ArticlePDF Available

Severe thrombocytopenia induced by tirofiban after percutaneous coronary intervention: a case report

Authors:

Abstract and Figures

Background Tirofiban is a nonpeptide glycoprotein IIb/IIIa receptor antagonist used widely in patients subjected to percutaneous coronary intervention. While the usage of tirofiban sets an important clinical benefit, severe thrombocytopenia can occur with use of this agent. Case presentation A 76-year-old Chinese man was admitted with 1-month history of sudden onset of chest tightness. He was diagnosed as having subacute inferior myocardial infarction, and percutaneous coronary intervention was performed. After the procedure, patient received tirofiban at 0.15 µg/kg/minute for 4 h. A blood sample was obtained for a complete blood count; severe thrombocytopenia was reported according to routine orders at our hospital. All antiplatelet drugs including tirofiban, aspirin, and clopidogrel were immediately discontinued. The patient received platelet transfusions and was treated with immunoglobulin G. Two days later, the patient’s platelet count had increased to 75 × 10 ⁹ /L. There was a significant improvement after day 5, and the platelet count was 112 × 10 ⁹ /L. Seven days after the acute thrombocytopenia, he was discharged with normal platelet count. Conclusions Clinicians should be particularly aware of tirofiban-induced thrombocytopenia in routine practice.
This content is subject to copyright. Terms and conditions apply.
Wangetal. Journal of Medical Case Reports (2023) 17:430
https://doi.org/10.1186/s13256-023-04169-5
CASE REPORT
Severe thrombocytopenia induced
bytiroban afterpercutaneous coronary
intervention: acase report
Ze‑Mu Wang1*, Bin Wang2, Ya‑Fei Li3, Bei Chen1, Qin Shen1, Dian‑Fu Li1 and Lian‑Sheng Wang1
Abstract
Background Tirofiban is a nonpeptide glycoprotein IIb/IIIa receptor antagonist used widely in patients subjected
to percutaneous coronary intervention. While the usage of tirofiban sets an important clinical benefit, severe throm‑
bocytopenia can occur with use of this agent.
Case presentation A 76‑year‑old Chinese man was admitted with 1‑month history of sudden onset of chest tight‑
ness. He was diagnosed as having subacute inferior myocardial infarction, and percutaneous coronary interven‑
tion was performed. After the procedure, patient received tirofiban at 0.15 µg/kg/minute for 4 h. A blood sample
was obtained for a complete blood count; severe thrombocytopenia was reported according to routine orders at our
hospital. All antiplatelet drugs including tirofiban, aspirin, and clopidogrel were immediately discontinued. The patient
received platelet transfusions and was treated with immunoglobulin G. Two days later, the patient’s platelet count
had increased to 75 × 109/L. There was a significant improvement after day 5, and the platelet count was 112 × 109/L.
Seven days after the acute thrombocytopenia, he was discharged with normal platelet count.
Conclusions Clinicians should be particularly aware of tirofiban‑induced thrombocytopenia in routine practice.
Keywords Glycoprotein IIb/IIIa receptor antagonists, Tirofiban, Acute coronary syndromes, Percutaneous coronary
intervention
Background
Glycoprotein IIb/IIIa receptor antagonists (GPRAs),
including abciximab, eptifibatide, and tirofiban, are
widely used in the treatment of patients with acute coro-
nary syndromes (ACS) [1]. ese agents have been exten-
sively studied in several randomized trials, which have
demonstrated that the use of GPRAs may reduce the
incidence of myocardial infarction (MI) and composite
cardiac outcomes in patients subjected to percutaneous
coronary intervention (PCI) [2]. However, severe throm-
bocytopenia can occur with use of these agents [3]. Drug-
induced thrombocytopenia may result from a number of
diverse etiologies; it is important for clinicians to make
an accurate diagnosis to guide treatment decisions and
to inform prognosis. Here, we report a case of severe
thrombocytopenia within 4 hours of tirofiban adminis-
tration after PCI for subacute inferior MI.
Case presentation
A 76-year-old Chineseman was admitted with 1-month
history of sudden onset of chest tightness. A month pre-
viously, the symptom started while he was doing exercise.
