ライフサイエンスコーパス: D-dimer

1 ctively, and a 12.5% (p = 0.042) decrease in D-dimer.

2 unts, tissue factor, soluble P-selectin, and D-dimer.

3 in plasminogen, and a 17.8% net increase in D-dimer.

4 sma levels of plasminogen activator and high D-dimers.

5 in C, plasminogen activator inhibitor-1, and D-dimers.

6 fibrinogen and von Willebrand factor; 9% for D-dimer, 1% for CRP, and 16% for t-PA.

7 .008; median [interquartile range]), higher D-dimer (16.1 [7.9-19.3] vs. 1.6 [1.1-4], p = .02 and 2.

8 studies, 5494 cases), 1.23 (1.16, 1.32) with D-dimer (18 studies, 6799 cases) and 1.16 (1.10, 1.22) w

9 antithrombin complex (14.5-50 microg/L), and D-dimers (6.00-27.0 mg/L) increased, whereas fibrinogen

10 tal addition of VACS Index components (10%), D-dimer (7%), and sCD14 (4%), but not from IL-6 (0%).

11 involved direct detection of CRP whereas for D-dimer a two-site immunoassay employing a biotinylated

12 D-dimer, a fibrin degradation product, generated followi

13 intravascular coagulation (DIC) (fibrinogen, D-dimer, alpha-2-antiplasmin, antitrombin, prothrombin t

14 .14) for t-PA antigen, 1.06 (1.00, 1.13) for D-dimer and 1.08 (1.02, 1.15) for VWF.

15 .33) for t-PA antigen, 1.01 (0.95, 1.07) for D-dimer and 1.11 (1.05, 1.18) for VWF.

16 d-dimer and cell injury markers (HMGB1, histones) confir

17 es PMA formation in vitro, along with plasma d-dimer and fibrinogen levels were also measured.

18 Increasing levels of D-dimer and inflammatory biomarkers are independently as

19 mong persons with PAD, circulating levels of D-dimer and inflammatory markers are higher in the 1 to

20 r there is any corelation of the Wells rule, D-dimer and LDH values with computerized tomography pulm

21 affecting lymphocytes, monocytes, platelets, D-dimer and liver function tests were observed 24 to 48

22 D-dimer and plasmin-antiplasmin complex levels increased

23 erone), thrombosis and endothelial function (D-dimer and plasminogen activator inhibitor type 1), and

24 flammation (C-reactive protein), hemostasis (D-dimer and plasminogen activator inhibitor-1), neurohor

25 rticipants, transient increases in levels of d-dimer and prothrombin fragments 1 and 2 were observed,

26 , amyloid-A, and amyloid-P) and coagulation (D-dimer and prothrombin-fragment 1+2) markers were deter

27 Addition of D-dimer and sCD14, but not IL-6, improves the predictive

28 D-dimer and soluble tissue factor levels were significan

29 ce, respectively, in natural-log-transformed D-dimer and together accounted for 1.8% of the total var

30 tissue plasminogen activator (t-PA) antigen, D-dimer and von Willebrand factor (VWF) with coronary he

31 Concentrations of t-PA antigen, D-dimer and VWF may be more modestly associated with fir

32 ng new preclinical safety tests, such as the d-dimer and/or the tissue plasminogen activator-to-plasm

33 , coagulation (prothrombin fragment F1+2 and d-dimer), and endothelial damage (thrombomodulin) marker

34 rleukin [IL]-6, and IL-10) and fibrinolysis (d-dimer), and lower coagulation biomarkers (antithrombin

35 mmation (interleukin 6 [IL-6]), coagulation (D-dimer), and monocyte activation (sCD14) also predict m

36 (interleukin-6 [IL-6]), altered coagulation (d-dimer), and monocyte activation (soluble CD14 [sCD14])

37 rs of Inflammation (CRP, IL-6), coagulation (D-dimer), and tissue fibrosis (HA) measured pre-ART and

38 hsCRP, IL-6, D-dimer, and cystatin C levels are elevated in persons w

39 ted in MESA study participants, hsCRP, IL-6, D-dimer, and cystatin C levels were 50%, 152%, 94%, and

