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1 in plasminogen, and a 17.8% net increase in D-dimer.
2 ctively, and a 12.5% (p = 0.042) decrease in D-dimer.
3 atriuretic peptide, interleukin-6 level, and D-dimers.
5 antithrombin complex (14.5-50 microg/L), and D-dimers (6.00-27.0 mg/L) increased, whereas fibrinogen
6 ive protein (198 vs. 107 mg/L, P = .010) and D-dimer (8.6 vs. 2.1 ug/mL, P = .004) levels, and lower
7 involved direct detection of CRP whereas for D-dimer a two-site immunoassay employing a biotinylated
9 e YF, we found high concentrations of plasma D-dimer, a fibrin split product, suggestive of a concurr
12 cile increase), and higher concentrations of D-dimer (aHR 1.10 [1.01-1.19] per decile increase) were
13 intravascular coagulation (DIC) (fibrinogen, D-dimer, alpha-2-antiplasmin, antitrombin, prothrombin t
19 OVID-19 presents with prominent elevation of D-dimer and fibrin/fibrinogen-degradation products, wher
22 r there is any corelation of the Wells rule, D-dimer and LDH values with computerized tomography pulm
25 rticipants, transient increases in levels of d-dimer and prothrombin fragments 1 and 2 were observed,
27 trunk and to study the relation between the D-dimer and the uni- or bilateralism of the lesions and
28 e at the interface of the two domains of the DS dimer and confirms the design strategy for allosteric
30 of coagulation (eg, as measured with plasma D-dimer) and thrombocytopenia have emerged as prognostic
31 , coagulation (prothrombin fragment F1+2 and d-dimer), and endothelial damage (thrombomodulin) marker
33 lder age; elevated C-reactive protein (CRP), D-dimer, and fibrinogen levels; tachycardia; thrombocyto
35 tes mellitus, higher body mass index, higher d-dimer, and greater severity of hypoxemia on ICU admiss
38 ifference was observed in the levels of FDP, D-dimer, and MPV among the three groups of the patients.
40 ng high-sensitivity C-reactive protein, IL6, d-dimer, and systemic tumor necrosis factor receptors I
42 sminogen activator inhibitor type 1 [PAI-1], D-dimer, and von Willebrand factor [vWF]) were measured
43 al pro B-type natriuretic peptide, ferritin, D-dimers, and cardiac troponin in addition to high C-rea
45 f coagulation exacerbation as fibrinogen and D-dimers, and were increased in patients requiring invas
46 14 [sCD14]), coagulation cascade activation [D-dimer], and fibrosis (hyaluronic acid [HA]) were measu
48 , activated partial thromboplastin time, and d-dimer as well as the DIC score differed significantly
53 s in patient characteristics, use of various d-dimer assays, and limited statistical power to assess
54 n peptides that are responsible for covalent D-dimer association, as well as dozens of novel cross-li
55 Measurement of clinical plasma sample with a D-dimer at concentration of 437 ng/mL with 15 biofunctio
57 enia, and elevation in inflammatory markers, D-dimer, B-type natriuretic peptide, IL-6, and IL-10 lev
58 suggest the potential for implementation of D-dimer based protocols to reduce low-yield CTPA orderin
59 26.6%-29.9%) and 337 patients (11.6%) had a D-dimer between 500 microg/L and their age-adjusted cuto
60 e bedside tools (clinical decision rules and D-dimer blood tests) for patients with low pretest proba
61 44-85%; P<0.001 for both), and reductions in D-dimer by 24% (95% CI, -30% to -18%), von Willebrand fa
63 dly elevated inflammatory markers (ferritin, D-dimer, C-reactive protein) and elevated neutrophil:lym
64 patients testing positive for COVID-19, and d-dimer can be used to stratify patients in terms of PE
