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Amanda Walborn

· Assistant Professor of Anesthesia and Critical CareVerified

University of Chicago · Pharmacology

Active 2015–2025

h-index12
Citations632
Papers537 last 5y
Funding
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About

Amanda Walborn, MD, is an Assistant Professor of Anesthesia and Critical Care at UChicago Medicine. She specializes in anesthesiology and practices at the Duchossois Center for Advanced Medicine in Hyde Park, Chicago. Dr. Walborn completed her medical education at Loyola University Chicago Stritch School of Medicine, followed by an internship, residency, and fellowship at the University of Chicago. Her professional role involves clinical care in anesthesiology, and she is affiliated with UChicago Medicine, where she contributes to patient care, research, and teaching in her specialty.

Research signals

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Research topics

  • Internal medicine
  • Medicine
  • Intensive care medicine
  • Immunology
  • Pharmacology
  • Biochemistry
  • Emergency medicine
  • Virology
  • Gastroenterology
  • Chemistry
  • Biology

Selected publications

  • Caring for the Transplant Patient for Non-transplant Anesthesia

    International Anesthesiology Clinics · 2025-05-22

    articleCorresponding
  • Effect of Thromboprophylaxis on Clinical Outcomes After COVID-19 Hospitalization

    Annals of Internal Medicine · 2023 · 36 citations

    • Medicine
    • Intensive care medicine
    • Emergency medicine

    BACKGROUND: Patients hospitalized with COVID-19 have an increased incidence of thromboembolism. The role of extended thromboprophylaxis after hospital discharge is unclear. OBJECTIVE: To determine whether anticoagulation is superior to placebo in reducing death and thromboembolic complications among patients discharged after COVID-19 hospitalization. DESIGN: Prospective, randomized, double-blind, placebo-controlled clinical trial. (ClinicalTrials.gov: NCT04650087). SETTING: Done during 2021 to 2022 among 127 U.S. hospitals. PARTICIPANTS: Adults aged 18 years or older hospitalized with COVID-19 for 48 hours or more and ready for discharge, excluding those with a requirement for, or contraindication to, anticoagulation. INTERVENTION: 2.5 mg of apixaban versus placebo twice daily for 30 days. MEASUREMENTS: The primary efficacy end point was a 30-day composite of death, arterial thromboembolism, and venous thromboembolism. The primary safety end points were 30-day major bleeding and clinically relevant nonmajor bleeding. RESULTS: Enrollment was terminated early, after 1217 participants were randomly assigned, because of a lower than anticipated event rate and a declining rate of COVID-19 hospitalizations. Median age was 54 years, 50.4% were women, 26.5% were Black, and 16.7% were Hispanic; 30.7% had a World Health Organization severity score of 5 or greater, and 11.0% had an International Medical Prevention Registry on Venous Thromboembolism risk prediction score of greater than 4. Incidence of the primary end point was 2.13% (95% CI, 1.14 to 3.62) in the apixaban group and 2.31% (CI, 1.27 to 3.84) in the placebo group. Major bleeding occurred in 2 (0.4%) and 1 (0.2%) and clinically relevant nonmajor bleeding occurred in 3 (0.6%) and 6 (1.1%) apixaban-treated and placebo-treated participants, respectively. By day 30, thirty-six (3.0%) participants were lost to follow-up, and 8.5% of apixaban and 11.9% of placebo participants permanently discontinued the study drug treatment. LIMITATIONS: The introduction of SARS-CoV-2 vaccines decreased the risk for hospitalization and death. Study enrollment spanned the peaks of the Delta and Omicron variants in the United States, which influenced illness severity. CONCLUSION: The incidence of death or thromboembolism was low in this cohort of patients discharged after hospitalization with COVID-19. Because of early enrollment termination, the results were imprecise and the study was inconclusive. PRIMARY FUNDING SOURCE: National Institutes of Health.

  • Effects of inflammation on thrombosis and outcomes in COVID-19: secondary analysis of the ATTACC/ACTIV-4a trial

