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Huffman T, Gleaves E, Lenoir G, Rafeedheen R. Delayed-onset eptifibatide-induced thrombocytopenia. Am J Health Syst Pharm 2024; 81:106-111. [PMID: 37884759 DOI: 10.1093/ajhp/zxad271] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/24/2023] [Indexed: 10/28/2023] Open
Abstract
PURPOSE We present a unique case of delayed-onset, profound eptifibatide-induced thrombocytopenia that occurred 5 days after initiation of the drug. SUMMARY Eptifibatide is a platelet glycoprotein IIb/IIIa receptor inhibitor with indications for use in patients with acute coronary syndromes. Eptifibatide-induced thrombocytopenia is uncommon but well studied and typically occurs within 24 hours of initiation of the drug. In the case described here, a 62-year-old male with a past history of coronary artery disease (including percutaneous coronary intervention within the past 12 months) was started on eptifibatide at a dosage of 2 µg/kg per minute for management of significant thrombus burden prior to a planned cardiac revascularization procedure; heparin for anticoagulation was also initiated. About 5 days after initiation of eptifibatide, the patient developed severe thrombocytopenia, with the platelet count dropping precipitously from 249 × 103/µL on admission to less than 1 × 103/µL. After eptifibatide and heparin therapy were discontinued and the patient was switched to argatroban, the platelet count recovered to 38 × 103/µL over the next 2 days. An eptifibatide platelet antibody assay was positive for IgG-mediated reactions consistent with eptifibatide-induced thrombocytopenia. Scoring of this case with the Naranjo scale yielded a score of 4, suggesting a possible adverse reaction to eptifibatide. CONCLUSION This is the first published case report of profound eptifibatide-induced thrombocytopenia occurring more than 24 hours after eptifibatide initiation and serves to bring awareness that a delayed reaction can occur.
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Affiliation(s)
- Travis Huffman
- University of Kentucky-Bowling Green Campus, Bowling Green, KY, and The Medical Center, Bowling Green, KY, USA
| | - Evan Gleaves
- University of Kentucky-Bowling Green Campus, Bowling Green, KY, and The Medical Center, Bowling Green, KY, USA
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Rikken SAOF, van 't Hof AWJ, ten Berg JM, Kereiakes DJ, Coller BS. Critical Analysis of Thrombocytopenia Associated With Glycoprotein IIb/IIIa Inhibitors and Potential Role of Zalunfiban, a Novel Small Molecule Glycoprotein Inhibitor, in Understanding the Mechanism(s). J Am Heart Assoc 2023; 12:e031855. [PMID: 38063187 PMCID: PMC10863773 DOI: 10.1161/jaha.123.031855] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/20/2023]
Abstract
Thrombocytopenia is a rare but serious complication of the intravenous glycoprotein IIb/IIIa (GPIIb/IIIa; integrin αIIbβ3) receptor inhibitors (GPIs), abciximab, eptifibatide, and tirofiban. The thrombocytopenia ranges from mild (50 000-100 000 platelets/μL), to severe (20 000 to <50 000/μL), to profound (<20 000/μL). Profound thrombocytopenia appears to occur in <1% of patients receiving their first course of therapy. Thrombocytopenia can be either acute (<24 hours) or delayed (up to ~14 days). Both hemorrhagic and thrombotic complications have been reported in association with thrombocytopenia. Diagnosis requires exclusion of pseudothrombocytopenia and heparin-induced thrombocytopenia. Therapy based on the severity of thrombocytopenia and symptoms may include drug withdrawals and treatment with steroids, intravenous IgG, and platelet transfusions. Abciximab-associated thrombocytopenia is most common and due to either preformed antibodies or antibodies induced in response to abciximab (delayed). Readministration of abciximab is associated with increased risk of thrombocytopenia. Evidence also supports an immune basis for thrombocytopenia associated with the 2 small molecule GPIs. The latter bind αIIbβ3 like the natural ligands and thus induce the receptor to undergo major conformational changes that potentially create neoepitopes. Thrombocytopenia associated with these drugs is also immune-mediated, with antibodies recognizing the αIIbβ3 receptor only in the presence of the drug. It is unclear whether the antibody binding depends on the conformational change and whether the drug contributes directly to the epitope. Zalunfiban, a second-generation subcutaneous small molecule GPI, does not induce the conformational changes; therefore, data from studies of zalunfiban will provide information on the contribution of the conformational changes to the development of GPI-associated thrombocytopenia.
