scholarly journals Thrombocytopenia with and without Thrombosis Following COVID-19 Vaccination

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 1062-1062
Author(s):  
Melissa Ge ◽  
Danyal Ladha ◽  
Jennifer Lymer ◽  
Stefana Pancic ◽  
Marc Carrier ◽  
...  

Abstract Introduction: Vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) were rapidly developed during the COVID-19 pandemic. There is emerging evidence of adverse hematologic effects including thrombocytopenia, for recipients of both mRNA and adenovirus-vector vaccines. We report findings in 9 patients diagnosed with thrombocytopenia following administration of an approved COVID-19 vaccine and managed according to the ASH COVID-19 Thrombosis with Thrombocytopenia Syndrome (TTS) recommendations [https://www.hematology.org/covid-19/vaccine-induced-immune-thrombotic-thrombocytopenia]. Methods: The study population included adults >18 years of age presenting to a large Canadian tertiary care centre, between April 1 st, 2021 and May 31 st, 2021, with new-onset thrombocytopenia within 31 days of receiving COVID-19 vaccination. Vaccines approved during this time period in Canada included BNT162b2 (Pfizer-BioNTech, mRNA) vaccine, mRNA-1273 (Moderna, mRNA) vaccine, and ChAdOx1-S (AstraZeneca (AZ), adenovirus vector-based) vaccine. We report on the initial presentation, management and 90-day outcomes. Results : Among 9 patients with thrombocytopenia included in this cohort, the median age was 55 years (range 24 to 73), and 5 patients (56%) were female. Seven patients received AZ and 2 had Pfizer vaccines. All events occurred after the first dose of COVID-19 vaccine with a median of 11 days between vaccination and presentation to hospital (range 2 to 31). All patients admitted to hospital tested negative for COVID-19 by PCR. Four patients developed TTS, as confirmed on both HIT ELISA and serotonin release assay, following AZ vaccination. Two patients presented with headaches and were diagnosed with cerebral vein thrombosis (CVT); and 2 presented with dyspnea and were diagnosed with venous thromboembolism (VTE). Platelet counts at presentation ranged 14-136 and D-dimer ranged 4000 to >44,000. HIT ELISA optical densities were persistently elevated. Three patients were admitted to hospital and received non-heparin parenteral anticoagulation, IVIG, and steroids. One patient had refractory thrombocytopenia with extension of CVT prompting use of therapeutic plasma exchange. Two patients had recurrent thrombocytopenia within 30 days of discharge and responded to repeat IVIG treatment. Five patients developed immune thrombocytopenic purpura (ITP), four without associated thrombosis and one patient with history of ITP and splenectomy, maintained on Revolade, presented with ITP flare and deep vein thrombosis. Presenting complaints included petechial rash and minor bleeding such as epistaxis. Platelet counts ranged from undetectable to 67; D-dimer levels were normal in all at presentation. Four patients were admitted to hospital and received IVIG +/- steroids. Two patients had recurrent severe thrombocytopenia within 14 days of discharge, requiring repeat steroid pulse. See Table for summary of all patients. Conclusion: In summary, application of the ASH TTS guidance to patients presenting with thrombocytopenia, with and without thrombosis, following COVID-19 vaccination was instrumental in the early identification and successful management of these complications. Figure 1 Figure 1. Disclosures Carrier: Sanofi: Honoraria; Pfizer: Honoraria, Research Funding; Servier: Honoraria; Bayer: Honoraria; Leo Pharma: Honoraria, Research Funding; BMS: Honoraria, Research Funding. Le Gal: BMS: Honoraria; Aspen: Honoraria; Bayer: Honoraria; LEO Pharma: Honoraria; Pfizer: Honoraria; Sanofi: Honoraria. Castellucci: BMS: Honoraria; Pfizer: Honoraria; Amag Pharmaceuticals: Honoraria; The Academy: Honoraria.

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 4258-4258
Author(s):  
Maged Al-Ammari ◽  
Abdul Ali Peer Zada ◽  
Ibraheem H. Motabi ◽  
Belal M. Albtoosh ◽  
Syed Y. Altaf ◽  
...  