Open Access
© The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which
permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the
original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or
other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line
to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory
regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this
licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecom
mons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
Journal of
Medical Case Reports
*Correspondence:
Ze‑Mu Wang
zemu.wang@njmu.edu.cn
1 Department of Cardiology, The First Affiliated Hospital of Nanjing
Medical University, Nanjing, China
2 Institute of Nephrology, Zhong Da Hospital, Southeast University School
of Medicine, Nanjing, China
3 Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing
Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing
Medical University, Suzhou, China
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Page 2 of 5
Wangetal. Journal of Medical Case Reports (2023) 17:430
It was associated with diaphoresis and shortness of
breath, without chest pain. e resting 12-lead electro-
cardiogram (ECG) showed abnormal Q waves in leads II,
III, and aVF, and the cardiac troponin T was elevated. He
was diagnosed as having ACS and was treated at a local
hospital. Owing to the fact that the hospital was unable
to perform coronary angiography (CAG), the patient was
discharged home several days later on aspirin (100 mg
qd), clopidogrel (75 mg qd), metoprolol (12.5 mg qd),
and rosuvastatin (10mg qn). On admission to our hos-
pital, the patient still had a mildly elevated level of high-
sensitivity cardiac troponin T (21.58 ng/L). His initial
ECG showed abnormal Q waves in the inferior (II, III,
and avF) leads (Fig.1), which may indicate subacute infe-
rior MI. His routine blood test was normal, including a
platelet count of 201 × 109/L and a white blood cell count
of 5.86 × 109/L. He had no history of blood dyscrasia and
denied any history of smoking or drinking. e patient
underwent CAG in our hospital after admission. CAG
revealed evidence of left main (LM) and three-vessel
coronary artery disease (Fig.2). Low-dose heparin (2000
units) was given during the procedure. We consider the
optimal revascularization technique for this patient to be
coronary artery bypass graft (CABG) surgery and did not
perform PCI. However, the patient decide to be treated
with PCI rather than CABG. Four days later, CAG was
performed again; multivessel coronary intervention was
performed with drug-eluting stents and drug-coated
balloon. e procedure lasted for about 2 hours, and
the dose of heparin given was 6500 units. After the
procedure, the patient was transferred in stable condi-
tion to the ward and treated by intravenous tirofiban at
0.15µg/kg/minute. Post-PCI medications included aspi-
rin 100mg qd, clopidogrel 75mg qd, metoprolol succi-
nate 12.5mg qd, rosuvastatin 10mg qn, and benazepril
5mg qd. A blood sample was obtained for a complete
blood count 4 hours after the procedure, according to
routine orders at our hospital. His platelet count was
21 × 109/L, which was confirmed by manual examina-
tion of the blood film. e patient’s hemoglobin level was
119g/L. Tirofiban infusion was stopped by 4hours, and
other antiplatelet drugs including aspirin and clopidogrel
were immediately discontinued. A heparin-induced
thrombocytopenia (HIT) platelet factor 4 antibody test
was performed, and the result was negative [4]. Over the
next 12hours, the patient received 10 unit platelet trans-
fusions to prevent hemorrhage, and his platelet count
had increased to 49 × 109/L. Another analysis completed
later indicated that his platelet count was 37 × 109/L.
Additionally, immunoglobulin G (10g) was given. Aspi-
rin and clopidogrel were resumed the next day, and the
patient received another 10 unit platelet transfusions.
Two days later, the patient’s platelet count had increased
to 75 × 109/L. e course of the patient’s platelet count
is shown in Fig.3. ere was a significant improvement
after day 5, and the platelet count was 112 × 109/L. Seven
days after the acute profound thrombocytopenia, his
platelet count was 138 × 109/L, and he was discharged
with no hemorrhagic sequelae.