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Affiliation(s)
- Sem A. O. F. Rikken
- Department of CardiologySt. Antonius HospitalNieuwegeinThe Netherlands
- Cardiovascular Research Institute Maastricht (CARIM)MaastrichtThe Netherlands
| | - Arnoud W. J. van 't Hof
- Cardiovascular Research Institute Maastricht (CARIM)MaastrichtThe Netherlands
- Department of CardiologyMUMC+MaastrichtThe Netherlands
- Department of CardiologyZuyderland Medical CentreHeerlenThe Netherlands
| | - Jurriën M. ten Berg
- Department of CardiologySt. Antonius HospitalNieuwegeinThe Netherlands
- Cardiovascular Research Institute Maastricht (CARIM)MaastrichtThe Netherlands
- Department of CardiologyMUMC+MaastrichtThe Netherlands
| | - Dean J. Kereiakes
- The Christ Hospital Heart and Vascular Institute and Lindner Clinical Research CenterCincinnatiOHUSA
| | - Barry S. Coller
- Allen and Frances Adler Laboratory of Blood and Vascular BiologyRockefeller UniversityNew YorkNYUSA
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Abstract
INTRODUCTION Platelets play a key role in arterial thrombosis and antiplatelet therapy is pivotal in the treatment of cardiovascular disease. Current antiplatelet drugs target different pathways of platelet activation and show specific pharmacodynamic and pharmacokinetic characteristics, implicating clinically relevant drug-drug interactions. AREAS COVERED This article reviews the role of platelets in hemostasis and cardiovascular thrombosis, and discusses the key pharmacodynamics, drug-drug interactions and reversal strategies of clinically used antiplatelet drugs. EXPERT OPINION Antiplatelet therapies target distinct pathways of platelet activation: thromboxane A2 synthesis, adenosine diphosphate-mediated signaling, integrin αIIbβ3 (GPIIb/IIIa), thrombin-mediated platelet activation via the PAR1 receptor and phosphodiesterases. Key clinical drug-drug interactions of antiplatelet agents involve acetylsalicylic acid - ibuprofen, clopidogrel - omeprazole, and morphine - oral P2Y12 inhibitors, all of which lead to an attenuated antiplatelet effect. Platelet function and genetic testing and the use of scores (ARC-HBR, PRECISE-DAPT, ESC ischemic risk definition) may contribute to a more tailored antiplatelet therapy. High on-treatment platelet reactivity presents a key problem in the acute management of ST-elevation myocardial infarction (STEMI). A treatment strategy involving early initiation of an intravenous antiplatelet agent may be able to bridge the gap of insufficient platelet inhibition in high ischemic risk patients with STEMI.