Abstract Background: JAK2 GGCC 46/1 haplotype can be represented by four main SNPs (rs3780367, rs10974944, rs12343867, and rs1159782) which replace one cytosine and three thymidines by two guanosines and two cytosines, generating a "GGCC" combination. These four SNPs located on JAK2 introns 10, 12, 14, and 15, respectively, and are always inherited together, being in complete linkage disequilibrium. The 46/1 component of the name came from Jones et al. study where the haplotype structure of the JAK2 gene was mapped using 14 SNPs genotyped by the Wellcome Trust Case Control Consortium (WTCCC) in 1500 healthy blood donors. Two haplotypes (numbers 46 and 1) were found to be identical except for one SNP, and they have a combined frequency of 0.24 in healthy individuals. Numerous observational studies associate this haplotype with myeloproliferative neoplasms (MPNs), as well as splanchnic vein thrombosis (SVT) and non-splanchnic vein thrombosis (non-SVT). In contrast to 24% frequency noted in healthy population, the frequency goes up to 40-80% in JAK2 V617F mutated MPN, and in 64% of those with JAK2 exon 12 mutations (Anelli et al. IJMS, 2018). We herein report our study of JAK2 GGCC (46/1) Haplotype in unprovoked Venous Thrombotic Events (VTE) in patients with negative thrombophilia workup, including negative JAK2 V617F mutation. Methods: We retrospectively identified patients positive for one of the two SNPs (rs12343867 and rs10974900) and unprovoked venous thrombotic among adult patients with negative thrombophilia workup (including JAK2 mutation) treated at tertiary care center from January 2018 to January 2021. Results: We have identified 8 patients, Table (1), that were positive for JAK2 46/1 haplotype SNPs, of whom 62.5% were homozygous 2/2, 25% heterozygous 1/2, while only 12.5% harbor homozygous 1/1 (a normal variant of JAK2 haplotype). The median age 48.5 years (23-65), and the majority (87.5%) were females. Thrombosis site was noted to be SVT in half of the patients, while non-SVT was noted in the other half (12.5% had cerebral vein thrombosis, 12.5% had deep venous thrombosis, 12.5% had a pulmonary embolism, and 12.5% had jugular vein thrombosis). Half of the patients had more than one site venous thrombosis and the other half had only one site. Around 37.50% of the patients had recurrent venous thrombosis on top of therapeutic anticoagulation. Two patients (25%) had high hemoglobin (17.4/16.7) g/dl, but did not fulfill the criteria for polycythemia vera diagnosis (of whom one is a male smoker and one was a female). None of the patients had leukocytosis or thrombocytosis. By imaging, one patient had mild splenomegaly which could be related to SVT. Conclusion: We report on a potential correlation between unprovoked thrombotic events, mainly venous thrombotic events, with JAK2 46/1 haplotype in patients with a negative thrombophilia workup, a finding that merit further investigation. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4175-4175 ◽  
Author(s):  
Claire N Harrison ◽  
Aaron T. Gerds ◽  
Jean-Jacques Kiladjian ◽  
Konstanze Döhner ◽  
Sarah A Buckley ◽  
...  