Fig. 1 Initial electrocardiogram of a 76‑year‑old man admitted with 1‑month history of chest tightness
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Page 3 of 5
Wangetal. Journal of Medical Case Reports (2023) 17:430
Discussion andconclusions
Tirofiban is a nonpeptide glycoprotein (GP) IIb/IIIa
receptor antagonist used in patients subjected to PCI for
the prevention of acute stent thrombosis and reduction
of major adverse coronary events [5]. It inhibits platelet
aggregation by preventing the attachment of fibrino-
gen and von Willebrand factor to the GP IIb/IIIa recep-
tor on the thrombocyte surface [6]. While the usage of
GP IIb/IIIa inhibitors sets an important clinical benefit,
the reported incidence of thrombocytopenia induced by
tirofiban ranges from 0.4% to 5.6% [7]. us, clinicians
should be particularly aware of tirofiban-induced throm-
bocytopenia in routine practice.
Besides tirofiban, aspirin and clopidogrel are widely
used as antiplatelet agents; they have also been reported
to be associated with thrombocytopenia [8]. How-
ever, the described patient had used these two drugs for
1 month before admission, and his routine blood test
showed a normal platelet count after admission. ere-
fore, the thrombocytopenia was not caused by the dual
antiplatelet therapy.
e most well-known medication that can induce
thrombocytopenia is heparin [9]. HIT is the most impor-
tant complication of heparin therapy during PCI in car-
diac patients. ere are two types of HIT. Type I HIT is a
transient, mild drop in platelet counts 48–72hours after
initiation of heparin therapy. It occurs because of direct
heparin-induced platelet aggregation and is usually clini-
cally harmless [7]. Type II HIT is an adverse immune-
mediated reaction due to antibodies formed against
heparin–platelet factor 4 complexes, which is usually
associated with thrombosis risk. It is more severe than
type I HIT and should be suspected when patients show
Fig. 2 Coronary angiography revealed an evidence of left main and three vessel coronary artery disease
Fig. 3 Platelet count trend during hospitalization
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Page 4 of 5
Wangetal. Journal of Medical Case Reports (2023) 17:430
a reduction in the platelet count to less than 100,000 per
cubic millimeter or more than 50% of the baseline value
5–15days after initiation of heparin therapy [10, 11]. e
4T’s score (theseverity of rombocytopenia, itsTiming
of heparin exposure, appearance of new rombosis, and
differential diagnosis by exclusion of oer causes) has
been utilized as a clinical assessment tool to evaluate the
likelihood of HIT [11, 12]. Our patient’s 4T’s score was 3
points. us, the suspicion for HIT was low. In addition,
we carried out an immunoassay to examine the presence
of HIT antibodies; the negative result indicated that our
patient did not have an HIT type II reaction. It is impor-
tant to exclude HIT and other causes of thrombocyto-
penia to diagnose tirofiban-induced thrombocytopenia
accurately and treat patients appropriately.
A recent study based on pre-procedural character-
istics for early prediction of thrombocytopenia before
patients were exposed to tirofiban has developed a sim-
ple risk model to predict thrombocytopenia associated
with periprocedural tirofiban exposure [7]. Five inde-
pendent risk factors, including age 65years (2 points),
white blood cell 12 × 109 /L (1 point), diabetes mel-
litus (2 points), congestive heart failure (2 points), and
chronic kidney disease (1 point), were identified as risk
factors in the scoring system. According to the scoring
system, 7 points, 3–6 points, and 2 points indicate
high risk, moderate risk and low risk. For our patient, this
score only indicates a moderate risk (4 points), calculated
based on age and congestive heart failure. erefore, a
further predictive model is still needed to help doctors
identify high-risk patients in clinical practice [7].
e efficacy of tirofiban for patients with MI who
undergo PCI was positively correlated with its dose; high
dose can enhance the clinical effects, but also increase
the hemorrhagic risk [13]. e appropriate dose could be
adopted by reference to the specific conditions of patients
under assessment of bleeding risk, and a common recom-
mended clinical dose of 10 µg/kg may be appropriate for
patients without high hemorrhagic risk, followed by con-
tinuous intravenous injection at 0.15µg/kg/minute [13].