40 eactive protein (hsCRP), interleukin (IL)-6, D-dimer, and cystatin C were compared in 494 HIV-infecte

41 CRP, TNF, sIL-6R, I-FABP, sCD14, D-dimer, and HA levels were elevated in acute HIV infect

42 st time, that higher levels of inflammation, D-dimer, and homocysteine are associated with more adver

43 re-ART and 1-month C-reactive protein (CRP), D-dimer, and interleukin 6 (IL-6) levels and pre-ART hya

44 Myeloperoxidase, D-dimer, and matrix metalloproteinase 9 were not modifie

45 ifference was observed in the levels of FDP, D-dimer, and MPV among the three groups of the patients.

46 Willebrand factor, prothrombin fragment 1-2, D-dimer, and plasmin antiplasmin) were measured.

47 Fibrinolytic components, d-dimer, and plasminogen activators were measured using

48 s calculated based on platelets, fibrinogen, d-dimer, and prothrombin index.

49 he VACS Index was more correlated with IL-6, D-dimer, and sCD14 than the Restricted Index (P < .001).

50 igher white blood cell count, blood glucose, D-dimer, and serum uric acid levels; and were more likel

51 ast, five markers (sICAM-1, IL-8, TNF-alpha, D-dimer, and sVCAM-1), all with ORs for the 3(rd) versus

52 sminogen activator inhibitor type 1 [PAI-1], D-dimer, and von Willebrand factor [vWF]) were measured

53 The PAI-1/tPA complexes, D-dimers, and prothrombin fragment F1 + 2 were measured

54 14 [sCD14]), coagulation cascade activation [D-dimer], and fibrosis (hyaluronic acid [HA]) were measu

55 D-dimer antigen can exist on fibrin degradation products

56 of 2 sections: in the first, the dynamics of D-dimer antigen formation is discussed and an overview o

57 The D-dimer antigen is a unique marker of fibrin degradation

58 ble evidence for the clinical utilization of D-dimer antigen measurement in VTE, as well as emerging

59 n gamma chains was selected to represent the D-dimer antigen.

60 e fibrin degradation products and expose the D-dimer antigen.

61 tions of tumor necrosis factor, IL-6, IL-10, d-dimer, antithrombin-III, and factor IX (adjusted HR =

62 We measured D-dimers, antithrombin, endogenous thrombin potential (E

63 Elevated levels of inflammatory markers and D-dimer are associated with greater functional impairmen

64 veloping an immunoassay that is specific for D-dimer arises from the inherent heterogeneity in its st

65 , activated partial thromboplastin time, and d-dimer as well as the DIC score differed significantly

66 nd markers of coagulation activation such as D-dimer, as well as predictive modeling.

67 ity, and diagnostic likelihood ratios of the D-dimer assay results were calculated.

68 perfusion lung scan, venous ultrasonography, d-dimer assay, and clinical assessment.

69 ) and underwent CT pulmonary angiography and D-dimer assay.

70 Wells score, in combination with a negative d-dimer assay.

71 obability of pulmonary embolism and negative d-dimer assay.

72 esults may not be generalizable to different D-dimer assays from the one used in the study.

73 ed and an overview of commercially available D-dimer assays is provided.

74 Results may not be generalizable to all D-dimer assays or patients with previous DVT, study pers

75 s in patient characteristics, use of various d-dimer assays, and limited statistical power to assess

76 in (beta=-0.21 per 1-SD increment; P=0.008), D-dimer (beta=-0.18 per 1-SD increment; P=0.041), total

77 26.6%-29.9%) and 337 patients (11.6%) had a D-dimer between 500 microg/L and their age-adjusted cuto

78 1 [sICAM-1]), and thrombotic (fibrinogen and D-dimer) biomarkers in a group of 32 untreated HIV-infec

79 likelihood that PE is present, followed by a D-dimer blood test and/or CTPA.

80 e bedside tools (clinical decision rules and D-dimer blood tests) for patients with low pretest proba

81 44-85%; P<0.001 for both), and reductions in D-dimer by 24% (95% CI, -30% to -18%), von Willebrand fa

82 Circulating levels of fibrinogen, fibrin D-dimer, C-reactive protein (CRP), tissue plasminogen ac

83 mbophilia, and inflammation (LDH, bilirubin, D-dimer, C-reactive protein [CRP]) improved.