Background: Myelofibrosis (MF) is a life-limiting condition with severe morbidity in advanced stages. Patients with MF and severe thrombocytopenia (platelet counts <50,000/mL) have a particularly poor prognosis, with more frequent anemia and leukopenia, higher rates of hemorrhagic and thrombotic complications, and worse overall survival (~15 months) compared to the overall MF population (Scotch AH, et al, Leuk Res. 2017; Masarova L, et al, Eur J Haematol. 2018). Moreover, effective treatment options are limited in this high-risk population as the currently approved JAK inhibitor, ruxolitinib (RUX), is associated with treatment-related thrombocytopenia and often requires dose reductions for patients with platelet counts <100,000/mL, with reduced efficacy compared to patients able to tolerate higher doses. Further, there is no approved dose of RUX for patients with platelet counts <50,000/mL, and NCCN guidelines encourage physicians to consider clinical trials for such patients given the lack of approved therapies. Pacritinib (PAC) is an oral JAK2/IRAK1 inhibitor that has demonstrated clinical activity in MF patients in two prior Phase 3 studies (PERSIST-1, PERSIST-2) as well as a Phase 2 dose-finding study (PAC203), including patients with severe thrombocytopenia. The PACIFICA trial has been designed to evaluate the efficacy and safety of PAC 200 mg BID vs. physician's choice (P/C) therapy in patients with MF and severe thrombocytopenia. Study Design and Methods: PACIFICA is a randomized, controlled Phase 3 trial of PAC vs. P/C in adult patients with primary or secondary MF who are not candidates for stem cell transplant, with DIPSS intermediate- or high-risk disease, ECOG PS ≤2, and platelet counts <50,000/mL, who have had up to 90 days of prior treatment with a JAK2 inhibitor or are JAK2 inhibitor-naïve. Additional exclusion criteria exist for patients with recent cardiac or hemorrhagic events, ejection fraction <50%, QTc >450 msec, or use of medications that increase the risk of hemorrhage or QT prolongation. On the PAC arm, patients receive continuous PAC 200mg BID. On the P/C arm, one of the following agents is selected prior to randomization: low-dose ruxolitinib (no more than 5 mg BID while platelet counts remain <50,000/mL), thalidomide, lenalidomide, corticosteroids, or hydroxyurea. The primary objective is to compare the efficacy of PAC vs. P/C based on the proportion of patients achieving a ≥35% spleen volume response (SVR) at Week 24. Secondary objectives include comparisons of the proportion of patients achieving a ≥50% reduction in total symptom score (TSS) at Week 24, overall survival, and proportion of patients who self-assess as "very much improved" or "much improved" as measured by the patient global impression of change (PGIC). Tertiary endpoints include alternative methods of evaluating SVR improvement, hematologic improvement (transfusion independence and improvement in anemia and thrombocytopenia), improvement in fatigue as measured by the PROMIS - Fatigue - Short form 7a, and changes in mutated allelic burden and gene expression (including correlation with response data). The study will enroll ~180 patients in a 2:1 ratio (PAC to P/C), which will have >80% power to achieve the primary endpoint. Enrollment is anticipated to begin in Q3 2019, as PACIFICA is expected to open as an amendment to the Phase 2 PAC203 study (NCT03165734) in select sites. Disclosures Harrison: Janssen: Speakers Bureau; Celgene: Honoraria, Speakers Bureau; CTI: Speakers Bureau; Roche: Honoraria; Gilead: Speakers Bureau; AOP: Honoraria; Promedior: Honoraria; Novartis: Honoraria, Research Funding, Speakers Bureau; Sierra Oncology: Honoraria. Gerds:Roche: Research Funding; CTI Biopharma: Consultancy, Research Funding; Celgene Corporation: Consultancy, Research Funding; Pfizer: Consultancy; Sierra Oncology: Research Funding; Imago Biosciences: Research Funding; Incyte: Consultancy, Research Funding. Kiladjian:Novartis: Honoraria, Research Funding; Celgene: Consultancy; AOP Orphan: Honoraria, Research Funding. Döhner:Daiichi: Honoraria; Jazz: Honoraria; Novartis: Honoraria; Celgene: Honoraria; Janssen: Honoraria; CTI Biopharma: Consultancy, Honoraria. Buckley:CTI BioPharma: Employment, Equity Ownership. Smith:CTI BioPharma: Employment, Equity Ownership. Craig:CTI BioPharma: Employment, Equity Ownership, Membership on an entity's Board of Directors or advisory committees. Mascarenhas:Incyte: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Research Funding; Roche: Consultancy, Research Funding; Merck: Research Funding; Celgene: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; CTI Biopharma: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Janssen: Research Funding; Promedior: Research Funding; Merus: Research Funding; Pharmaessentia: Consultancy, Membership on an entity's Board of Directors or advisory committees. Verstovsek:Incyte: Research Funding; Celgene: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Sierra Oncology: Research Funding; Pharma Essentia: Research Funding; Gilead: Research Funding; Promedior: Research Funding; CTI BioPharma Corp: Research Funding; Genetech: Research Funding; Blueprint Medicines Corp: Research Funding; Astrazeneca: Research Funding; Ital Pharma: Research Funding; Protaganist Therapeutics: Research Funding; Constellation: Consultancy; Pragmatist: Consultancy; NS Pharma: Research Funding; Roche: Research Funding.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4217-4217
Author(s):  
Barry E Rosenbloom ◽  
Sarah Kulke ◽  
John Taylor ◽  
Neal J. Weinreb