    Research and Practice in Thrombosis and Haemostasis · 2023-09-15 · 1 citations

    articleOpen access1st author

    Background: Patients hospitalized for COVID-19 are at high risk of thrombotic complications and organ failure, and often exhibit severe inflammation, which may contribute to hypercoagulability. Objectives: To determine whether patients hospitalized for COVID-19 experience differing frequencies of thrombotic and organ failure complications and derive variable benefits from therapeutic-dose heparin dependent on the extent of systemic inflammation and whether observed benefit from therapeutic-dose anticoagulation varies depending on the degree of systemic inflammation. Methods: We analyzed data from 1346 patients hospitalized for COVID-19 enrolled in the ATTACC and ACTIV-4a platforms who were randomized to therapeutic-dose heparin or usual care for whom levels of C-reactive protein (CRP) were reported at baseline. Results: Increased CRP was associated with worse patient outcomes, including a >98% posterior probability of increased organ support requirement, hospital length of stay, risk of 28-day mortality, and incidence of major thrombotic events or death (patients with CRP 40-100 mg/L or ≥100 mg/L compared to patients with CRP <40 mg/L). Patients with CRP 40 to 100 mg/L experienced the greatest degree of benefit from treatment with therapeutic doses of unfractionated or low molecular weight heparin compared with usual-care prophylactic doses. This was most significant for an increase in organ support-free days (odds ratio: 1.63; 95% confidence interval, 1.09-2.40; 97.9% posterior probability of beneficial effect), with trends toward benefit for other evaluated outcomes. Conclusion: Moderately ill patients hospitalized for COVID-19 with CRP between 40 mg/L and 100 mg/L derived the greatest benefit from treatment with therapeutic-dose heparin.

  • Biomarkers of Platelet Activation and Their Prognostic Value in Patients With Sepsis-Associated Disseminated Intravascular Coagulopathy

    Clinical and Applied Thrombosis/Hemostasis · 2021 · 54 citations

    • Medicine
    • Internal medicine
    • Gastroenterology

    Sepsis-associated disseminated intravascular coagulation (DIC) is related to marked hemostatic changes such as transient thrombocytopenia secondary to the endogenous activation and consumption of platelets. This study measured markers of platelet function in 103 adult ICU patients with clinically established sepsis-associated DIC to determine the biomarker association with disease severity. Patients were categorized as having no DIC, nonovert DIC, or overt DIC using the International Society of Thrombosis and Hemostasis scoring system. Plasma levels of CD40L, platelet factor 4 (PF4), platelet-derived microparticles, and microparticle-associated tissue factor were quantified. Markers of platelet activation were significantly elevated in patients with DIC compared to healthy individuals. This increase was independent of platelet count. Levels of PF4 differed based on the severity of DIC and differentiated nonsurvivors and survivors. These findings suggest that the markers of platelet activation in DIC may not be regulated by the number of circulating platelets and may be independent of the factors leading to their consumption.

  • Plasma MCP-1 levels in bipolar depression during cyclooxygenase-2 inhibitor combination treatment

    Journal of Psychiatric Research · 2020 · 17 citations

    • Pharmacology
    • Medicine
    • Internal medicine
  • RELATIONSHIP BETWEEN ATRIAL FIBRILLATION AND ANGIOPOIETIN-2 ELEVATION REMAINS SIGNIFICANT FOLLOWING 1-YEAR INTERVAL

    Journal of the American College of Cardiology · 2020-03-01

    article
  • Procalcitonin as a Marker of Comorbid Atrial Fibrillation in Chronic Kidney Disease and History of Sepsis

    Clinical and Applied Thrombosis/Hemostasis · 2020-01-01 · 8 citations

    articleOpen access

    Cardiovascular disease and infection are the leading causes of mortality in patients with stage 5 chronic kidney disease on hemodialysis (CKD5-HD). Inflammation is a large component in the pathogenesis of both atrial fibrillation (AF) and sepsis and may link these conditions in CKD5-HD. Procalcitonin (PCT) is an inflammatory biomarker elevated in systemic infection and CKD5-HD, yet its value with regard to comorbid AF has not been thoroughly investigated. The aim of this study sought to evaluate circulating inflammatory markers, including PCT, Angiopoietin-1, Angiopoetin-2, CD40-L, C-reactive protein, d-dimer, and von Willebrand factor in relation to these conditions. Plasma levels of inflammatory markers were measured by enzyme linked immunosorbent assay method in CKD5-HD (n = 97) patients and controls (n = 50). Procalcitonin levels were significantly elevated ( P = .0270) in CKD5-HD with comorbid AF compared to those without AF. Further analysis of patients with a history of sepsis demonstrated significantly elevated levels of PCT ( P = .0405) in those with comorbid AF (160.7 ± 39.5 pg/mL) compared to those without AF (117.4 ± 25.3 pg/mL). This study demonstrates that the inflammatory biomarker PCT is further elevated in the presence of both AF and a history of sepsis in hemodialysis patients and suggests that underlying chronic inflammation following sepsis resolution may place these patients at greater risk of developing AF.

