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  • JAMA April 21, 2015

    Figure 4: Platelet Reconstitution After Gene Therapy

    A, Change over time in platelet count in each patient. The lower normal value is indicated by a dotted line. Solid lines connecting the triangles indicate continuous platelet transfusions; dashed lines, continuous administration of romiplostim. B, Wiskott-Aldrich syndrome protein (WASp) expression in platelets, as measured by flow cytometry.
  • JAMA April 21, 2015

    Figure 5: Correlation Between Platelet Reconstitution and Number of Transduced Cells Infused

    The platelet count at last follow-up (Table 3) was plotted against the number of transduced CD34+ cells infused per kilogram of body weight, which was calculated by taking account of vector copy number values below 1.0 in the infused product (Table 2).
  • Effect of Oral Eliglustat on Splenomegaly in Patients With Gaucher Disease Type 1: The ENGAGE Randomized Clinical Trial

    Abstract Full Text
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    JAMA. 2015; 313(7):695-706. doi: 10.1001/jama.2015.459

    This international randomized clinical trial found that among adults with Gaucher disease type 1, treatment with eliglustat for 9 months resulted in significant improvements in spleen volume, hemoglobin level, liver volume, and platelet count compared with placebo.

  • Transfusion of Plasma, Platelets, and Red Blood Cells in a 1:1:1 vs a 1:1:2 Ratio and Mortality in Patients With Severe Trauma: The PROPPR Randomized Clinical Trial

    Abstract Full Text
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    JAMA. 2015; 313(5):471-482. doi: 10.1001/jama.2015.12

    This randomized trial reports that among patients with severe trauma and major bleeding, early administration of plasma, platelets, and red blood cells in a 1:1:1 ratio compared with a 1:1:2 ratio did not result in significant differences in mortality at 24 hours or at 30 days.

  • JAMA February 3, 2015

    Figure 1: Flow of Patients in the Pragmatic, Randomized Optimal Platelet and Plasma Ratios (PROPPR) Trial

    CPR indicates cardiopulmonary resuscitation; ED, emergency department; RBC, red blood cell.aIncluded patients with the following: 6 known pregnancies, 5 with physicians who refused to randomize, 4 with known do-not-resuscitate order prior to randomization, 3 with burns covering more than 20% of total body surface area, 1 with a documented inhalation injury, 1 who opted out upon arrival to the ED, 1 unknown reason.bThe vital statistic data were obtained for patients who withdrew consent when available. Patients who withdrew consent at 24 hours are included in the count of those who withdrew at 30 days.
  • JAMA February 3, 2015

    Figure 4: Distribution of Blood Product Amounts Within Period up to 24 Hours After Admission

    Prerandomization blood products include those given prior to hospital arrival. The lower and upper edges of the boxes are the 25th and 75th percentiles, the whiskers extend to ± 1.5 × the interquartile range, and the points outside are the outliers. The thick line inside the box represents the median and the circle is the mean. Five or 6 U pools of whole blood–derived platelets were considered equivalent to 1 U of apheresis platelets (eg, an adult dose of platelets).
  • Platelet Function During Extended Prasugrel and Clopidogrel Therapy for Patients With ACS Treated Without Revascularization: The TRILOGY ACS Platelet Function Substudy

    Abstract Full Text
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    JAMA. 2012; 308(17):1785-1794. doi: 10.1001/jama.2012.17312
    Gurbel and coauthors compare the effect of clopidogrel with prasugrel on platelet reactivity among 2564 patients—who were part of a substudy of the TRILOGY ASC trial—whose acute coronary syndromes, which did not include ST-segment elevation, were managed medically. In an editorial, Price discusses implications of the study for clinical practice and future research.
  • Measured Drug Effect and Cardiovascular Outcomes in Patients Receiving Platelet P2Y 12 Receptor Antagonists: Clarifying the Time and Place for Intensive Inhibition

    Abstract Full Text
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    JAMA. 2012; 308(17):1806-1808. doi: 10.1001/jama.2012.34011
  • JAMA November 7, 2012

    Figure 4: Kaplan-Meier Event Curves for the Primary Efficacy End Point, All-Cause Death, and All Myocardial Infarction Events

    Starting at the 30-day landmark time point and continuing through 30 months are shown for patients with vs without high platelet reactivity from the 30-day platelet function measurement. High platelet reactivity was defined as more than 208 P2Y12 reaction units (PRUs) and as more than 230 PRUs, as detailed in the “Methods” section. The P values shown on each panel compare the hazard between the 2 groups. The raw number of total events from 30 days through 30 months by those with or without high platelet reactivity for each panel are as follows: panel A: 133 vs 81; panel B: 87 vs 52; panel C: 78 vs 47; panel D: 150 vs 64; panel E: 95 vs 44; and panel F: 90 vs 35, respectively.
  • JAMA January 18, 2012