66 C-reactive protein, procalcitonin, ferritin, D-dimer, cardiac troponin T, and N-terminal pro-B-type n
68 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
71 levels increased soon after start of NMP and D-dimer concentrations correlated significantly with lev
73 ponin-T, creatine kinase-MB, fibrinogen, and D-Dimer concentrations were measured at baseline, at 1,
74 te ED patients who had any of the following: D-dimer, CTPA, scintillation ventilation perfusion lung
76 s 50.7%) when compared with the conventional D-dimer cutoff level to rule out thromboembolic disease
77 stimated glomerular filtration rate-adjusted D-dimer cutoff levels (> 333 ug/L [estimated glomerular
81 acteristics were also observed when adjusted D-dimer cutoff levels were applied in patients with acut
85 cal probability assessment with age-adjusted D-dimer cutoff was associated with a larger number of pa
92 ive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and i
94 physiology was observed as platelet counts, d-dimer, fibrinogen levels, and serum chemistries remain
95 roponins, plasminogen activator inhibitor-1, D-dimer, fibrinogen, C-reactive protein, sST2, galectin-
97 nhibitor-1, aldosterone, C-reactive protein, D-dimer, fibrinogen, homocysteine, and growth differenti
98 L-6 appeared to be a stronger predictor than D-dimer for CVD and non-AIDS-defining malignancies, but
99 s results, suggests a model in which the PGL DD dimer forms a fundamental building block for P-granul
100 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%
102 lized ratio (INR) 1.3, fibrinogen 199 mg/dL, D-dimer greater than 1.0 mug/mL, and fibrin split produc
104 ciated complications during hospitalization (D-dimer >2500 ng/mL, adjusted odds ratio [OR] for thromb
108 (hazard ratio, 1.09 [95% CI, 1.08-1.11]) and D-dimer (hazard ratio, 1.10 [95% CI, 1.02-1.20]) predict
109 essment score, lower PaO2/FIO2 ratio, higher D-dimer, higher C-reactive protein, and receipt of mecha
110 lipoprotein particle concentration, leptin, d-dimer, homoarginine, and N-terminal pro B-type natriur
111 etermination of C-reactive protein (CRP) and D-dimer in human blood plasma based on a white light int
113 e investigated whether persistently negative D-dimers in patients with vein recanalization or stable
114 oluble [s]CD14 and sCD163), and coagulation (D-dimer) in HIV-infected and uninfected never, former, a
119 Ultrasound evaluation is recommended if D-dimer is greater than 2,000 ng/mL (sensitivity 95%, sp
120 %) and empiric anticoagulation considered if D-dimer is greater than 5,500 ng/mL (sensitivity 53%, sp
123 p = 0.013) and in patients with a decline in D-dimer less than or equal to 50% (odds ratio, 2.76; p =
124 tPA and uPA, attenuated ICH, lowered plasma d-dimers, lessened thrombocytopenia, and improved neurol
125 2.32), interleukin 6 level (aHR, 2.34), and D-dimer level (aHR, 1.95) were associated with mortality
126 inclusive cohorts: patients with an elevated d-dimer level (cohort 1), patients with an elevated d-di
128 4.1 +/- 1.1 [95% CI: 13.8, 14.4]; P = .035), d-dimer level (P < .001), lactate dehydrogenase level (P
129 gh-sensitivity C-reactive protein level, and D-dimer level all strongly predicted mortality, even aft
131 sTNFR-I level, sTNFR-II level, KT ratio, and D-dimer level at year 1 were associated with the occurre
133 The 3-month failure rate in patients with a D-dimer level higher than 500 microg/L but below the age
134 ical probability, 817 patients (28.2%) had a D-dimer level lower than 500 microg/L (95% CI, 26.6%-29.