It is important to monitor platelet counts closely after
initiation of tirofiban infusion [14]. For these patients,
testing platelet counts before treatment, 2–4 h following
the start of infusion, and at 24 h would detect most cases
of acute thrombocytopenia [1, 15]. Discontinuation of
tirofiban is usually sufficient for treatment of thrombocy-
topenia because it is cleared from the circulation within
the first hours of cessation of the drug [14, 16].
In conclusion, this report demonstrates an example of
acute severe thrombocytopenia induced by tirofiban and
endorses the importance of platelet count monitoring
after initiating therapy with this agent in clinical practice.
Abbreviations
ACS Acute coronary syndromes
CABG Coronary artery bypass graft
CAG Coronary angiography
ECG Electrocardiogram
GP Glycoprotein
GPRAs Glycoprotein IIb/IIIa receptor antagonists
HIT Heparin‑induced thrombocytopenia
hs‑cTnT High‑sensitivity cardiac troponin T
LAD Left anterior descending
LCX Left circumflex artery
LM Left main
MI Myocardial infarction
PCI Percutaneous coronary intervention
RCA Right coronary artery
Acknowledgements
Not applicable.
Author contributions
Z‑MW wrote the manuscript. Z‑MW, BW, and Y‑FL analyzed and interpreted the
patient data. BC and QS collected the relevant materials including the figures
and medical records. D‑FL performed the PCI procedure. L‑SW was a major
contributor in proof reading and manuscript correction. All authors read and
approved the final manuscript.
Funding
This work was supported by grants from the National Natural Science Founda‑
tion of China (no. 81703213) and the Natural Science Youth Foundation of
Jiangsu Province of China (no. BK20151034) to Z‑MW.
Availability of data and materials
Not applicable.
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patient for publication of
this case report and any accompanying images. A copy of the written consent
is available for review by the Editor‑in‑Chief of this journal.
Competing interests
The authors declare that they have no competing interests.
Received: 17 October 2021 Accepted: 9 September 2023
References
1. Huxtable LM, Tafreshi MJ, Rakkar AN. Frequency and management of
thrombocytopenia with the glycoprotein IIb/IIIa receptor antagonists.
Am J Cardiol. 2006;97:426–9.
2. Karvouni E, Katritsis DG, Ioannidis JP. Intravenous glycoprotein IIb/IIIa
receptor antagonists reduce mortality after percutaneous coronary
interventions. J Am Coll Cardiol. 2003;41:26–32.
3. Sharma A, Ferguson C, Bainey KR. Thrombocytopenia in acute coronary
syndromes: etiologies and proposed management. Can J Cardiol.
2015;31:809–11.
4. Rauova L, Zhai L, Kowalska MA, Arepally GM, Cines DB, Poncz M. Role
of platelet surface PF4 antigenic complexes in heparin‑induced throm
bocytopenia pathogenesis: diagnostic and therapeutic implications.
Blood. 2006;107:2346–53.
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Page 5 of 5
Wangetal. Journal of Medical Case Reports (2023) 17:430
fast, convenient online submission
thorough peer review by experienced researchers in your field
rapid publication on acceptance
support for research data, including large and complex data types
gold Open Access which fosters wider collaboration and increased citations
maximum visibility for your research: over 100M website views per year
At BMC, research is always in progress.
Learn more biomedcentral.com/submissions
Ready to submit your research
Ready to submit your research
? Choose BMC and benefit from:
? Choose BMC and benefit from:
5. Giordano A, Musumeci G, D’Angelillo A, Rossini R, Zoccai GB, Messina S,
et al. Effects Of glycoprotein IIb/IIIa antagonists: anti platelet aggregation
and beyond. Curr Drug Metab. 2016;17:194–203.
6. Ede H, Erkoç MF, Alüzüm H, Özdemir ZT, Erbay AR. Tirofiban induced
anemia without thrombocytopenia. Int J Cardiol. 2015;179:500–1.
7. Yi YH, Yin WJ, Gu ZC, Fang WJ, Li DY, Hu C, et al. A simple clinical pre‑
procedure risk model for predicting thrombocytopenia associated with
periprocedural use of tirofiban in patients undergoing percutaneous
coronary intervention. Front Pharmacol. 2018;9:1456.