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Affiliation(s)
- Georg Gelbenegger
- Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
| | - Bernd Jilma
- Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
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Masood F, Hashmi S, Chaus A, Hertsberg A, Ehrenpreis ED. Complications and Management of Eptifibatide-Induced Thrombocytopenia. Ann Pharmacother 2021; 55:1467-1473. [PMID: 33813877 DOI: 10.1177/10600280211006645] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022] Open
Abstract
BACKGROUND Eptifibatide is used in acute coronary syndromes to reversibly block platelet aggregation by inhibiting the platelet glycoprotein IIb/IIIa receptor. A serious adverse effect of eptifibatide is a profound drop in platelet count, termed eptifibatide-induced thrombocytopenia (EIT). OBJECTIVE To provide insight into the types of complications and management of EIT. METHODS Cases of EIT submitted to the Food and Drug Administration adverse event reporting system were evaluated. Data analyses included management of EIT, complications of thrombocytopenia, initial platelets, and platelet nadir following eptifibatide. RESULTS 103 cases of EIT were reported from January 2010 to 2019; 57 cases met the Naranjo scale and were included. Only 37 of those cases contained information on how EIT was managed. Eptifibatide administration was withheld in all 37 of those cases. Platelet transfusions were administered in 20 cases (54%). Two cases were managed with steroids (5.4%), and 1 case used intravenous immunoglobulin G to reverse EIT (2%). The median initial platelet count prior to administration of eptifibatide was 207 000 cells/mm3 (SD = 69 000; n = 27), and median platelet nadir was 9000 cells/mm3 (SD = 19 000; n = 35) The majority of complications of EIT included bleeding events (16/28, 57%). Delayed procedures, prolonged stay, allergic reactions, and thrombosis were each reported in 3 patients (10.75%). CONCLUSION AND RELEVANCE Most cases of EIT were managed by withholding eptifibatide with platelet transfusion if necessary. The majority of complications included bleeding. However, significant procedure delays, prolonged hospital stay, thrombosis, and allergic reactions were also reported.
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Affiliation(s)
- Faisal Masood
- Advocate Lutheran General Hospital, Park Ridge, IL, USA
| | - Saad Hashmi
- Advocate Lutheran General Hospital, Park Ridge, IL, USA
| | - Adib Chaus
- Advocate Lutheran General Hospital, Park Ridge, IL, USA
| | | | - Eli D Ehrenpreis
- Advocate Lutheran General Hospital, Park Ridge, IL, USA
- Rosalind Franklin University, North Chicago, IL, USA
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5
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Abstract
Eptifibatide is a commonly and widely used drug for management of acute coronary syndrome and during percutaneous coronary intervention. It is usually well tolerated with no major adverse effects. We report a rare case of life-threatening thrombocytopenia secondary to eptifibatide along with a literature review of available evidence.
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6
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Serebruany VL, Sibbing D, DiNicolantonio JJ. Dyspnea and reversibility of antiplatelet agents: ticagrelor, elinogrel, cangrelor, and beyond. Cardiology 2013; 127:20-4. [PMID: 24192670 DOI: 10.1159/000354876] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/15/2013] [Accepted: 07/17/2013] [Indexed: 02/02/2023]
Abstract
CONTEXT Oral reversible platelet P2Y12 receptor inhibitors (ticagrelor and elinogrel) cause double-digit rates of dyspnea, while irreversible oral antiplatelet drugs (aspirin, ticlopidoine, clopidogrel, and prasugrel) or intravenous glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, or tirofiban) do not increase the incidence of dyspnea in randomized trials. Dyspnea after oral reversible antiplatelet agents remains unexplained. A transfusion-related acute lung injury (TRALI) hypothesis has been proposed. The dyspnea risks after cangrelor, an intravenous reversible antiplatelet agent, are not well defined but may offer a universal mechanism linking TRALI, dyspnea, and reversible platelet inhibition. OBJECTIVE We analyzed safety data from recent head-to-head randomized trials with reversible antiplatelet agents (ticagrelor, elinogrel, and cangrelor) compared to irreversible (clopidogrel/placebo) comparators. RESULTS All three reversible antiplatelet agents cause excess dyspnea. In contrast to the high double-digit rates after oral ticagrelor or elinogrel, the dyspnea risks after intravenous cangrelor were smaller (<2%) but still consistently and significantly higher than in the corresponding control arms. CONCLUSIONS The clinical utility of reversible antiplatelet strategies has been challenged. Despite a potential advantage of fewer bleeding events during heart surgery, reversible antiplatelet agents carry the risk of potential autoimmune reactions manifesting as dyspnea. Repeated binding and unbinding cycles, impaired platelet turnover, and lung sequestration or apoptosis of overloaded destructive platelets are among the potential mechanism(s) responsible for dyspnea after reversible antiplatelet agents.