135 luded 315 patients who had a low C-PTP and a d-dimer level of 500 to 999 ng per milliliter (95% CI, 0
137 st that pulmonary embolism is ruled out by a d-dimer level of less than 1000 ng per milliliter in pat
138 esting in outpatients with a low C-PTP and a d-dimer level of less than 1000 ng per milliliter or wit
139 linical pretest probability (C-PTP) and by a d-dimer level of less than 500 ng per milliliter in pati
140 dered to be ruled out with a low C-PTP and a d-dimer level of less than 500 ng per milliliter would r
142 level (cohort 1), patients with an elevated d-dimer level or an age of at least 75 years (cohort 2),
143 clinical or laboratory findings of elevated D-dimer level or elevated lactate dehydrogenase (LDH) le
144 atients with a Wells score </=4 and a normal d-dimer level or no d-dimer testing) (override group) an
146 none of the three criteria were met and the d-dimer level was less than 1000 ng per milliliter or if
148 f the pulmonary trunk and the correlation of D-dimer level with the uni-or bilateralism of the lesion
150 group (25 of 589 studies, none with a normal d-dimer level) and 11.2% in the adherent group (270 of 2
152 asma biomarkers (interleukin 6 [IL-6] level, D-dimer level, high-sensitivity C-reactive protein [hsCR
153 e dehydrogenase (LDH) level, ferritin level, d-dimer level, neutrophil count, and neutrophil-to-lymph
154 cutely ill medical patients with an elevated d-dimer level, there was no significant difference betwe
157 </=3500 ng/mL), whereas significantly higher D-dimer levels (>3500 ng/mL) were in found in livers wit
159 hite blood cell count (P = .005), and higher D-dimer levels (P = .044) were also significantly associ
160 vs 5, p<0.002), were associated with higher D-dimer levels (p<0.01) and were associated with more se
161 I (P=0.003), higher WBC (P=0.005) and higher D-dimer levels (P=0.044) were also significantly associa
162 atient group in terms of elevated LDH or/and D-dimer levels (P=0.263 and P=1.000, respectively).
164 mia patients had higher fibrinogen but lower d-dimer levels and platelet counts than drowning patient
165 strongest" weak correlation resulted between D-dimer levels and the axial diameter of the pulmonal tr
166 -sensitivity C-reactive protein (hsCRP), and D-dimer levels are linked to adverse outcomes in human i
171 ly reported fever and myalgia, and had lower D-dimer levels compared to White patients (p&0.05).
172 ary embolisms and the degree of elevation of D-dimer levels does not differ between patients with COV
173 e [CLT]) and a 5% slower rate of increase in D-dimer levels during clot degradation (D-Drate; all P <
175 tudy was to evaluate the correlation between D-dimer levels in positive thromboembolic thoracic compu
178 rter reaction times compared with those with D-dimer levels less than or equal to 2,000 (4.8 vs 5.6 m
179 line low BMI and hemoglobin and high CRP and D-dimer levels may be clinically useful predictors of IR
181 There were no significant differences in D-dimer levels or the location of pulmonary embolisms be
188 2550 [310-8410] mug/l saline); median plasma D-dimer levels were decreased by Day 7 in both groups (4
191 CCR5(+) monocytes positively associated with D-dimer levels, CCR2(+) monocytes were inversely associa
192 was reflected by up to 1,000-fold increased d-dimer levels, greater than 5-fold elevated plasmin ant
193 s stasis activated fibrinolysis, measured by D-dimer levels, in alpha2AP(-/-) mice vs alpha2AP(+/+) m
194 ignificant effect on plasma interleukin-6 or D-dimer levels, nor on monocyte/T-cell activation, mucos
208 a-free hemoglobin, platelets, and decline in D-dimer <= 50% the day after decannulation), cannula siz
209 ine low BMI and hemoglobin, and high CRP and D-dimer may be clinically useful predictors of IRIS and
211 Clinicians should obtain a high-sensitivity d-dimer measurement as the initial diagnostic test in pa
215 icularly computed tomography (CT) and plasma d-dimer measurement, may not improve care while potentia
216 2-level Wells score for PE; highly sensitive D-dimer measurement; and computed tomography pulmonary a
218 CTICE ADVICE 2: Clinicians should not obtain d-dimer measurements or imaging studies in patients with
221 ge, renal function, or biomarkers except for D-dimer (median, 12,858 ng/mL [interquartile range, 3,17
222 We have discovered that the domain-swapped (DS) dimer of hCRBPII undergoes a large and robust confor