8. Hu Y, Yuan M, Lu X. Thrombocytopenia induced by both aspirin and clopi‑
dogrel in the same patient. Int J Clin Pharmacol Ther. 2013;51:228–31.
9. Cuker A, Arepally GM, Chong BH, Cines DB, Greinacher A, Gruel Y, et al.
American Society of Hematology 2018 guidelines for management of
venous thromboembolism: heparin‑induced thrombocytopenia. Blood
Adv. 2018;2:3360–92.
10. Cicco N, Gerken G, Frey M, et al. Heparin‑induced thrombocytopenia.
Intensivmed. 2000;37(Suppl 1):S099. https:// doi. org/ 10. 1007/ s0039 00070
012.
11. Lassila R, Antovic JP, Armstrong E, Baghaei F, Dalsgaard‑Nielsen J, Hillarp
A, et al. Practical viewpoints on the diagnosis and management of hepa‑
rin‑induced thrombocytopenia. Semin Thromb Hemost. 2011;37:328–36.
12. Liu W, Zhang C, Bai Q, Zhang Z. Rare heparin induced thrombocytopenia
type I reaction in a hemodialysis patient: case report. Medicine (Balti‑
more). 2018;97: e13609.
13. Wang H, Feng M. Influences of different dose of tirofiban for acute ST
elevation myocardial infarction patients underwent percutaneous coro‑
nary intervention. Medicine (Baltimore). 2020;99: e20402.
14. Elcioglu OC, Ozkok A, Akpınar TS, Tufan F, Sezer M, Umman S, et al. Severe
thrombocytopenia and alveolar hemorrhage represent two types of
bleeding tendency during tirofiban treatment: case report and literature
review. Int J Hematol. 2012;96:370–5.
15. Shenoy C, Harjai KJ. Thrombocytopenia following percutaneous coronary
intervention. J Interv Cardiol. 2011;24:15–26.
16. Kondo K, Umemura K. Clinical pharmacokinetics of tirofiban, a nonpep‑
tide glycoprotein IIb/IIIa receptor antagonist: comparison with the mono‑
clonal antibody abciximab. Clin Pharmacokinet. 2002;41:187–95.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in pub‑
lished maps and institutional affiliations.
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
1.
2.
3.
4.
5.
6.
Terms and Conditions
Springer Nature journal content, brought to you courtesy of Springer Nature Customer Service Center GmbH (“Springer Nature”).
Springer Nature supports a reasonable amount of sharing of research papers by authors, subscribers and authorised users (“Users”), for small-
scale personal, non-commercial use provided that all copyright, trade and service marks and other proprietary notices are maintained. By
accessing, sharing, receiving or otherwise using the Springer Nature journal content you agree to these terms of use (“Terms”). For these
purposes, Springer Nature considers academic use (by researchers and students) to be non-commercial.
These Terms are supplementary and will apply in addition to any applicable website terms and conditions, a relevant site licence or a personal
subscription. These Terms will prevail over any conflict or ambiguity with regards to the relevant terms, a site licence or a personal subscription
(to the extent of the conflict or ambiguity only). For Creative Commons-licensed articles, the terms of the Creative Commons license used will
apply.
We collect and use personal data to provide access to the Springer Nature journal content. We may also use these personal data internally within
ResearchGate and Springer Nature and as agreed share it, in an anonymised way, for purposes of tracking, analysis and reporting. We will not
otherwise disclose your personal data outside the ResearchGate or the Springer Nature group of companies unless we have your permission as
detailed in the Privacy Policy.
While Users may use the Springer Nature journal content for small scale, personal non-commercial use, it is important to note that Users may
not:
use such content for the purpose of providing other users with access on a regular or large scale basis or as a means to circumvent access
control;
use such content where to do so would be considered a criminal or statutory offence in any jurisdiction, or gives rise to civil liability, or is
otherwise unlawful;
falsely or misleadingly imply or suggest endorsement, approval , sponsorship, or association unless explicitly agreed to by Springer Nature in
writing;
use bots or other automated methods to access the content or redirect messages
override any security feature or exclusionary protocol; or
share the content in order to create substitute for Springer Nature products or services or a systematic database of Springer Nature journal
content.