Abstract Abstract 4217 Background: Patients with Gaucher disease frequently experience a delay in diagnosis despite clinical signs and/or symptoms. This delay is thought to stem from the rarity of the disease and physicians' inexperience with the constellation of disease manifestations that often overlap those of more common hematological illnesses. It has been the authors' experience that, in the absence of palpable splenomegaly, physicians are even less likely to consider the possibility of Gaucher disease in patients who have other typical manifestations such as chronic bone pain or hematological cytopenias. Using data submitted to the International Collaborative Gaucher Group (ICGG) Gaucher Registry, the largest single repository of Gaucher disease clinical information in existence, we sought to determine how commonly such patients are likely to be encountered. Purpose: To determine the frequency of patients with Gaucher disease who have little to no splenomegaly at diagnosis despite having concurrent moderate or severe thrombocytopenia. Methods: Data were evaluated from all patients with Gaucher disease type 1 enrolled in the ICGG Gaucher Registry as of June 3, 2011 who had not been splenectomized before diagnosis and whose spleen volumes and platelet counts at the time of diagnosis were reported to the Registry. Splenomegaly was quantitated by MRI, CT or ultrasonic volumetric measurements and categorized as mild/none (≤5 multiples of normal [MN] based on a normal value of 0.2% of body weight), moderate (>5 to ≤15 MN) and severe (> 15 MN). Platelet counts were categorized according to thrombocytopenia categories of mild/none (≥120 ×103/mm3), moderate (>60 to ≤120 × 103/mm3) and severe (<60 × 103/mm3). Results: A total of 612 patients with platelet counts and spleen volumes were identified. Of these, 96/612 (15.7%) had mild or no splenomegaly at the time of Gaucher diagnosis. Of these 96 patients, 37 (38.5%) had moderate thrombocytopenia and 6 (6.3%) had severe thrombocytopenia. Conclusions: Type 1 Gaucher patients often present with moderate to severe thrombocytopenia but with either normal spleen volumes or with splenomegaly that is not likely to be clinically apparent. These patients may be at particular risk for diagnostic delay but no less susceptible to Gaucher disease morbidity than patients with a more typical presentation. Further description of this cohort with respect to genotype, demographics, and other disease manifestations will be presented. Disclosures: Rosenbloom: Genzyme Corporation ; Shire Pharmaceuticals: Research Funding, Speakers Bureau; Genzyme Corp: Research Funding, Speakers Bureau. Kulke:Genzyme, a Sanofi Company: Employment. Taylor:Genzyme, a Sanofi Company: Employment. Weinreb:Genzyme Corporation: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Shire HGT: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Actelion Corporation: Speakers Bureau.


2007 ◽  
Vol 97 (02) ◽  
pp. 195-201 ◽  
Author(s):  
Thomas Arnason ◽  
Philip Wells ◽  
Alan Forster

