transfusion, compared to those who did not (<i>p</i> = .038). Baseline hemoglobin level <13 g/dl and TRAP test result ≤29.5 AUC increased the odds of bleeding by 5.4-fold and 6.8-fold, respectively, independent of other clinical variables. We conclude that in patients with TAAA undergoing bEVAR, platelet reactivity and platelet-rich thrombus formation decreased directly after the operation. Preoperative hemoglobin level and platelet reactivity in the TRAP test were independent predictors of postoperative bleeding complications.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2458622"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383222","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":"Association of thromboxane generation with the bleeding events in aspirin users.","authors":"Yawen Liu, Yijie Liu, Feiqing Liang, Lu Lin, Zhipeng Xie, Jinxia Mai, Zhuoyi Wu, Min Huang, Shilong Zhong","doi":"10.1080/09537104.2025.2473953","DOIUrl":"https://doi.org/10.1080/09537104.2025.2473953","url":null,"abstract":"<p><p>Coronary artery disease is among the leading causes of morbidity and mortality worldwide, posing a significant threat to human health and life. Aspirin is widely used in the treatment of coronary artery disease, however, long-term use may increase the risk of bleeding. Urinary 11-dehydro-TXB2, a biomarker indicative of platelet activation, has been associated with thrombotic events, but its association with bleeding events remains unexplored. This study aimed to assess the predictive value of TXB2-M levels for bleeding events in patients with coronary artery disease undergoing aspirin therapy. Multifactorial logistic regression analysis was employed to evaluate the potential of TXB2-M levels as a reliable marker for bleeding risk following aspirin use. Among patients with coronary artery disease treated with aspirin, those with lower TXB2-M levels exhibited an increased risk of bleeding events within three years (Hazard Ratio: 0.46; 95% Confidence Interval: 0.26-0.79; <i>P</i> < 0.05). Additionally, variations in TXB2-M levels were observed across different demographic groups. This study reinforces the validity of TXB2-M levels as a biomarker for identifying patients at elevated risk of bleeding, thus facilitating the implementation of personalized treatment strategies to minimize bleeding risks while preserving the efficacy of antithrombotic therapy.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2473953"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670778","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":"Management of a twin pregnancy patient with Glanzmann thrombasthenia might be caused by a novel <i>ITGA2B</i> gene mutation (c.2822G>A): a case report and family investigation.","authors":"Xiangcheng Liao, Ruikai Zhu, Zhigang Yang, Aiqiu Qin, Yucong Huang, Ping Li, Liling Liu, Zhuning Mo","doi":"10.1080/09537104.2025.2470758","DOIUrl":"https://doi.org/10.1080/09537104.2025.2470758","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Mutations in the ITGA2B or ITGB3 gene that encodes for the αIIbβ3 platelet integrin usually cause Glanzmann thrombasthenia (GT). This study aims to investigate the clinical characteristics of a pedigree exhibiting an inherited hemorrhagic disorder resembling GT, elucidate its molecular pathogenesis and evaluate the efficacy of blood management strategies for a proband who is pregnant with twins. The clinical data of the pedigree with inherited hemorrhagic disorder were collected, including the assessment of clinical, laboratory and thromboelastography (TEG) profiles. DNA samples were obtained for next-generation sequencing, encompassing the exons and flanking sequences of the ITGA2B and ITGB3 genes, as well as other genes associated with blood and immune deficiency. Bioinformatics software tools, such as PolyPhen-2, SIFT and MutationTaster, were employed to analyze the functional impact of mutations. Protein structural models for the new mutation type were generated using PyMOL. The phenotype of the proband in this pedigree with inherited platelet dysfunction and bleeding disorder was in accordance with GT. The proband shows persistent blood accumulation in the uterine cavity. Laboratory findings indicate normal PLT morphology, PLT count, MPV, and PDW. However, there is a decreased PLT aggregation induced by agonists ADP, collagen, and AA while maintaining a normal response to ristocetin. The initial TEG examination results indicated that the patient presented with a hypocoagulable state, characterize d by a reduction in α angle (46.9), an extended K value (4.6) and a decreased maximum amplitude (35.1). The younger sister demonstrated comparable TEG performance to that of the proband and has a documented history of abnormal bleeding. A novel heterozygous mutation of &lt;i&gt;ITGA2B&lt;/i&gt; at position c.2822 G&gt;A (p.Trp941*) was identified in the proband and her familial counterparts-father, brother and sister. MutationTaster software predicted the new mutation to be