In line with the restriction against commercial use, Springer Nature does not permit the creation of a product or service that creates revenue,
royalties, rent or income from our content or its inclusion as part of a paid for service or for other commercial gain. Springer Nature journal
content cannot be used for inter-library loans and librarians may not upload Springer Nature journal content on a large scale into their, or any
other, institutional repository.
These terms of use are reviewed regularly and may be amended at any time. Springer Nature is not obligated to publish any information or
content on this website and may remove it or features or functionality at our sole discretion, at any time with or without notice. Springer Nature
may revoke this licence to you at any time and remove access to any copies of the Springer Nature journal content which have been saved.
To the fullest extent permitted by law, Springer Nature makes no warranties, representations or guarantees to Users, either express or implied
with respect to the Springer nature journal content and all parties disclaim and waive any implied warranties or warranties imposed by law,
including merchantability or fitness for any particular purpose.
Please note that these rights do not automatically extend to content, data or other material published by Springer Nature that may be licensed
from third parties.
If you would like to use or distribute our Springer Nature journal content to a wider audience or on a regular basis or in any other manner not
expressly permitted by these Terms, please contact Springer Nature at
onlineservice@springernature.com
ResearchGate has not been able to resolve any citations for this publication.
Article
Full-text available
Tirofiban is widely used in patients with acute ST elevation myocardial infarction (STEMI) underwent percutaneous coronary intervention (PCI). This drug can efficiently improve myocardial perfusion and cardiac function, but its dose still remains controversial. We here investigated the effects of different dose of tirofiban on myocardial reperfusion and heart function in patients with STEMI. A total of 312 STEMI patients who underwent PCI in our hospital from March 2017 to March 2018 were enrolled and randomly divided into control group (75 cases, 0 μg/kg), low-dose group (79 cases, 5 μg/kg), medium-dose group (81 cases, 10 μg/kg) and high-dose group (77 cases, 20 μg/kg). The infarction-targeted artery flow grade evaluated by thrombolysis in myocardial infarction (TIMI), corrected TIMI frame count (CTFC) and sum-ST-segment resolution were recorded. At Day 7 and Day 30 after PCI, the left ventricular ejection fraction (LVEF), left ventricular end diastolic diameter, left ventricular end systolic diameter, major adverse cardiovascular events and the hemorrhage and thrombocytopenia were also evaluated. After PCI, the rate of TIMI grade 3, CTFC and incidence of sum-ST-segment resolution > 50% of high-dose group were significantly higher than those of control group, low-dose group and medium-dose group (P < .05), and the CTFC of medium -dose group were significantly higher than that of control group, low-dose group (P < .05). Moreover, the LVEF, left ventricular end diastolic diameter and left ventricular end systolic diameter of high-dose group were significantly improved than those of other groups, and the LVEF of medium-dose group was significantly superior to that of low-dose group (P < .05). However, the incidence of major adverse cardiac events in high-dose group was significantly decreased, while the hemorrhage and incidence of thrombocytopenia of high-dose group were significantly higher than those of other 3 groups (P < .05). The tirofiban can effectively alleviate the myocardial ischemia-reperfusion injury and promote the recovery of cardiac function in STEMI patients underwent PCI. Although the high-dose can enhance the clinical effects, it also increased the hemorrhagic risk. Therefore, the rational dosage application of tirofiban become much indispensable in view of patient's conditions and hemorrhagic risk, and a medium dose of 10 μg/kg may be appropriate for patients without high hemorrhagic risk.