SummaryIt was the objective of this study to determine the proportion of patients who undergo an appropriate diagnostic work-up following a D-dimer test performed to evaluate suspected pulmonary embolism (PE) or deep vein thrombosis (DVT). We performed a retrospective cohort study at a tertiary care hospital. We included patients if they underwent D-dimer testing between 2002 and 2005, if the D-dimer was performed for evaluation of VTE, and if the D-dimer test was successful. We classified: the patients’ clinical probability of DVT or PE according to theWells models,the imaging results,and the appropriateness of the testing algorithm. Of 1,000 randomly selected patients, 863 met our study criteria. Seven hundred nineteen patients (83%) had testing during an emergency department visit, while 144 were tested as inpatients (17%). Physicians performed the D-dimer test to evaluate DVT and PE in 238 (28%) and 625 (72%) patients, respectively. Overall, the testing strategy was appropriate in 69% (95% confidence interval [CI]: 66%–72%) of cases. The testing strategy was more likely to be appropriate for emergency department versus inpatients (75% vs. 39%, p < 0.05) and for DVT versus PE patients (84% vs. 63%, p < 0.05). Of all inappropriately tested patients, under-utilization of diagnostic imaging was more common than over-utilization (90% vs. 10%, p < 0.05). VTE was confirmed in 37 of 138 ‘DVT patients’ and 35 of 625 ‘PE patients’ (16% [95% CI: 11%–21%] and 6% [95% CI: 4%–8%], respectively). In conclusion, physicians often fail to use diagnostic testing strategies for VTE correctly following a D-dimer test.


2012 ◽  
Vol 10 (4) ◽  
pp. 582-589 ◽  
Author(s):  
F. DENTALI ◽  
A. SQUIZZATO ◽  
C. MARCHESI ◽  
M. BONZINI ◽  
J. M. FERRO ◽  
...  

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5778-5778
Author(s):  
Monika Oliver ◽  
Mohammad Karkhaneh ◽  
Jacqueline Karathra ◽  
Mariam Goubran ◽  
Cynthia M. Wu

Introduction The D-dimer has been validated for use in the diagnosis of venous thromboembolism (VTE). The high sensitivity of the assay allows for safe exclusion of VTE in patients with low pre-test probability. Pre-test probability scores such as the Wells score for Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) have been established to help guide physicians on when to order a D-dimer in patients with suspected VTE. We sought to explore the landscape of D-dimer ordering at our institution and what clinical circumstances trigger D-dimer ordering. Methods We conducted a retrospective chart review of 237 patients in whom a D-dimer has been ordered over a 3-month period from January to March 2018 at the University of Alberta Hospital, Edmonton, Canada. Charts were reviewed for the following parameters: Specialty of ordering physician, apparent indication for ordering, patient risk factors for VTE and evidence of pre-test probability calculation. If no pre-test probability was recorded, we retrospectively calculated Wells DVT or PE scores depending on the apparent indication. We then reviewed subsequent investigations thought to be influenced by interpretation of the D-dimer. These included ventilation/perfusion scans (V/Q scan), ultrasound Doppler studies and Computerized Tomography pulmonary angiography (CTPA). Results Of the 237 charts reviewed, 84.4% of D-dimers were ordered in the Emergency Department while only 14.3% were drawn on admitted patients. Sixty-nine percent of the patients were identified as having at least one risk factor for the development of VTE with prolonged hospitalization (5.5%) and personal history of VTE (4.2%) being the most common. Indication for ordering was suspected VTE in 76.3% of patients while the indications was unclear in 12.7% of patients. An initial pre-test probability score was recorded for only 3 patients. Of the D-dimers ordered, 47.7% were above the upper limit of normal (≥ 0.50 mg/L) and considered a positive test. Forty five CTPAs and 27 V/Q scans were performed with only 4 (1.69%) and 6 (2.53%) confirming the presence of pulmonary emboli, respectively. Doppler ultrasounds were performed on 18 patients (7.6%) with only one confirming a DVT. Conclusions Our data shows that the majority of physicians at our institution fail to utilize pre-test probability tools prior to ordering a D-dimer. This leads to unnecessary costs, overuse of imaging studies and results in low rates of positive scans. Disclosures Wu: Bayer: Other: Local PI for trial ; BMS-Pfizer: Other: Local PI for trial ; Daiichi-Sankyo: Other: Local PI for trial .


Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 3517-3517
Author(s):  
Siraj Mithoowani ◽  
Andrea Cervi ◽  
Nishwa Shah ◽  
Resham Ejaz ◽  
Rebecca Barty ◽  
...  