pathogenic; however, PolyPhen-2 and SIFT software did not provide correlated predictions. The p.Trp941* mutation resulted in the premature termination of translation at residue 940Trp, leading to impaired protein function. Successful management was achieved during the perioperative period by administration of human immunoglobulin, platelets and antifibrinolytic drugs, followed by recombinant factor VIIa (rFVIIa), according to the thromboelastography tracings. The laboratory findings of the proband are consistent with GT, and a novel mutation in the ITGA2B gene at position c.2822 G&gt;A (p.Trp941*) has been identified as a potential cause of GT. However, since GT is a recessive disorder and both the proband and her family members are heterozygous, it cannot be excluded that they may possess additional bleeding risk factors, including the presence of other undetected variants. This study also illustrates the significance of multidisciplinary planning, TEG analysis and judicious utilization of ","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2470758"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692846","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":"From reticulated platelets to immature platelet fraction: structure, function, and clinical applications.","authors":"Yuxin Zhang, Ziyun Wang, Pan Zhou, Hongwei Zhang","doi":"10.1080/09537104.2025.2467383","DOIUrl":"https://doi.org/10.1080/09537104.2025.2467383","url":null,"abstract":"<p><p>In comparison to mature platelets, reticulated platelets (RPs) are newly released from the bone marrow and exhibit a larger size, higher reactivity, and a greater quantity of RNA, and can be an agile indicator of platelet turnover. The transcriptome associated with platelet function is significantly upregulated in RPs, which is a possible explanation for RPs intrinsic hyper-reactivity. We presented a comprehensive overview of the detection techniques for RPs. Current methods to quantify RPs in clinical routine are flow cytometry and fully automated hematology analyzers (Sysmex-XE/XN, Abbott, ADVIA, Mindray), which make the detection of RPs simpler, faster and more affordable. The proportion of RPs increased in the circulation has potential diagnostic and prognostic values in multiple clinical settings (risk stratification in cardiovascular diseases, the effect on antiplatelet drugs, differential diagnosis of thrombocytopenia, monitor platelet recovery after bone marrow or stem cell transplantation, and other diseases). There have been several studies focusing on RPs in recent years, particularly in cardiovascular disease and thrombocytopenia. In this review we summarizes the current study with regard to RPs and discuss their likely contribution in clinical routine.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2467383"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143543018","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":"Cardiometabolic risk factor burden associates with an immature platelet profile.","authors":"Carine E Hamo, Matthew Muller, Emily Rosenfeld, Yuhe Xia, Adedoyin Akinlonu, Elliot Luttrell-Williams, Tessa J Barrett, Jeffrey S Berger","doi":"10.1080/09537104.2025.2459800","DOIUrl":"10.1080/09537104.2025.2459800","url":null,"abstract":"<p><p>Cardiometabolic risk factors, obesity, diabetes and hyperlipidemia contribute to cardiovascular disease (CVD). While platelets are involved in CVD pathogenesis, the relationship between risk factor burden on platelet indices and the platelet transcriptome remains uncertain. Blood was collected from CVD-free adults, measuring platelet count, mean platelet volume (MPV), immature platelet fraction (IPF), and absolute immature platelet fraction (AIPF) by hemogram. Platelets were isolated and analyzed via RNA sequencing. Participants were stratified by number of cardiometabolic risk factors (diabetes, obesity, hyperlipidemia). We calculated median (IQR) values of platelet indices and p-for-trend via linear regression across risk factor burden. To evaluate the association between risk factor burden and platelet transcripts, we performed multivariable linear regression adjusting for age, sex, and race/ethnicity. Among 141 participants, (50.5 ± 14.8 years, 42% male, 26% Black) risk factor burden was associated with increasing platelet size, IPF, and AIPF but not platelet count. Platelet RNA sequencing identified 100 differentially expressed transcripts (<i>p</i> < .01; 66 upregulated, 34 downregulated). Gene ontology enrichment analysis demonstrated upregulated pathways of secondary metabolic processes (NES = 1.96, <i>p</i> < .01), and hematopoietic stem cell proliferation (NES = 1.95, <i>p</i> < .01). Greater cardiometabolic risk factor burden is associated with increased platelet size and immaturity and suggesting novel platelet-mediated mechanisms linking risk factor burden with CVD.