84 Higher levels of D-dimer, C-reactive protein, and serum amyloid A were as

85 e plasminogen activator antigen, fibrinogen, D-dimer, C-reactive protein, insulin, and hemoglobin A(1

86 ted markers of the 18 tested (interleukin-6, d-dimer, coagulation factor VIII, von Willebrand factor,

87 n in whom plasma factor VIII activity and/or D-dimer concentration were elevated at diagnosis, from w

88 ted with VTE risk up to Day 10 (P=0.017) and D-dimer concentration with VTE risk up to Day 35 (P=0.00

89 As a result, D-dimer concentrations at 6, and 8 hours, and blood fibr

90 levels increased soon after start of NMP and D-dimer concentrations correlated significantly with lev

91 Baseline plasma D-dimer concentrations ranged from 0.6 to 1.7 mug/L for

92 ponin-T, creatine kinase-MB, fibrinogen, and D-Dimer concentrations were measured at baseline, at 1,

93 heir homes and blood-sampled for fibrinogen, D-dimer, CRP, t-PA, and von Willebrand factor.

94 Compared with a fixed D-dimer cutoff of 500 microg/L, the combination of prete

95 ants on the basis of a negative age-adjusted D-dimer cutoff result.

96 cal probability assessment with age-adjusted D-dimer cutoff was associated with a larger number of pa

97 Plasma levels of the coagulation biomarker D-dimer (DD) correlate with increased mortality and card

98 D-dimer (DD) is highly sensitive for AAS but is inadequa

99 D-dimer declined with ATV/r and DRV/r and was unchanged

100 Levels of PTF1+2, FDP, and D-dimer decreased as symptoms improved.

101 its detection; and 3) discusses the role of D-dimer determination in these various conditions.

102 High concentrations of D-dimer early after start of NMP can be considered a mar

103 D-dimer exhibited a peak at 14:00 hours, CRP at 15:00 ho

104 ive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and i

105 Reduced levels of D-dimer (fibrin degradation product) were evident in tic

106 physiology was observed as platelet counts, d-dimer, fibrinogen levels, and serum chemistries remain

107 Higher baseline D-dimer, fibrinogen, and C-reactive protein portended a

108 tests including ESR, CBC with differential, D-dimer, fibrinogen, C3, C4, IL-6, etc.

109 nhibitor-1, aldosterone, C-reactive protein, D-dimer, fibrinogen, homocysteine, and growth differenti

110 L-6 appeared to be a stronger predictor than D-dimer for CVD and non-AIDS-defining malignancies, but

111 s of tissue plasminogen activator, and lower d-dimer formation compared with nondiabetic AdMSCs.

112 s results, suggests a model in which the PGL DD dimer forms a fundamental building block for P-granul

113 in whom PE could be excluded on the basis of D-dimer from 43 of 673 patients (6.4% [95% CI, 4.8%-8.5%

114 s was revealed by a crystal structure of the D-dimer from human fibrinogen cocrystallized with GHRPYa

115 TF ELISA, soluble P-selectin, d-dimer, FVIII, and C-reactive protein were assayed.

116 lized ratio (INR) 1.3, fibrinogen 199 mg/dL, D-dimer greater than 1.0 mug/mL, and fibrin split produc

117 7.82 (1.95-31.38) in validation cohort for a D-dimer >4 mg/L vs </=4 mg/L.

118 In addition, D-dimer has been evaluated for determining the optimal d

119 Consequently, D-dimer has been extensively investigated for the diagno

120 lipoprotein particle concentration, leptin, d-dimer, homoarginine, and N-terminal pro B-type natriur

121 lasma concentrations of inflammatory markers D-dimer, IFN-gamma, and monokine induced by IFN-gamma th

122 ls and significant 1-month increases in CRP, D-dimer, IL-6, interleukin 8, CXCL10, TNF-alpha, and int

123 etermination of C-reactive protein (CRP) and D-dimer in human blood plasma based on a white light int

