Search

Introduction: Recent animal studies show rADAMTS13 (vWF cleaving protease) to block tPA-induced BBB opening, reducing tPA-related hemorrhage and augmenting tPA’s thrombolytic effect. From proteomic screening, we found ADAMTS13/vWF to be an important pathway in tPA responders. Thus, the vWF/ADAMTS13 (vWF cleaving protease) axis may be an important modifier of tPA response in the clinical setting. But the effect of tPA on the ADAMTS13/vWF balance has not been studied directly in stroke patients post-tPA. Here we measured vWF and ADAMTS13 in acute ischemic stroke patients post IV tPA to investigate their clinical utility to follow tPA response. Methods: Quantitative Mass Spectrometry (MS), latex immuno-turbidimetric assay, and ELISA were performed in acute ischemic stroke plasma over time, with clinical outcome measured at 3 months. Response was defined per NINDS trial as mRankins= 4 points improvement on NIHSS. Results: Post tPA (up to 72 hours), ADAMTS13 is persistently and significantly higher in tPA responders than in non-responders (Figure 1A). Conversely, within 72 hrs post tPA, the ratio of vWF/ADAMTS13 (a measure of clot burden vs clot lysis) is significantly higher in tPA patients who did not improve compared to those who did. tPA patients also had lower vWF/ADAMTS13 ratios than non-tPA strokes (Figure 1B). Conclusion: Through dynamic changes detected in the vWF/ADAMTS13 pathway, our data suggest the balance of clot burden vs lysis is crucial in tPA response as measured in patient plasma in real time. More vWF degradation in tPA patients via ADAMTS13 is correlated to better clinical outcome within the first 72 hours, and conversely, increased clot burden was found in tPA non-responders. Studying endogenous ADAMTS13 activity in tPA response is an initial step to obtain evidence for its potential clinical utility. And vWF/ADAMTS13 ratio may be a biologically relevant and potentially clinically useful marker of clotting/lytic status in early thrombolysis.

Objective To identify characteristics differentiating the node-first presentation of Kawasaki disease (NFKD) from bacterial cervical lymphadenitis (BCL) and typical Kawasaki disease (KD). Study design From our prospectively collected database, we compared clinical, laboratory, and imaging characteristics of NFKD and BCL cohorts and performed multivariable logistic regression to identify variables that distinguish NFKD from BCL. We then compared outcomes of patients with NFKD and patients with typical KD treated during the same period. Results Over 7 years, 57 patients were hospitalized for NFKD, 78 for BCL, and 287 for typical KD. Patients with NFKD were older and had more medical encounters and longer duration of illness before the correct diagnosis was made than did patients with BCL. Of patients with NFKD, 33% had an admission diagnosis of bacterial adenitis or abscess. Compared with patients with BCL, patients with NFKD had lower leukocyte (white blood cell), hemoglobin, and platelet counts and higher absolute band counts (ABCs), C-reactive protein (CRP), alanine transaminase and γ-glutamyl transpeptidase levels, and erythrocyte sedimentation rates. In the multivariable analysis, smaller nodes, lower white blood cell count, and higher ABC and CRP were independently associated with NFKD. Patients with NFKD had multiple enlarged solid nodes and comparable rates of retropharyngeal edema. Compared with patients with typical KD, patients with NFKD were older, had more severe inflammation, and had similar rates of coronary artery abnormalities and resistance to intravenous immune globulin. Conclusions High ABC and CRP values and multiple enlarged solid nodes in febrile patients with cervical adenopathy should prompt consideration of NFKD to prevent delayed diagnosis of KD. Retropharyngeal edema on radiography should not dissuade from the diagnosis of NFKD.

Overcrowding and prolonged patient length-of-stay (LOS) in emergency departments (EDs) are growing problems. We evaluated the impact of implementing a rapid whole blood quantitative D-dimer test (Biosite Triage, Biosite Diagnostics, San Diego, CA) in our ED satellite laboratory on 252 patients before vs 211 patients after implementation. All patients also underwent testing with the existing central laboratory method (VIDAS D-dimer, bioMérieux, Durham, NC). D-dimer turnaround time (from blood draw to result) decreased approximately 79% (approximately 2 hours vs 25 minutes). The mean ED LOS declined from 8.46 to 7.14 hours (P = .016). Hospital admissions decreased 13.8%, ED discharges increased 7.3%, and the number of patients admitted for observation increased 6.4% (P = .005). No difference in the utilization of radiologic studies was observed (P = .86). At 3 months' follow-up, none of the after-implementation patients with negative D-dimer results were admitted for subsequent venous thromboembolic disease. The rapid D-dimer test was associated with a shorter ED LOS and fewer hospital admissions.