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Affiliation(s)
- Victor L Serebruany
- HeartDrug™ Research Laboratories, Johns Hopkins University, Towson, Md., USA
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Chong BH, Choi PYI, Khachigian L, Perdomo J. Drug-induced immune thrombocytopenia. Hematol Oncol Clin North Am 2013; 27:521-40. [PMID: 23714310 DOI: 10.1016/j.hoc.2013.02.003] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
Thrombocytopenia is caused by immune reactions elicited by diverse drugs in clinical practice. The activity of the drug-dependent antibodies produces a marked decrease in blood platelets and a risk of serious bleeding. Understanding of the cellular mechanisms that drive drug-induced thrombocytopenia has advanced recently but there is still a need for improved laboratory tests and treatment options. This article provides an overview of the different types of drug-induced thrombocytopenia, discusses potential pathologic mechanisms, and considers diagnostic methods and treatment options.
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Affiliation(s)
- Beng H Chong
- Haematology Department, St George Hospital, Kogarah, NSW 2217, Australia.
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Antibodies causing thrombocytopenia in patients treated with RGD-mimetic platelet inhibitors recognize ligand-specific conformers of αIIb/β3 integrin. Blood 2012; 119:6317-25. [PMID: 22490676 DOI: 10.1182/blood-2012-01-406322] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
Arginine-glycine-aspartic acid (RGD)-mimetic platelet inhibitors act by occupying the RGD recognition site of α(IIb)/β(3) integrin (GPIIb/IIIa), thereby preventing the activated integrin from reacting with fibrinogen. Thrombocytopenia is a well-known side effect of treatment with this class of drugs and is caused by Abs, often naturally occurring, that recognize α(IIb)/β(3) in a complex with the drug being administered. RGD peptide and RGD-mimetic drugs are known to induce epitopes (ligand-induced binding sites [LIBS]) in α(IIb)/β(3) that are recognized by certain mAbs. It has been speculated, but not shown experimentally, that Abs from patients who develop thrombocytopenia when treated with an RGD-mimetic inhibitor similarly recognize LIBS determinants. We addressed this question by comparing the reactions of patient Abs and LIBS-specific mAbs against α(IIb)/β(3) in a complex with RGD and RGD-mimetic drugs, and by examining the ability of selected non-LIBS mAbs to block binding of patient Abs to the liganded integrin. Findings made provide evidence that the patient Abs recognize subtle, drug-induced structural changes in the integrin head region that are clustered about the RGD recognition site. The target epitopes differ from classic LIBS determinants, however, both in their location and by virtue of being largely drug-specific.
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Garbe E, Andersohn F, Bronder E, Salama A, Klimpel A, Thomae M, Schrezenmeier H, Hildebrandt M, Späth-Schwalbe E, Grüneisen A, Meyer O, Kurtal H. Drug-induced immune thrombocytopaenia: results from the Berlin Case–Control Surveillance Study. Eur J Clin Pharmacol 2011; 68:821-32. [DOI: 10.1007/s00228-011-1184-3] [Citation(s) in RCA: 40] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/10/2011] [Accepted: 11/22/2011] [Indexed: 10/14/2022]
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Abstract
BACKGROUND Thrombocytopenia following percutaneous coronary intervention (PCI) is an underappreciated condition that is often clinically challenging. There are no guidelines on the management of patients with this condition. OBJECTIVE To review recent data in etiologies, risk factors, prevention, management, and prognostic implications of thrombocytopenia following PCI. EVIDENCE ACQUISITION Search of MEDLINE, EMBASE, the Cochrane Database, and Google Scholar using the term thrombocytopenia + PCI and other relevant keywords to identify systematic reviews, clinical trials, cohort studies, case series, and case reports. The review was limited to English-language articles published between January 1980 and June 2009. Articles on patients with baseline thrombocytopenia prior to PCI were excluded. EVIDENCE SYNTHESIS Thrombocytopenia is not infrequent following PCI. The typical patient with post-PCI thrombocytopenia is on multiple therapies that can potentially cause a decrease in the platelet count. Identification of the cause is critical because management of the condition varies significantly based on the etiology. The severity of the thrombocytopenia also determines the clinical management of the patient. Several observational studies have demonstrated the adverse prognostic impact of the complication on clinical outcomes and have identified risk factors. CONCLUSIONS Judicious use of therapies that can cause thrombocytopenia, efficient detection of the cause of the decrease in platelet count, and appropriate management of the condition can potentially improve the quality of care and outcomes following PCI. Further research into risk factors that predispose post-PCI patients to developing thrombocytopenia is warranted.