Abstract Background Severe bleeding is a rare but serious complication of immune thrombocytopenia (ITP). A standard approach to treatment is lacking and the delivery of emergency care is often disjointed. The objective of this study was to describe 1) the treatments and outcomes of ITP patients who present to the emergency department (ED) with severe thrombocytopenia and bleeding; and 2) predictors of worsening bleeding or death among ITP patients presenting to the ED. Methods We did a retrospective cohort study of all patients with ITP who presented to the ED with severe thrombocytopenia (platelet count <20 x109/L) and bleeding in 4 academic hospitals affiliated with McMaster University in Hamilton, Canada between January 2008 and April 2016. Patients were followed from arrival to the ED until 10 days after hospital admission, discharge or death. We extracted demographic data, bleeding symptoms at presentation, all ITP treatments administered, new or worsening bleeding, thrombosis and mortality. Bleeding was graded using the ITP Bleeding Score. We defined major bleeding as intracranial hemorrhage (ICH), pulmonary bleeding, or gross gastrointestinal bleeding (GIB). We summarized the results descriptively by frequencies (percentage), and medians (interquartile range [IQR]). Ethics approval was obtained from the Hamilton Integrated Research Ethics Board. Funding was provided by the Platelet Disorder Support Association. Results We identified 110 patients who presented to the ED (n=139 ED visits) with platelets <20 x109/L and bleeding. Median age was 59 years (IQR: 38-74) and 57% were female. For 63 patients (57%), this was their initial presentation of ITP; for the remaining 47 patients, 36% had previously been treated for ITP and had received a median of 3 (IQR: 2-4) ITP therapies. Twenty-eight patients presented to the ED with major bleeding; the remaining 82 patients had ED visits with minor bleeding only. There were 31 ED visits with major bleeding at presentation including GIB (n=23 visits), ICH (n=4), pulmonary hemorrhage (n=3) and GIB plus ICH (n=1). Median platelet count among patients with major bleeding was 3 x109/L (IQR: 3-8 x109/L). Patients received a median of 3 ITP therapies (IQR: 2-4) after presentation to the ED, including intravenous immune globulin (IVIG; 90% of visits), corticosteroids (77% of visits), platelet transfusions (74% of visits), and romiplostim (3% of visits). Median time from ED presentation to first treatment was 7.6 (4.5-9.5) hours. Treatment for bleeding was initiated by Internal Medicine or Hematology consultants in 19/31 visits (61%) or Emergency Department physicians in 12/31 visits (39%). One patient developed arterial thrombosis and 2 patients died, both from bleeding. There were 6 patients who initially presented to the ED with minor bleeding but who subsequently developed major bleeding after a median of 2 days (range: 1-7). All 6 patients had oral purpura and 4 had frank hematuria before or coincident with the development of major bleeding. Conclusions Management of ITP-associated bleeding in the ED consisted mostly of IVIG, corticosteroids and platelet transfusions. Time to first ITP treatment was greater than 7 hours from ED presentation. Oral purpura and hematuria were associated with the development of new or worsening bleeding. A standardized protocol for the management of ITP bleeding in the ED would help identify patients at risk for new or worsening bleeding, and improve health care delivery by making appropriate treatments available in a timely manner. Disclosures Arnold: Amgen: Consultancy, Research Funding; UCB: Consultancy; UCB: Consultancy; Amgen: Consultancy, Research Funding; Bristol Myers Squibb: Research Funding; Novartis: Consultancy, Research Funding; Bristol Myers Squibb: Research Funding; Novartis: Consultancy, Research Funding.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4452-4452
Author(s):  
Girish N Viswanathan ◽  
Gnanamoorthy Mayurathan ◽  
John Hardy ◽  
Sheila Jamieson ◽  
Patrick Kestevan ◽  
...  

