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Ivanova J.I.,Analysis Group Inc. | Bergman R.,Analysis Group Inc. | Birnbaum H.G.,Analysis Group Inc. | Colice G.L.,Washington Hospital Center | And 2 more authors.
Journal of Allergy and Clinical Immunology | Year: 2012

Background: Health care costs increase in patients with more severe asthma, but the effect of asthma exacerbations on costs among patients with more severe asthma has not been quantified. Objective: This study compared direct health care costs between patients with moderate/severe persistent asthma with and without exacerbations. Methods: Patients who had an asthma diagnosis (International Classification of Diseases-ninth revision-Clinical Modification code 493.x), were 12 to 64 years old, and were receiving controller therapy were identified from a large administrative claims database. Patients were categorized as having moderate/severe persistent asthma and were further evaluated for exacerbations during a 12-month exacerbation identification period. Patients with 1 or more exacerbations (asthma-related inpatient or emergency department visit or corticosteroid prescription) were matched to patients without exacerbations on demographic characteristics and asthma severity. Total and asthma-related health care costs during the 1-year study period after the exacerbation index date were calculated. Results: Patients with exacerbations had significantly higher total health care costs ($9223 vs $5011, P <.0001) and asthma-related costs ($1740 vs $847, P <.0001). The cost differences remained significant after controlling for patient differences by using multivariate models. Patients with exacerbations (n = 3830) had higher rates of sinusitis, allergy-related diagnoses or medications, pneumonia, and mental disorders and higher average Charlson Comorbidity Index scores at baseline. Patients with exacerbations filled their prescriptions for controllers more often and had higher asthma-related drug costs. Conclusions: Patients with moderate/severe persistent asthma who had exacerbations had higher total and asthma-related health care costs than those without exacerbations. Moreover, controller medication use was higher in patients with exacerbations. © 2011 American Academy of Allergy, Asthma & Immunology. Source

Spyropoulos A.C.,University of Rochester | McGinn T.,North Shore LIJ Health System | Khorana A.A.,University of Rochester
Thrombosis and Haemostasis | Year: 2012

Summary Formalised risk assessment models (RAMs) for venous thromboembol-ism (VTE) using weighted and scored variables have only recently been widely incorporated into international antithrombotic guidelines. Scored and weighted VTE RAMs have advantages over a simplified group-specific VTE risk approach, with the potential to allow more tailored strategies for thromboprophylaxis and an improved estimation of the risk/benefit profile for a particular patient. The derivation of VTE RAMs should be based on variables that are a priori defined or identified in a univariate analysis and the predictive capability of each variable should be rigorously assessed for both clinical and statistical significance and internal consistency and completeness. The assessment of the RAM should include the goodness of fit of the model and con-struction of a prognostic index score. Any VTE RAM which has been derived must undergo validation of that model before it can be used in clinical practice. Validation of the model should be performed in a "deliberate" prospective fashion across several diverse clinical sites using pre-defined criteria using basic standards for performing model validation. We discuss the basic concepts in the derivation of recent scored and weighted VTE RAMs in hospitalised surgical and medical patients and cancer outpatients, the mechanisms for accurate external validation of the models, and implications for their use in clinical practice. © Schattauer 2012. Source

Arad A.,Beth Israel Deaconess Medical Center | Proulle V.,Beth Israel Deaconess Medical Center | Furie R.A.,North Shore LIJ Health System | Furie B.C.,Beth Israel Deaconess Medical Center | Furie B.,Beth Israel Deaconess Medical Center
Blood | Year: 2011

Antiphospholipid syndrome is characterized by thrombosis, recurrent fetal loss, and the presence of the lupus anticoagulant, anticardiolipin antibodies, or anti-β2-glycoprotein-1 (anti-β2-GP1) antibodies. Although anti-β2-GP1 antibodies have been documented as a biomarker for diagnosis of antiphospholipid syndrome, their direct role in the pathogenesis of thrombosis is unknown. We have demonstrated using intravital microscopy that anti-β2-GP1 autoantibodies purified from the sera of patients with antiphospholipid syndrome complicated by thrombosis greatly amplify thrombus size after laser-induced vessel wall injury in live mice. Anti-β2-GP1 autoantibodies from 3 patients with antiphospholipid syndrome were affinity-purified using human β2-GP1 bound to agarose. The effects of purified anti-β2-GP1 IgG autoantibodies, of anti-β2-GP1- depleted IgG, and of IgG from normal human sera on thrombus formation were measured in mice after arterial injury in the cremaster muscle. Before injury, purified anti-β2-GP1 IgG autoantibodies, anti- β2-GP1 antibody-depleted IgG, or IgG from normal human sera were infused. Increasing amounts of purified anti-β2-GP1 autoantibodies increased thrombus size in a dose-dependent manner, whereas neither anti-β2-GP1 antibody-depleted IgG nor IgG from normal serum affected thrombus size. These results indicate that anti- β2-GP1 IgG autoantibodies in antiphospholipid syndrome patient sera are not only a marker of antiphospholipid syndrome but are directly involved in the pathogenesis of thrombosis. © 2011 by The American Society of Hematology. Source

The classic idea that arterial narrowing, called vasospasm (VSP), represents the hallmark of secondary injury after subarachnoid hemorrhage, has been challenged. The more complex and pleiotropic pathophysiological repercussions from the irruption of arterial blood into the subarachnoid layers go beyond the ascribed VSP. Putting adjectives in front of this term, such as “symptomatic,” “microdialytic,” or “angiographic” VSP, is misleading. Delayed cerebral ischemia (DCI) is a better term but remains restrictive to severe hypoperfusive injury and neglects oligemia, edema, and metabolic nonischemic injuries. In recognition of these issues, the international conference on VSP integrated “neurovascular events” into its name (www.vasospasm2013.com) and a multidisciplinary research group was formed in 2010 to study subgroups of DCI/VSP and their respective signifi cance. In three parts, this tiered article provides a broader defi nitional envelope for DCI and secondary neurovascular insults after SAH, with a rubric for each subtype of delayed neuronal dysfunction. First, it pinpoints the need for nosologic precision and covers current terminological inconsistency. Then, it highlights the input of neuroimaging and neuromonitoring in defi ning secondary injurious processes. Finally, a new categorization of deteriorating patients is proposed, going beyond a hierarchical or dichotomized defi nition of VSP/DCI, and common data elements are suggested for future trials. © Springer International Publishing Switzerland 2015. Source

Kassavin D.S.,North Shore LIJ Health System | Constantinopoulos G.,Monmouth Medical Center
Journal of Endovascular Therapy | Year: 2012

Purpose: To describe the use of in situ fenestration to facilitate management of a disconnected iliac stent-graft limb that could not be repaired by conventional endovascular techniques. Technique: An 85-year-oldman who had a Zenith endovascular graft deployed 3 years earlier for a 10-cm infrarenal abdominal aortic aneurysm presented with separation of the right iliac stent-graft limb from the main body, resulting in type III endoleak and sac enlargement. The disconnected limb occluded the ostiumof themain stent-graft body, blocking all conventional endovascular techniques to traverse the graft limb-main body intersection. To overcome the problem, the cephalad portion of the proximal disconnected limb overlying the main body gate was successfully fenestrated with an endoscopic FNA needle and continuity restored with a Viabahn stent-graft across the balloon-modeled fenestration. Conclusion: In situ fenestration of endovascular stent-grafts may be a useful adjunct in performing rescues of late complications in patients not suitable for open repair. © 2012 by the International Society of Endovascular Specialists. Source

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