Article
Full-text available
Rationale Heparin-induced thrombocytopenia (HIT) is a common antibody-mediated adverse reaction that occurs after heparin exposure. However, few case reports exist regarding nonantibody-mediated HIT. Patient concerns and diagnoses An 81-year-old female diagnosed with rapidly progressive glomerulonephritis (RPGN) presented with atypical presentation of non antibody-meditated HIT after using heparin during hemodialysis. Interventions and outcomes Patient was initiated on hemodialysis and presented with thrombocytopenia following administration of heparin during dialysis. After ruling out all other causes of thrombocytopenia, HIT was suspected to be the cause. Patient's 4Ts score was 6 points, and Naranjo adverse drug reaction probability scale was a score of 10. However, enzyme-linked immunoassay for platelet factor 4 (PF4)/heparin antibodies was negative, indicating non-antibody mediated HIT. Patient eventually continued hemodialysis without heparin. Lessons This patient case presented a rare presentation of HIT type I reaction due to heparin and demonstrated the importance of timely recognition of thrombocytopenia, appropriate diagnosis and management, and possible existence of a new atypical or subtype of HIT reaction.
Article
Full-text available
Background: No risk model for predicting thrombocytopenia associated with periprocedural tirofiban exposure is available. The purpose of this study was to develop a simple clinical pre-procedure risk model based on pre-procedural characteristics for early prediction of thrombocytopenia before patients were exposed to tirofiban. Methods: The series included 1862 patients who underwent percutaneous coronary intervention with tirofiban exposure. Baseline demographic and clinical characteristics were collected from the hospital information system on admission. The earliest pro-procedural platelets within 72 h were used to evaluate the thrombocytopenia incidence. Risk factors associated with thrombocytopenia in patients with tirofiban exposure were investigated by univariable and multivariable analyses. Locally weighted scatterplot smoothing procedure was used to identify the cut points for the numeric variables. The discriminatory power of the scoring system was assessed with the receiver operating characteristic (ROC) curve analysis. Results: The occurrence of thrombocytopenia was 4.02% (75 of 1862), 4.01% (56 of 1396), and 4.08% (19 of 466) in the overall, developmental, and validation data sets, respectively. The risk score was developed based on five independent predictors: age ≥65y, white blood cell ≥12 × 10⁹/L, diabetes mellitus, congestive heart failure, and chronic kidney disease. This tool was well calibrated (Hosmer Lemeshow χ² = 6.914; P = 0.546) and good discrimination was well obtained in validation data set (C-statistic, 0.82). Conclusion: The clinical pre-procedure risk model is a simple and accurate tool for early identification of high-risk patients of thrombocytopenia before tirofiban exposure, allowing for timely and appropriate intervention.
Article
Full-text available
Background: The use of inhibitors of glycoprotein IIb/IIIa (GPIIb/IIIa) has provided dramatic results in terms of the prevention of acute stent thrombosis and a reduction in major adverse coronary events in patients subjected to percutaneous coronary intervention. GPIIb/IIIa or αIIbβ3 is a member of the β3 subfamily of integrins, which also includes αVβ3. GPIIb/IIIa functions as a receptor for fibrinogen and several adhesion proteins sharing an arginine-glycine-aspartic acid (RGD) sequence. GPIIb/IIIa antagonists, through blockade of the receptor, prevent platelet aggregation. Among the three GPIIb/IIIa antagonists used in therapy, abciximab is an anti-β3 monoclonal antibody, while tirofiban and eptifibatide mimic the binding sequence of the fibrinogen ligand. Although antiplatelet aggregation represents the central function of GPIIb/IIIa inhibitors, further actions have been documented for these compounds. Objective: The aim of the present article is to review the structures and functions of GPIIb/IIIa antagonists and to highlight the clinical outcomes and results of randomized trials with these compounds. Hypotheses on the unexplored potential of GPIIb/IIIa antagonists will be put forward. Conclusion: GPIIb/IIIa inhibitors were developed to prevent platelet aggregation, however, these compounds can exert further biological functions, both platelet- and non-platelet-related. Large-scale studies comparing the efficacy and safety of GPIIb/IIIa antagonists are lacking. More insights into the functions of these compounds may lead to generation of novel small molecules able to antagonize platelet aggregation while promoting vascular repair.