124 The structure, containing L- and D-dimers in a centrosymmetric space group, revealed unex

125 e investigated whether persistently negative D-dimers in patients with vein recanalization or stable

126 oluble [s]CD14 and sCD163), and coagulation (D-dimer) in HIV-infected and uninfected never, former, a

127 WR also increases blood level of D-dimer, indicative of ongoing coagulation and thromboly

128 Detectable hyaluronic acid and higher d-dimer, interleukin 6, interleukin 8, and soluble CD14

129 Matriptase processes the FL-D dimer into a GFD dimer (GFD-D) in a stepwise manner, i

130 D-dimer is a product of the coagulation cascade and is a

131 D-dimer is a soluble fibrin degradation product that res

132 This review: 1) describes how D-dimer is generated; 2) reviews the assays used for its

133 tPA and uPA, attenuated ICH, lowered plasma d-dimers, lessened thrombocytopenia, and improved neurol

134 , hsCRP level (-46% vs +15%; P < .0001), and D-dimer level (-40% vs +6%; P < .0001).

135 2.32), interleukin 6 level (aHR, 2.34), and D-dimer level (aHR, 1.95) were associated with mortality

136 inclusive cohorts: patients with an elevated d-dimer level (cohort 1), patients with an elevated d-di

137 ex, age older than 65 years, and an elevated D-dimer level 1 month after discontinuing anticoagulant

138 gh-sensitivity C-reactive protein level, and D-dimer level all strongly predicted mortality, even aft

139 sTNFR-I level, sTNFR-II level, KT ratio, and D-dimer level at year 1 were associated with the occurre

140 btain any imaging studies in patients with a d-dimer level below the age-adjusted cutoff.

141 The 3-month failure rate in patients with a D-dimer level higher than 500 microg/L but below the age

142 ly specific method for the quantification of D-dimer level in human plasma.

143 ical probability, 817 patients (28.2%) had a D-dimer level lower than 500 microg/L (95% CI, 26.6%-29.

144 level (cohort 1), patients with an elevated d-dimer level or an age of at least 75 years (cohort 2),

145 clinical or laboratory findings of elevated D-dimer level or elevated lactate dehydrogenase (LDH) le

146 atients with a Wells score </=4 and a normal d-dimer level or no d-dimer testing) (override group) an

147 ts with Wells score >4 or </=4 with elevated d-dimer level) (adherent group).

148 group (25 of 589 studies, none with a normal d-dimer level) and 11.2% in the adherent group (270 of 2

149 Intensification also reduced the D-dimer level, a coagulation biomarker that is predictiv

150 a statistically significant decrease in the D-dimer level, compared to placebo (P = .045).

151 asma biomarkers (interleukin 6 [IL-6] level, D-dimer level, high-sensitivity C-reactive protein [hsCR

152 cutely ill medical patients with an elevated d-dimer level, there was no significant difference betwe

153 el, kynurenine-to-tryptophan (KT) ratio, and D-dimer level.

154 esting for all participants (DVT excluded at D-dimer levels <0.5 microg/mL).

155 with low or moderate C-PTP (DVT excluded at D-dimer levels <1.0 microg/mL [low C-PTP] or <0.5 microg

156 </=3500 ng/mL), whereas significantly higher D-dimer levels (>3500 ng/mL) were in found in livers wit

157 blood platelet counts (P < .001) and higher D-dimer levels (P < .001).

158 Patients with high-grade tumors had higher D-dimer levels (P = .008) and leukocyte counts (P < .001

159 Valsartan and ramipril both lowered D-dimer levels (P<0.01 for both), whereas only ramipril

160 atient group in terms of elevated LDH or/and D-dimer levels (P=0.263 and P=1.000, respectively).

161 Normal D-dimer levels after withdrawal of anticoagulant therapy

162 mia patients had higher fibrinogen but lower d-dimer levels and platelet counts than drowning patient

163 Although elevated plasma D-dimer levels are associated with increased morbidity a

164 -sensitivity C-reactive protein (hsCRP), and D-dimer levels are linked to adverse outcomes in human i

165 Among all DIC parameters, D-dimer levels are most predictive for thrombosis with a

166 e PE is highly unlikely in these patients if d-dimer levels are normal.