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Affiliation(s)
- Chetan Shenoy
- Guthrie Clinic, One Guthrie Square, Sayre, Pennsylvania, USA
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11
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Russell KN, Schnabel JG, Rochetto RP, Tanner MC. Acute Profound Thrombocytopenia Associated with Readministration of Eptifibatide: Case Report and Review of the Literature. Pharmacotherapy 2009; 29:867-74. [DOI: 10.1592/phco.29.7.867] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
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12
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Megakaryocyte impairment by eptifibatide-induced antibodies causes prolonged thrombocytopenia. Blood 2009; 114:1250-3. [PMID: 19429867 DOI: 10.1182/blood-2009-02-203034] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
Abstract
Glycoprotein (GP) IIbIIIa inhibitors are used in the treatment of acute coronary syndromes. Transient immune-mediated acute thrombocytopenia is a recognized side effect of GPIIbIIIa inhibitors. We provide evidence that GPIIbIIIa inhibitor-induced antibodies can affect megakaryocytes in the presence of eptifibatide. In a patient with acute coronary syndrome, acute thrombocytopenia occurred after a second exposure to eptifibatide 20 days after the initial treatment. Despite the short half-life of eptifibatide (t(1/2) = 2 hours), thrombocytopenia less than 5 x 10(9)/L and gastrointestinal and skin hemorrhage persisted for 4 days. Glycoprotein-specific enzyme-linked immunosorbent assay showed eptifibatide-dependent, GPIIbIIIa-specific antibodies. Bone marrow examination showed predominance of early megakaryocyte stages, and platelet transfusion resulted in an abrupt platelet count increase. Viability of cultured cord blood-derived megakaryocytes was reduced in the presence of eptifibatide and patient IgG fraction. These findings can be explained by impaired megakaryocytopoiesis complicating anti-GPIIbIIIa antibody-mediated immune thrombocytopenia. This mechanism may also apply to some patients with autoimmune thrombocytopenia.
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14
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Abstract
Recent randomised studies suggest that experimental oral reversible platelet P2Y12 receptor inhibitor, AZD6140, causes dyspnoea. This also raises similar concerns about the parent compound, and another adenosine triphosphate (ATP) analogue (AR-69931MX or cangrelor), which is currently in Phase 3 trial in patients undergoing coronary interventions. We analysed package inserts, and available clinical trials safety data for antiplatelet agents with regard to the incidence of dyspnoea. We found that dyspnoea is a very rare complication of the presently approved platelet inhibitors, mostly caused by underlying disease, rather than antiplatelet therapy per se. The main reasons for respiratory distress after oral (AZD6140), and intravenous (cangrelor) agents may be the development of mild asymptomatic thrombotic thrombocytopenic purpura, fluid retention and dyspnoea because of the reversible nature of these drugs. Also, these agents are ATP analogues, which rapidly metabolise to adenosine, a well-known bronchoprovocator causing dyspnoea as well. In summary, dyspnoea is seldom considered, there are no treatment algorithms when it does occur, plausible mechanisms exist and despite these plausible mechanisms, the true cause of dyspnoea in these exposed individuals is unknown. Additional pulmonary function testing, immunological investigations and platelet receptor studies are urgently needed to determine the cause of dyspnoea after AZD6140, and to point out how such serious adverse reactions can be prevented, or at least minimised, raising potential concerns about this drug.