Abstract Abstract 4452 Introduction Glycoprotein IIb/IIIa inhibitors (GPI) improve outcomes in patients following percutaneous coronary intervention (PCI) and troponin positive acute coronary syndrome. However, GPI's can result in severe but transient thrombocytopenia (platelet count <50×109 cells/l). Guidelines on management of this complication are lacking. Minimal data exist on clinical outcomes of this cohort of patients and routine prophylactic use of blood products for these patients is controversial. Aim We aimed to study the clinical course and outcomes of patients with coronary artery disease who were admitted for coronary revascularisation and developed severe thrombocytopenia in coronary care unit of our tertiary cardiac centre. Methods We undertook review of 50 consecutive patients who had severe thrombocytopenia. Patients were divided in to two groups, severe thrombocytopenia following GPI usage and severe thrombocytopenia without exposure to GPI (control group). Severe thrombocytopenia in control group was due to co-existent sepsis (4), drugs other than GPI (4), myelodysplasia (4) and unknown aetiology (7). Patients with heparin induced thrombocytopenia, pseudo thrombocytopenia and bypass surgery associated thrombocytopenia and who died within 48 hours were excluded (one in each group). We chose in-hospital mortality, 30-day mortality, repeat coronary intervention and major bleeding as defined by TIMI criteria, as our combined primary endpoint. Results Data from 27 patients with severe thrombocytopenia following GPI administration and 19 age-matched controls were included for analysis. The GPI group had more males (92.6% vs.78.9%), smokers (29.6% vs.3.7%) and patients with a history of hypertension (59.3% vs.57.9%) and dyslipidaemia (66.7% vs.57.9%). Baseline platelet counts were higher in GPI group (in X109 Cells/l, mean, (SD), 201.63 (78.69) vs. 92.2 (8.02), p<0.05). More number of patients in the GPI group had PCI procedures and coronary stents. Patients in GPI group had major fluctuations and quicker recovery of platelet counts (Figure 1). This group had more patients with minor bleeding without any increase in major bleeding (Table 1). GPI group received fewer blood product transfusions (mean units, blood: 0.07 vs.1.32, p<0.05, platelets: 0.22 vs.1.05, p<0.05). GPI group had significant favourable outcomes such as, lower combined primary end point (3.7% vs.42.1%, p<0.05), lower in hospital mortality (3.7% vs.26.3%, p<0.05) and shorter duration of hospital stay (mean days 3.92 vs.25.08, p<0.05) compared to no-GPI group. Conclusion GPI related severe thrombocytopenia was not associated with an increase in bleeding complications or adverse cardiovascular events. A conservative approach with minimal blood product replacement was safe in this group of patients. These findings may have implications in minimising blood product support in this cohort of patients. Disclosures: Zaman: British Heart Foundation/FS/07/033: Research Funding.


1998 ◽  
Vol 79 (03) ◽  
pp. 517-519 ◽  
Author(s):  
Stephane Heymans ◽  
Raymond Verhaeghe ◽  
Luc Stockx ◽  
Désiré Collen

SummaryThe feasibility of catheter-directed thrombolysis with recombinant staphylokinase was evaluated in six selected patients with deep vein thrombosis. The patients underwent intrathrombus infusion of recombinant staphylokinase (2 mg bolus followed by a continuous infusion of 1 mg/h). Heparin was given via the catheter as a bolus (5000 U) and as a continuous infusion (1000 U/h). Complete lyis was obtained in five patients and partial lysis in one patient. Complications consisted of minor bleeding in four subjects. Symptomatic reocclusion occurred in one. Debulking of the thrombus mass by a high speed rotating impeller (n = 1) and stenting (n = 3) were used as additional interventions. An underlying anatomical abnormality was present in two patients. Long term follow up revealed normal patency in all patients and normal valve function in four patients. Symptomatic venous insufficiency with valve dysfunction was present in the two with a second thrombotic episode.Thus catheter-directed infusion of recombinant staphylokinase in patients with deep vein thrombosis appears feasible and may be associated with a high frequency of thrombolysis. Larger studies to define the clinical benefit of this treatment appear to be warranted.


Sign in / Sign up

Export Citation Format

Share Document