167 -sensitivity C-reactive protein (hsCRP), and D-dimer levels at baseline and weeks 24 and 48.

168 terminal pro-B-type natriuretic peptide, and d-dimer levels at baseline.

169 e [CLT]) and a 5% slower rate of increase in D-dimer levels during clot degradation (D-Drate; all P <

170 21%), an unlikely score combined with normal d-dimer levels excluded UEDVT.

171 d-Dimer levels in blood specimens were drastically incre

172 In both patients, plasma D-dimer levels increased with clinical evidence of disea

173 cholesterol decreased significantly, whereas D-dimer levels increased.

174 We present 2 cases that indicate that D-dimer levels may be useful as a potential biochemical

175 Thus, quantification of D-dimer levels serves an important role in guiding thera

176 omal chromosomes and natural-log-transformed D-dimer levels using linear regression in additive genet

177 tigation of the genomic correlates of plasma D-dimer levels was conducted among 21 052 European-ances

178 PT, PTT, Va, VIIIa, PC aPC t-PA, and D-dimer levels were assayed.

179 Elevated plasma D-dimer levels were associated with acute C1-INH-HAE att

180 Higher sCD14, CRP, and D-dimer levels were associated with higher peripheral bl

181 rtiles and log2-transformed IL-6, hsCRP, and D-dimer levels were calculated using Cox models.

182 Median plasma D-dimer levels were comparable across treatment groups a

183 2550 [310-8410] mug/l saline); median plasma D-dimer levels were decreased by Day 7 in both groups (4

184 Plasma D-dimer levels were elevated in 80% of the patients (med

185 terminal pro-B-type natriuretic peptide, and d-dimer levels were measured at baseline.

186 nd small HDLp) and higher IL-6, sICAM-1, and D-dimer levels, and the relationship of these markers to

187 CCR5(+) monocytes positively associated with D-dimer levels, CCR2(+) monocytes were inversely associa

188 was reflected by up to 1,000-fold increased d-dimer levels, greater than 5-fold elevated plasmin ant

189 F5 and FGA loci known to be associated with D-dimer levels, there was no evidence of an additional a

190 ; in those with an unlikely score and normal d-dimer levels, UEDVT was excluded.

191 To identity genetic loci influencing D-dimer levels, we performed the first large-scale, geno

192 ch clinical disease activity correlates with D-dimer levels.

193 onth-old chronic residual thrombi and normal D-dimer levels.

194 omplexes, endogenous thrombin potential, and D-dimer levels.

195 ggested on the basis of isolated measures of D-dimer levels.

196 Three genes were associated with fibrin D-dimer levels.

197 f plasminogen activator inhibitor-1 and high D-dimer levels.

198 ad a Wells score of 4 or less and had normal d-dimer levels.

199 gnificantly associated with higher sCD14 and D-dimer levels.

200 levels but normalization of TNF, sIL-6R, and D-dimer levels.

201 n test showed no correlation between LDH and D-dimer levels.

202 fected C-reactive protein, interleukin 6, or D-dimer levels.

203 ctor-a, sE-selectin, von Willebrand factors, d-dimers, matrix metalloproteinases, oxidative stress an

204 ntify high short-term risk, whereas elevated D-dimer may be suggestive of high midterm risk.

205 Clinicians should obtain a high-sensitivity d-dimer measurement as the initial diagnostic test in pa

206 The clinical utility of D-dimer measurement has been established in some scenari

207 Despite its importance, D-dimer measurement has limited clinical utility due in

208 Clinicians should not obtain a d-dimer measurement in patients with a high pretest prob

209 D-dimer measurement is an important step in the diagnost

210 Serial D-dimer measurement is suitable in clinical practice for

211 icularly computed tomography (CT) and plasma d-dimer measurement, may not improve care while potentia

212 2-level Wells score for PE; highly sensitive D-dimer measurement; and computed tomography pulmonary a

213 We show the potential value of D-dimer measurements as a marker of vasculocentric and/o

214 CTICE ADVICE 2: Clinicians should not obtain d-dimer measurements or imaging studies in patients with

215 They received serial D-dimer measurements using commercial assays with predef

216 Fibrin fragment D-dimer, one of several peptides produced when crosslink

217 , 2.25; 95% CI, 1.60-3.16, respectively) and d-dimer (OR, 1.97; 95% CI, 1.44-2.71, OR, 1.68; 95% CI,

218 Higher D-dimer (p < 0.001), sVCAM-1 (p < 0.001), and homocystei

219 and P = .02), sICAM-1 (P < .01 for both) and D-dimer (P = .03 and p < .01).