227 Linear regression showed that increased D-dimer ordering correlated with increased PE yield rate
229 IP-10 (P = .0011), TNF-RII (P = .0002), and D-dimer (P = .0444) were also found in coinfected patien
230 f IL-6 (P < .001) but not hsCRP (P = .15) or D-dimer (P = .20) as a predictor for different end point
232 prothrombin fragment F1 + 2 (P = 0.031) and D-dimers (P = 0.044) were significantly lower in plasma
233 >=2 dose-adjustment criteria, reductions in D-dimers (p interaction = 0.20) and PF1+2 (p interaction
234 oximal DVT alone, higher C-reactive protein, D-dimer, peak thrombin, lower Ks, shorter lag phase, dec
235 t F1 + 2 (marker of coagulation activation), D-dimer, plasmin-antiplasmin complex, tissue plasminogen
236 sus warfarin on population pharmacokinetics, D-dimer, prothrombin fragment 1 + 2 (PF1+2), and clinica
237 In 319 patients (78%) who had 2 negative D-dimer results and did not restart anticoagulant therap
238 ith a first unprovoked VTE who have negative D-dimer results is not low enough to justify stopping an
241 active protein, interleukin-6 (IL-6), GlycA, D-dimer, soluble CD14 (sCD14), sCD163, and sIL-2r; blood
243 processing regulates the deposition of PDGF-D dimer species into the extracellular matrix (ECM) with
245 moderate C-PTP (40 patients) and a negative d-dimer test (i.e., <1000 or <500 ng per milliliter, res
246 rly if concomitant proximal DVT), a positive d-dimer test after stopping anticoagulation, an antiphos
248 n a "PE-unlikely" Wells score and a negative d-dimer test result (efficiency) was estimated using fix
250 f the low specificity and sensitivity of the d-dimer test, all pregnant women with suspected pulmonar
251 Wells score of 4 or less but did not undergo d-dimer testing and 26 had a Wells score of 4 or less an
252 ssessment of pretest probability followed by D-dimer testing and imaging with venous ultrasonography.
254 ng thromboembolic disease typically includes D-dimer testing and use of clinical scores in patients w
255 lls score of 4 or less, CDS alerts suggested d-dimer testing because acute PE is highly unlikely in t
258 e index event was PE rather than DVT, and/or d-dimer testing is positive 1 month after stopping antic
262 score </=4 and a normal d-dimer level or no d-dimer testing) (override group) and those in whom prov
263 he combination of a clinical decision score, d-dimer testing, and ultrasonography can safely and effe
264 gorithm combining a clinical decision score, d-dimer testing, and ultrasonography has not been evalua
270 ADVICE 4: Clinicians should use age-adjusted d-dimer thresholds (age x 10 ng/mL rather than a generic
271 ge x 10 microg/L in patients aged >50 years) d-dimer thresholds; their 3-month incidence of symptomat
272 tions of tissue plasminogen activator (tPA), d-dimer, thrombin-antithrombin complex, and cytokines (I
273 tor, interleukin-6, and -10); "coagulation" (D-dimers, thrombin-antithrombin complex); "oxidative str
274 hrombin time international normalized ratio, D-dimer, tissue plasminogen activator (tPA), plasminogen
275 rinogen, activated partial prothrombin time, D-dimer, tissue plasminogen activator (tPA), plasminogen
278 markers (white blood cell count, fibrinogen, D-dimer, troponin T, N-terminal pro-brain natriuretic pe
279 d-dimer level was 1774 ng/mL and 6432 ng/mL d-dimer units in CT pulmonary angiography-negative and C
283 us disease 2019 include obesity, an elevated d-dimer value, elevated C-reactive protein level, and a
287 -A, fibroblast growth factor-2), thrombosis (D-dimer, von Willebrand factor, thrombin-antithrombin II
288 diography was 86% to 100% sensitive, whereas D-dimer was 51.7% to 100% sensitive and 32.8% to 89.2% s
291 AT (thrombin-antithrombin complex), APC, and D-dimer were monitored over 8 hours after infusion of re
292 okines, thrombin-antithrombin complexes, and D-dimer were not different between nonsurvivors and surv
293 tion during NMP, perfusate levels of ALT and D-dimers were low (</=3500 ng/mL), whereas significantly
295 tivity, thrombin-antithrombin complexes, and D-dimers were measured as procoagulant markers and marke
298 evels of fibrin degradation products (plasma D-dimers) were assessed before study drug administration
299 ated an allosteric metal binding site in the DS dimer, where ligand binding results in a reversible 5
300 ed in 528 (52.3%) with persistently negative D-dimer who subsequently experienced 25 recurrences (3.0