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Affiliation(s)
- V L Serebruany
- HeartDrug Research Laboratories, Johns Hopkins University, Towson, MD, USA.
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15
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Lee CM, Leung TK, Wang HJ, Lee WH, Shen LK, Liu JD, Chang CC, Chen YY. Evaluation of the effect of partial splenic embolization on platelet values for liver cirrhosis patients with thrombocytopenia. World J Gastroenterol 2007; 13:619-22. [PMID: 17278231 PMCID: PMC4065987 DOI: 10.3748/wjg.v13.i4.619] [Citation(s) in RCA: 46] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the effect of partial splenic embolization (PSE) on platelet values in liver cirrhosis patients with thrombocytopenia and to determine the effective embolization area for platelet values improvement.
METHODS: Blood parameters and liver function indicators were measured on 10 liver cirrhosis patients (6 in Child-Pugh grade A and 4 in grade B) with thrombocytopenia (platelet values < 80 × 103/μL) before embolization. Computed tomography scan was also needed in advance to acquire the splenic baseline. After 2 to 3 d, angiography and splenic embolization were performed. A second computed tomography scan was made to confirm the embolization area after 2 to 3 wk of embolization. The blood parameters of patients were also examined biweekly during the 1 year follow-up period.
RESULTS: According to the computed tomography images after partial splenic embolization, we divided all patients into two groups: low (< 30%), and high (≥ 30%) embolization area groups. The platelet values were increased by 3 times compared to baseline levels after 2 wk of embolization in high embolization area group. In addition, there were significant differences in platelet values between low and high embolization area groups. GPT values decreased significantly in all patients after 2 wk of embolization. The improvement in platelet and GPT values still persisted until 1 year after PSE. In addition, 3 of 4 (75%) Child-Pugh grade B patients progressed to grade A after 2 mo of PSE. The complication rate in < 30% and ≥ 30% embolization area groups was 50% and 100%, respectively.
CONCLUSION: Partial splenic embolization is an effective method to improve platelet values and GPT values in liver cirrhosis patients with thrombocytopenia and the ≥ 30% embolization area is meaningful for platelet values improvement. The relationship between the complication rate and embolization area needs further studies.
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Affiliation(s)
- Chi-Ming Lee
- Department of Diagnostic Radiology, Taipei Medical University Hospital, 110, Taipei, Taiwan, China
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Said SM, Hahn J, Schleyer E, Müller M, Fiedler GM, Buerke M, Prondzinsky R. Glycoprotein IIb/IIIa inhibitor-induced thrombocytopenia. Clin Res Cardiol 2006; 96:61-9. [PMID: 17146606 DOI: 10.1007/s00392-006-0459-7] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/16/2005] [Accepted: 09/27/2006] [Indexed: 10/23/2022]
Abstract
Thrombocyte glycoprotein IIb/IIIa inhibitors prevent fibrinogen binding and thereby thrombocyte aggregation. The inhibition of thrombocyte activation at the damaged coronary plaque is the target of the new therapeutic strategies in treating acute coronary syndrome. This reduces the ischemic complications associated with the non-STelevation myocardial infarction (NSTEMI) and percutaneous coronary intervention (PCI). Thrombocytopenia is a known complication of glycoprotein (GP) IIb/IIIa inhibitors. Although, in general, GP IIb/IIIa inhibitor-induced thrombocytopenia is a harmless side effect which responds readily to thrombocyte transfusion, it can occasionally be a very serious complication associated with serious bleeding. In addition patients developing thrombocytopenia have unfavorable outcome (e.g., death, myocardial infarction, bypass surgery or additional PCI) in comparison to patients without thrombocytopenia. Advanced age (> 65 years), low BMI and a low initial thrombocyte count (<180,000/microl) are independent risk factors of thrombocytopenia. The risk of bleeding is higher with this form of thrombocytopenia not only due to the low thrombocyte count but also to the impaired function of the remaining thrombocytes. It is important to closely monitor platelet count during GP IIb/IIIa antagonist treatment. Platelet count monitoring two, six, twelve and 24 hour after starting the treatment reveals most cases of acute thrombocytopenia. Side effects can be avoided by the early discontinuation of the GP IIb/IIIa antagonist treatment. This article reviews the diagnosis and treatment of glycoprotein IIb/IIIa inhibitor-induced thrombocytopenia and summarizes the differential diagnosis from heparin-induced thrombocytopenia and laboratory-related pseudothrombocytopenia.