220 IP-10 (P = .0011), TNF-RII (P = .0002), and D-dimer (P = .0444) were also found in coinfected patien

221 but not with C-reactive protein (P = .65) or D-dimer (P = .08) among patients with HIV.

222 f IL-6 (P < .001) but not hsCRP (P = .15) or D-dimer (P = .20) as a predictor for different end point

223 Higher levels of D-dimer (p = 0.014), C-reactive protein (CRP) (p = 0.002

224 Fibrinogen (P<0.05) and D-Dimer (P<0.05) concentrations were significantly eleva

225 prothrombin fragment F1 + 2 (P = 0.031) and D-dimers (P = 0.044) were significantly lower in plasma

226 , tissue factor, prothrombin split products, D-dimer, P-selectin, factor VIII and C-reactive protein.

227 oximal DVT alone, higher C-reactive protein, D-dimer, peak thrombin, lower Ks, shorter lag phase, dec

228 t F1 + 2 (marker of coagulation activation), D-dimer, plasmin-antiplasmin complex, tissue plasminogen

229 ted to plasma levels of interleukin-6 and to D-dimer products of fibrinolysis.

230 ed levels and future VTE have been found for d-dimer, prothrombin fragment 1+2, and soluble P-selecti

231 d-dimer, prothrombin fragment F1.2 and TATc concentratio

232 ight velocity was positively associated with D-dimer (ratio of geometric means = 1.11, 95% CI: 1.01,

233 levels also correlated with plasma levels of D-dimers, reflective of in vivo clot formation and fibri

234 meter grafts without an apparent increase in D-dimer release from thrombi, and prevented the occlusio

235 Age, sex, referral setting, and D-dimer result, as well as seven possible risk factors,

236 In 319 patients (78%) who had 2 negative D-dimer results and did not restart anticoagulant therap

237 D-Dimer results have high NPV and sensitivity for PE in

238 ith a first unprovoked VTE who have negative D-dimer results is not low enough to justify stopping an

239 D-Dimer results were positive in 171 patents (85%).

240 Numerous studies have shown that D-dimer serves as a valuable marker of activation of coa

241 active protein, interleukin-6 (IL-6), GlycA, D-dimer, soluble CD14 (sCD14), sCD163, and sIL-2r; blood

242 processing regulates the deposition of PDGF-D dimer species into the extracellular matrix (ECM) with

243 Age-adjusted cutoff levels increase D-dimer specificity and may decrease overuse of imaging

244 n a "PE-unlikely" Wells score and a negative d-dimer test result (efficiency) was estimated using fix

245 Anticoagulant therapy was stopped if D-dimer test results were negative and was not restarted

246 an unlikely clinical probability and normal D-dimer test was 0.5% (95% confidence interval [CI], 0.0

247 solely with a negative result from a plasma D-dimer test.

248 Wells score of 4 or less but did not undergo d-dimer testing and 26 had a Wells score of 4 or less an

249 up and the proportion of patients undergoing D-dimer testing and ultrasonography.

250 lls score of 4 or less, CDS alerts suggested d-dimer testing because acute PE is highly unlikely in t

251 uced the proportion of patients who required D-dimer testing by 21.8 percentage points (CI, 19.1 to 2

252 ts, or uniform testing (n = 863), defined as D-dimer testing for all participants (DVT excluded at D-

253 e C-PTP]) and venous ultrasonography without D-dimer testing for outpatients with high C-PTP and inpa

254 Selective testing (n = 860), defined as D-dimer testing for outpatients with low or moderate C-P

255 Most overrides were due to the lack of d-dimer testing in patients unlikely to have PE.

256 cluded based on a clinical decision rule and D-dimer testing in patients with a delayed clinical pres

257 the utility of clinical prediction rules and D-dimer testing in the diagnosis of VTE in the patient w

258 Age-adjusted d-dimer testing is associated with a 5% absolute increas

259 e index event was PE rather than DVT, and/or d-dimer testing is positive 1 month after stopping antic

260 D-Dimer testing is sensitive but not specific for diagno

261 A selective D-dimer testing strategy seems as safe as and more effic

262 d-Dimer testing was done locally.