    Figure 2: Distribution of Platelet Reactivity During The Overall Study

    Platelet reactivity as assessed by PRU using the VerifyNow P2Y12 assay during the study time course (at baseline and up to 7 days of study drug infusion (2A) and at last sample taken prior to CABG (2B). Data are presented as median and interquartile range. PRU indicates P2Y12 reactivity units; CABG, coronary artery bypass grafting; dotted line, cut-off level of 240 PRU; ITT, intention to treat.
  • Bridging Antiplatelet Therapy With Cangrelor in Patients Undergoing Cardiac Surgery: A Randomized Controlled Trial

    Abstract Full Text
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    JAMA. 2012; 307(3):265-274. doi: 10.1001/jama.2011.2002
  • JAMA December 28, 2011

    Figure 1: Relationship Between CYP2C19 Genotype, Active Drug Metabolite, and Platelet Reactivity

    A, The expected mean active clopidogrel metabolite concentration in a white population for all individuals treated with 75 mg and for individuals with loss-of-function and normal/increased-function CYP2C19 alleles.a indicates mean active clopidogrel metabolite concentration regardless of genotype, area under the plasma concentration-time curve from the time of administration to the last measurable concentration (AUC0-t) = 0.35 μM × hr;b indicates difference in clopidogrel active metabolite concentration between *2 through *8 and *1 or *17, AUC0-t = 0.14 μM × hr. The central tendency and measure of dispersion are obtained from Mega et al: CYP2C19 *1 or *17 summary estimates were pooled from ultra and extensive metabolizer groups and *2 through*8 from intermediate and poor metabolizer groups. The heights of the plots are proportional to the allele frequency of *2 (the most common loss-of-function * allele; rs4244285 mean allele frequency = 0.13; European ancestry [NCBI Single Nucleotide Polymorphism database, http://www.ncbi.nlm.nih.gov/projects/SNP]); ie, as *1 is more common (87%) than *2 (13%), the height of the plot for the *1 or *17 group is higher than that for *2, reflecting the number within the population that will harbor this genotype. B, Meta-analysis of 4 treatment-only studies (4341 individuals) reporting CYP2C19 genotype and platelet reactivity after 600 mg of clopidogrel (using various assays). Error bars indicate 95% CIs.
  • JAMA November 23, 2011

    Figure 2: On-Treatment Platelet Reactivity Across Genotype and Clopidogrel Daily Dose

    VASP PRI indicates vasodilator-stimulated phosphoprotein phosphorylation assay platelet reactivity index.
  • JAMA November 23, 2011

    Figure 4: Difference in Platelet Reactivity Between CYP2C19*2 Heterozygotes Treated With Increasing Doses of Clopidogrel vs Noncarriers Treated With 75 mg of Clopidogrel Daily

    Data are reported as least squares differences and 95% confidence intervals for platelet reactivity between CYP2C19*2 heterozygotes at clopidogrel doses of 75 mg (n = 76), 150 mg (n = 73), 225 mg (n = 75), and 300 mg (n = 73) and noncarriers at 75 mg of clopidogrel (n = 237). Differences in least squares means were tested using asymptotic methods (normal z test). VASP indicates vasodilator-stimulated phosphoprotein phosphorylation assay.
  • Dosing Clopidogrel Based on CYP2C19 Genotype and the Effect on Platelet Reactivity in Patients With Stable Cardiovascular Disease

    Abstract Full Text
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    JAMA. 2011; 306(20):2221-2228. doi: 10.1001/jama.2011.1703
  • High Residual Platelet Reactivity After Clopidogrel Loading and Long-term Cardiovascular Events Among Patients With Acute Coronary Syndromes Undergoing PCI

    Abstract Full Text
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    JAMA. 2011; 306(11):1215-1223. doi: 10.1001/jama.2011.1332
  • JAMA September 21, 2011

    Figure 2: Kaplan-Meier Survival Curves for Primary End Point Events and for Cardiac Mortality in Patients With HRPR and LRPR

    HRPR indicates high residual platelet reactivity; LRPR, low residual platelet reactivity. Primary end point events included cardiac death, myocardial infarction, any urgent coronary revascularization, and stroke.
  • JAMA September 21, 2011

    Figure 3: Kaplan-Meier Landmark Analysis Survival Curves for Primary End Point Events and for Cardiac Mortality Beginning at 6 Months in Patients With HRPR and LRPR

    HRPR indicates high residual platelet reactivity; LRPR, low residual platelet reactivity. Primary end point events included cardiac death, myocardial infarction, any urgent coronary revascularization, and stroke.
  • JAMA March 16, 2011

    Figure 3: Pharmacodynamic Effect of High- and Standard-Dose Clopidogrel in Randomized Patients With High On-Treatment Platelet Reactivity

    High-dose clopidogrel resulted in significantly lower levels of on-treatment platelet reactivity at 30 days and 6 months than standard-dose clopidogrel (P < .001, respectively, not corrected for multiple comparisons). The horizontal line in the middle of each box indicates the median; the top and bottom borders of each box indicate the interquartile range (IQR). The whiskers above and below the box indicate plus/minus 1.5 IQRs, respectively.