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2459800"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067532","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":"Extracellular thiol isomerase ERp5 regulates integrin αIIbβ3 activation by inhibition of fibrinogen binding.","authors":"Kaifei Sun, Yaqiong Zhang, Aizhen Yang, Yuxin Zhang, Zhenzhen Zhao, Xiaofeng Yan, Yi Lu, Yue Han, Depei Wu, Freda Passam, Jingyu Zhang, Yi Wu","doi":"10.1080/09537104.2025.2455743","DOIUrl":"https://doi.org/10.1080/09537104.2025.2455743","url":null,"abstract":"<p><p>Recent studies have shown that anti-ERp5 antibodies inhibit platelet activation and thrombus formation; Moreover, ERp5-deficient platelets exhibit enhanced platelet reactivity via regulation of endoplasmic reticulum (ER) stress. In this study, we used a new ERp5-knockout mouse model as well as recombinant ERp5 (rERp5) protein, to examine the role of ERp5 in platelet function and thrombosis. Although platelet-specific ERp5-deficient mice had decreased platelet count, the mice had shortened tail-bleeding times and enhanced platelet accumulation in FeCl₃-induced mesenteric artery injury, compared with wild-type mice. Using platelet-specific ERp5-deficient mice, we found that ERp5 deficiency increased platelet aggregation, granule secretion, and integrin αIIbβ3 activation. Wild-type recombinant ERp5 protein (rERp5-wt) and inactive mutant ERp5 protein (rERp5-mut) both inhibited human platelet aggregation and the binding of fibrinogen to human platelets, indicating that ERp5 protein interferes with the interaction between integrin αIIbβ3 and its ligand fibrinogen, and its enzymatic activity is not required for this process. Consistently, wild-type mice injected with rERp5-wt or rERp5-mut protein had prolonged tail-bleeding times. Our results provide important evidence that platelet ERp5 negatively regulates platelet activation and thrombus formation, via steric hindrance interfering with integrin αIIbβ3 ligation.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2455743"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143067537","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":"Transcriptomic and functional characterization of megakaryocytic-derived platelet-like particles: impaired aggregation and prominent anti-tumor effects.","authors":"Kaitlin Garofano, Vera Mariani, Kameron Rashid, Sumanun Suwunnakorn, Alfateh Sidahmed, Anelia Horvath, Sanjay B Maggirwar, Travis J O'Brien, Minoli A Perera, Michael Whalen, Norman H Lee","doi":"10.1080/09537104.2024.2449344","DOIUrl":"10.1080/09537104.2024.2449344","url":null,"abstract":"<p><p>Platelet-like particles (PLPs), derived from megakaryocytic cell lines MEG-01 and K-562, are widely used as a surrogate to study platelet formation and function. We demonstrate by RNA-Seq that PLPs are transcriptionally distinct from platelets. Expression of key genes in signaling pathways promoting platelet activation/aggregation, such as the PI3K/AKT, protein kinase A, phospholipase C, and α-adrenergic and GP6 receptor pathways, was missing or under-expressed in PLPs. Functionally, PLPs do not aggregate following epinephrine, collagen, or ADP stimulation. While PLPs aggregated in response to thrombin, they did not display enhanced expression of surface markers P-selectin and activated α_2bβ₃, in contrast to platelets. We have previously demonstrated that platelets physically couple to MDA-PCa-2b and RC77T/E prostate cancer (PCa) cells via specific ligand-receptor interactions, leading to platelet-stimulated cell invasiveness and apoptotic resistance, and reciprocal cell-induced platelet aggregation. In contrast, PLP interactions with PCa cells inhibited both cell invasion and apoptotic resistance while failing to promote PLP aggregation. Moreover, PLPs reduced platelet-PCa cell interactions and antagonized platelet-stimulated oncogenic effects in PCa cells. RNA-Seq analysis identified candidate ligand-transmembrane protein combinations involved in anti-tumorigenic signaling of PLPs to PCa cells. Antibody neutralization of the TIMP3-MMP15 and VEGFB-FGFR1 signaling axes reversed PLP-mediated anti-invasion and apoptotic sensitization, respectively. In summary, PLPs lack many transcriptomic, molecular and functional features of platelets and possess novel anti-tumorigenic properties. These findings indicate that PLPs may have a potential therapeutic role in targeting and disrupting the oncogenic signaling between platelets and cancer cells, offering a new avenue for anti-cancer strategies.