263 The failure rate of age-adjusted d-dimer testing was less than 3% in all examined subgrou

264 more efficient than having everyone undergo D-dimer testing when diagnosing a first episode of suspe

265 D-dimer testing yielded a sensitivity of 99% (95% CI, 96

266 score </=4 and a normal d-dimer level or no d-dimer testing) (override group) and those in whom prov

267 he combination of a clinical decision score, d-dimer testing, and ultrasonography can safely and effe

268 gorithm combining a clinical decision score, d-dimer testing, and ultrasonography has not been evalua

269 al application of a clinical decision score, d-dimer testing, and ultrasonography.

270 is of a clinical decision rule combined with D-dimer testing.

271 the dichotomized Wells rule and quantitative d-dimer testing.

272 g can be safely withheld compared with fixed d-dimer testing.

273 ts with chest pain, our carrying out LDH and D-Dimer tests will not exclude PTE without CTPA.

274 and MHRPYam) complexed with fibrin fragment D-dimer; the modeling of various other side chains showe

275 when the age-adjusted (instead of the fixed) d-dimer threshold was applied.

276 ADVICE 4: Clinicians should use age-adjusted d-dimer thresholds (age x 10 ng/mL rather than a generic

277 ge x 10 microg/L in patients aged >50 years) d-dimer thresholds; their 3-month incidence of symptomat

278 or inhibitor-1, plasmin-antiplasmin complex, D-dimer, thrombin activatable fibrinolysis inhibitor, an

279 factor IX, plasminogen activator inhibitor, d-dimer, thrombin antithrombin complex), and lymphocyte

280 tions of tissue plasminogen activator (tPA), d-dimer, thrombin-antithrombin complex, and cytokines (I

281 tor, interleukin-6, and -10); "coagulation" (D-dimers, thrombin-antithrombin complex); "oxidative str

282 d little difference among measured levels of D-dimer, tissue factor, or F1+2 between HIV-infected ind

283 tor, fibrinogen, factor XIII), fibrinolysis (D-dimer, tissue-type plasminogen activator, plasminogen

284 rix (ECM) with increased binding from the FL-D dimer, to the HD, and to the GFD-D.

285 markers (white blood cell count, fibrinogen, D-dimer, troponin T, N-terminal pro-brain natriuretic pe

286 urement in VTE, as well as emerging areas of D-dimer utilization as a marker of coagulation activatio

287 Patients with a D-dimer value between the conventional cutoff of 500 mic

288 -A, fibroblast growth factor-2), thrombosis (D-dimer, von Willebrand factor, thrombin-antithrombin II

289 diography was 86% to 100% sensitive, whereas D-dimer was 51.7% to 100% sensitive and 32.8% to 89.2% s

290 In addition, the concentration of D-dimer was elevated significantly.

291 Levels of IL-6, sICAM-1, and D-dimer were 65%-70% higher in HIV-infected participants

292 Plasma levels of D-dimer were measured independently in each of 13 cohort

293 ion, including C-reactive protein level, and D-dimer were not associated with sCD163 or plaque among

294 okines, thrombin-antithrombin complexes, and D-dimer were not different between nonsurvivors and surv

295 tion during NMP, perfusate levels of ALT and D-dimers were low (</=3500 ng/mL), whereas significantly

296 tivity, thrombin-antithrombin complexes, and D-dimers were measured as procoagulant markers and marke

297 on and PAC-1 binding, fibrinogen levels, and d-dimers were not associated with VTE.

298 evels of fibrin degradation products (plasma D-dimers) were assessed before study drug administration

299 ross-linked fibrin cleavage product protein, d-dimer, were significantly decreased in NP compared wit

300 ed in 528 (52.3%) with persistently negative D-dimer who subsequently experienced 25 recurrences (3.0