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Affiliation(s)
- S M Said
- Carl-von-Basedow-Klinikum Merseburg, Medizinische Klinik I, Germany.
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Epelman S, Nair D, Downey R, Militello M, Askari AT. Eptifibatide-induced thrombocytopenia and thrombosis. J Thromb Thrombolysis 2006; 22:151-4. [PMID: 17008982 DOI: 10.1007/s11239-006-8785-1] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/24/2022]
Abstract
Glycoprotein (GP) IIb/IIIa inhibitors have been shown to reduce morbidity and mortality in patients with acute coronary syndromes undergoing percutaneous coronary interventions (PCI). With their widespread use, there is a growing body of literature describing adverse outcomes, including severe thrombocytopenia. Here we report a case of a 75-year-old man who presented with an ST-elevation myocardial infarction, underwent primary PCI and stenting, and subsequently developed profound thrombocytopenia and thrombosis after eptifibatide administration. This report adds to the literature regarding eptifibatide-induced thrombocytopenia and also raises the possibility of a new syndrome of eptifibatide-induced thrombosis. A case is made to examine available databases for thrombosis after administration of eptifibatide and other GPIIb/IIIa inhibitors.
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Affiliation(s)
- Slava Epelman
- Division of Internal Medicine, The Cleveland Clinic, USA
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19
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Chevoya L. Anticoagulant and antiplatelet medications. Crit Care Nurse 2006. [DOI: 10.4037/ccn2006.26.3.19] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/01/2022]
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Aster RH, Curtis BR, Bougie DW, Dunkley S, Greinacher A, Warkentin TE, Chong BH. Thrombocytopenia associated with the use of GPIIb/IIIa inhibitors: position paper of the ISTH working group on thrombocytopenia and GPIIb/IIIa inhibitors. J Thromb Haemost 2006; 4:678-9. [PMID: 16460451 DOI: 10.1111/j.1538-7836.2006.01829.x] [Citation(s) in RCA: 51] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
Affiliation(s)
- R H Aster
- Blood Research Institute, Blood Center of Wisconsin, Milwaukee, WI 53201-2178, USA.
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Cheema AA, Teklinski AH, Maria V, Chilukuri K, Frank JJ, Gosselin MO. Recurrent Acute Profound Thrombocytopenia Related to Readministration of Eptifibatide. J Interv Cardiol 2006; 19:99-103. [PMID: 16483348 DOI: 10.1111/j.1540-8183.2006.00112.x] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/22/2023] Open
Abstract
We describe the case of an 86-year-old woman who presented with unstable angina. She was given heparin and eptifibatide, and she underwent percutaneous coronary intervention (PCI). Shortly thereafter, she developed acute profound thrombocytopenia (6,000 platelets/mm3), which resolved after the discontinuation of heparin and eptifibatide. Four months later, she presented again with unstable angina and underwent PCI. Soon after the procedure, she again developed acute profound thrombocytopenia (2,000 platelets/mm3). To our knowledge, acute profound thrombocytopenia due to eptifibatide treatment in the same patient at two different times has not been reported before.
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Affiliation(s)
- Aamir Adnan Cheema
- Department of Internal Medicine, Division of Cardiology, St. John Hospital and Medical Center, Detroit, MI 48236, USA.
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Current awareness: Pharmacoepidemiology and drug safety. Pharmacoepidemiol Drug Saf 2005. [DOI: 10.1002/pds.1030] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/10/2022]
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