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2449344"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142984432","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":"Regulation of lipid metabolism: a new strategy for platelet storage.","authors":"Jieyun Shi, Wenting Wang, Jinmei Xu, Wen Yin","doi":"10.1080/09537104.2025.2465321","DOIUrl":"https://doi.org/10.1080/09537104.2025.2465321","url":null,"abstract":"<p><p>Transfusions of platelets are often used as prophylaxis in patients with hematologic malignancies and as treatment for active bleeding. However, platelets are in short supply due to the fact that they could only be kept for 5-7 days in vitro and they lose some of their functionality as a result of platelet storage lesions. To address this issue, refrigeration, cryopreservation and platelet additive solutions have been researched to determine their abilities to extend platelet storage duration. However, refrigerated platelets are quickly cleared after transfusion, while platelets in platelet additive solutions still present issues such as platelets quality and the risk of allergic reactions. Recent studies showed that changes in lipid metabolites during platelet storage and inadequate of fatty acid metabolism may also limit platelet shelf life and function. In this review, we address the principles of lipid metabolism during platelet storage and discuss the strategies for effective platelet storage systems. The findings of this review highlight the role of lipid metabolism during platelet storage, providing insights into future research focused on extending the preservation period and function of platelet.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2465321"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414952","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":"Effect of aspirin dosage on oxidative stress and platelet reactivity in patients undergoing coronary artery bypass grafting (APRICOT): randomized controlled trial.","authors":"Aleksandra Gąsecka, Rafał Kaczorowski, Katarzyna Pomykała, Tomasz Kucharski, Magdalena Gajewska, Dominika Siwik, Katarzyna Karoń, Maciej Małyszko, Jaromir Hunia, Jakub Michal Zimodro, Paweł Kowalczyk, Oliwia Zagrocka-Stendel, Małgorzata Dutkiewicz, Katarzyna Koziak, Ceren Eyileten, Marek Postuła, Mateusz Wondołkowski, Marcin Grabowski, Mariusz Kuśmierczyk, Radosław Wilimski","doi":"10.1080/09537104.2025.2457415","DOIUrl":"https://doi.org/10.1080/09537104.2025.2457415","url":null,"abstract":"<p><p>Coronary artery bypass grafting (CABG) triggers oxidative stress and platelet activation. High acetylsalicylic acid (ASA) dose might mitigate the transient proinflammatory state. We compared the effect of three ASA dosages on post-CABG platelet reactivity, oxidative stress, and serum CD39 and CD73 levels. Thirty-six consecutive patients undergoing elective off-pump CABG, pre-treated with ASA 1 × 75 mg for ≥7 days, were randomized to continue the prior treatment regimen, switch to ASA 1 × 150 mg, or ASA 2 × 75 mg. Blood was collected on admission, 7 days, 1 month, and 3 months after CABG. Platelet reactivity was assessed using impedance aggregometry. Platelet oxidative stress was measured as platelet mitochondria extracellular oxygen consumption rate and oxidatively damaged whole-blood DNA cleavage. Serum CD39 and CD73 levels were determined using ELISA. Platelet reactivity and oxidative stress parameters were comparable in all groups. Patients treated with ASA 2 × 75 mg had higher CD39 levels at 7 days and 1 month (<i>p</i> = .049, <i>p</i> = .033), compared to the control group. ASA 2 × 75 mg was associated a beneficial effect on serum CD39 levels after off-pump CABG, without a significant effect on oxidative stress parameters.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2457415"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143190154","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":"Immune-induced thrombocytopenia by pembrolizumab: case report and review of literature.","authors":"Nathan El-Ghazzi, Anna Monier, Antoine Italiano, Aude Besson, Eurydice Angeli","doi":"10.1080/09537104.2025.2487767","DOIUrl":"10.1080/09537104.2025.2487767","url":null,"abstract":"<p><p>Immune-checkpoint blockades (ICBs) are now used in early-stage diseases like triple-negative breast cancer (TNBC). While effective, they can cause severe toxicities. We report the first case of life-threatening immune thrombocytopenia (ITP) induced by pembrolizumab during neoadjuvant chemo-immunotherapy for early TNBC. A 42-year-old woman with early-stage TNBC developed grade 4 thrombocytopenia, diagnosed as ITP, after 107 days of pembrolizumab treatment. She required intensive care unit (ICU) admission and high-dose steroids, and intravenous immunoglobulin therapy, leading to a rapid recovery. ITP is a rare but potentially fatal complication of immunotherapy, with an incidence of less than 1% and a mortality rate of up to 20% in affected patients. Immediate recognition and steroid therapy are critical, as platelet transfusion is usually ineffective. Diagnosis is often delayed due to its similarity to chemotherapy-induced marrow toxicity. Immunotherapy-induced ITP generally contraindicates further use of the treatment. ITP, although uncommon, is a serious complication of immunotherapy requiring immediate intervention. The growing use of immunotherapy necessitates increased awareness of its potential toxicities among healthcare providers.</p>","PeriodicalId":20268,"journal":{"name":"Platelets","volume":"36 1","pages":"2487767"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773088","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}