Article
Background: Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction mediated by platelet-activating antibodies that target complexes of platelet factor 4 and heparin. Patients are at markedly increased risk of thromboembolism. Objective: These evidence-based guidelines of the American Society of Hematology (ASH) are intended to support patients, clinicians, and other health care professionals in their decisions about diagnosis and management of HIT. Methods: ASH formed a multidisciplinary guideline panel balanced to minimize potential bias from conflicts of interest. The McMaster University GRADE Centre supported the guideline development process, including updating or performing systematic evidence reviews. The panel prioritized clinical questions and outcomes according to their importance for clinicians and patients. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach was used to assess evidence and make recommendations, which were subject to public comment. Results: The panel agreed on 33 recommendations. The recommendations address screening of asymptomatic patients for HIT, diagnosis and initial management of patients with suspected HIT, treatment of acute HIT, and special situations in patients with acute HIT or a history of HIT, including cardiovascular surgery, percutaneous cardiovascular intervention, renal replacement therapy, and venous thromboembolism prophylaxis. Conclusions: Strong recommendations include use of the 4Ts score rather than a gestalt approach for estimating the pretest probability of HIT and avoidance of HIT laboratory testing and empiric treatment of HIT in patients with a low-probability 4Ts score. Conditional recommendations include the choice among non-heparin anticoagulants (argatroban, bivalirudin, danaparoid, fondaparinux, direct oral anticoagulants) for treatment of acute HIT.
Article
Thrombocytopenia in acute coronary syndromes (ACS) can arise from a variety of etiologies. Glycoprotein IIb/IIIa receptor antagonists have improved clinical outcomes in ACS, however, profound thrombocytopenia can occur with use of these agents. We present a case of profound thrombocytopenia due to administration of a glycoprotein IIb/IIIa receptor antagonist, eptifibatide, after percutaneous coronary intervention for an inferior ST-elevation myocardial infarction. We review the major causes and suggest an approach for diagnosis and management of thrombocytopenia in ACS. Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
Article
Heparin-induced thrombocytopenia (HIT), next to bleeding complications, is the most important side-effect of heparin therapy in cardiac patients and the most frequently found thrombocytopenia induced by medication. Two types of HIT are distinguished on the basis of both severity of disease, and pathophysiology: type I HIT is an early, transient, clinically harmless form of thrombocytopenia, due to direct heparin-induced platelet aggregation. Thromboembolic complications are usually not seen. No treatment is required. A normalization of platelet count even if heparin is continued is a usual observation. Type II HIT is more severe than type I HIT and is frequently complicated by extension of preexisting venous thromboembolism or new arterial thrombosis. The thrombocytopenia is caused by a pathogenic heparin-dependent IgG antibody (HIT-IgG) that recognizes as its target antigen a complex consisting of heparin and platelet factor IV. Type II HIT should be suspected when the platelet count falls to less than 100,000 per cubic millimeter or less than 50% of the base line value 5 to 15 days after heparin therapy is begun, or sooner in a patient who received heparin in the recent past. The clinical diagnosis of type II HIT can be confirmed by several sensitive assays. In cases of type II HIT, heparin must be stopped immediately. However, if the patient requires continued anticoagulant therapy for an acute event such as deep venous thrombosis, substitution of an alternative rapid-acting anticoagulant drug is often needed. In the authors experience Danaparoid sodium, a low-sulfated heparinoid with a low cross-reactivity (10%) to heparin, can be regarded as an effective anticoagulant in patients with type II HIT. Preliminary experiences with intravenous recombinant hirudin are also encouraging and suggest that this direct thrombin inhibitor will emerge as a valuable alternative treatment for patients who suffer from HIT.
Article
Aspirin and clopidogrel are used widely as antiplatelet agents due to their efficacy, safety, and tolerability. In rare cases, these agents can cause thrombotic thrombocytopenic purpura, but no report has documented severe thrombocytopenia in response to both drugs in the same patient. A 73-yearold female developed severe thrombocytopenia following treatment with clopidogrel. Platelet count recovered within 6 months of drug withdrawal without additional thrombopoietic therapies. Seven months after the last dose of clopidogrel, thrombocytopenia recurred on aspirin therapy. Again, platelet count rebounded gradually and independently. This case suggests that some patients who experience thrombocytopenia in response to one antiplatelet agent may react similarly to other antiplatelet agents.