  • Development of an Algorithm to Predict Mortality in Patients With Sepsis and Coagulopathy

    Clinical and Applied Thrombosis/Hemostasis · 2020-01-01 · 9 citations

    articleOpen access1st author

    Sepsis is a systemic response to infection with a high rate of mortality and complex pathophysiology involving inflammation, infection response, hemostasis, endothelium, and platelets. The purpose of this study was to develop an equation incorporating biomarker levels at intensive care unit (ICU) admission to predict mortality in patients with sepsis, based on the hypothesis that a combination of biomarkers representative of multiple physiological systems would provide improved predictive value. Plasma samples and clinical data were collected from 103 adult patients with sepsis at the time of ICU admission. Biomarker levels were measured using commercially available methods. A 28-day mortality was used as the primary end point. Stepwise linear regression modeling was performed to generate a predictive equation for mortality. Differences in biomarker levels between survivors were quantified using the Mann-Whitney test and the area under the receiver operating curve (AUC) was used to describe predictive ability. Significant differences ( P &lt; .05) were observed between survivors and nonsurvivors for plasminogen activator inhibitor 1 (AUC = 0.70), procalcitonin (AUC = 0.77), high mobility group box 1 (AUC = 0.67), interleukin (IL) 6 (AUC = 0.70), IL-8 (AUC = 0.70), protein C (AUC = 0.71), angiopoietin-2 (AUC = 0.76), endocan (AUC = 0.58), and platelet factor 4 (AUC = 0.70). A predictive equation for mortality was generated using stepwise linear regression modeling, which incorporated procalcitonin, vascular endothelial growth factor, the IL-6:IL-10 ratio, endocan, and platelet factor 4, and demonstrated a better predictive value for patient outcome than any individual biomarker (AUC = 0.87). The use of mathematical modeling resulted in the development of a predictive equation for sepsis-associated mortality with performance than any individual biomarker or clinical scoring system which incorporated biomarkers representative of multiple systems.

  • Markers of Inflammation and Infection in Sepsis and Disseminated Intravascular Coagulation

    Clinical and Applied Thrombosis/Hemostasis · 2019-01-01 · 99 citations

    articleOpen access

    Sepsis is a severe systemic inflammatory response to infection that manifests with widespread inflammation as well as endothelial and coagulation dysfunction that may lead to hypotension, organ failure, shock, and death. Disseminated intravascular coagulation (DIC) is a complication of sepsis involving systemic activation of the fibrinolytic and coagulation pathways that can lead to multi-organ dysfunction, thrombosis, and bleeding, with a 2-fold increase in mortality. This study demonstrates the diagnostic and prognostic value of profiling various biomarkers of inflammation and infection in patients with sepsis-associated DIC to assess the severity of illness. Deidentified samples were obtained from adult patients with sepsis and suspected DIC. Platelet count, prothrombin time, D-dimer, and fibrinogen levels were used to assign International Society of Thrombosis and Hemostasis DIC scores to plasma samples from 103 patients with sepsis and suspected DIC. Using commercially available enzyme-linked immunosorbent assay, chromogenic assay, and RANDOX Biochip methods, levels of procalcitonin (PCT), extracellular nucleosomes, interleukin (IL) 6, IL-8, IL-10, and tumor necrosis factor α (TNFα) were measured in patients with sepsis and DIC and compared to levels in healthy individuals. Elevated levels of PCT, IL-6, IL-8, IL-10, and TNFα were observed in most patients with sepsis and DIC. Additionally, the levels of these markers show significant positive correlations with each other and with DIC score. Currently, no single biomarker can effectively diagnose DIC in patients with sepsis. This study lays the groundwork for the development of a diagnostic algorithm using several markers of inflammation and infection and DIC score as parameters in assessing severity of sepsis-associated coagulopathy in a clinical setting.

  • S95. Plasma MCP-1 Levels in Bipolar Depression During Cyclooxygenase-2 Inhibitor Combination Treatment

    Biological Psychiatry · 2019-05-01

    article

Frequent coauthors

  • Jawed Fareed

    50 shared
  • Debra Hoppensteadt

    Loyola University Chicago

    47 shared
  • Matthew T. Rondina

    University of Utah

    22 shared
  • Vinod Bansal

    Loyola University Chicago

    15 shared
  • Michael J. Mosier

    Oregon Clinic

    12 shared
  • Paula Maia

    Instituto Nacional de Traumatologia e Ortopedia

    11 shared
  • Jack Bontekoe

    10 shared
  • Jeffrey Liles

    Duke Medical Center

    10 shared

Labs

Education

  • MD

    Loyola University Chicago Stritch School of Medicine

    2020
  • PhD, Department of Molecular Pharmacology and Therapeutics

    Loyola University Chicago

    2018
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