Evidence map›Paper›PMID 40896543›Full record

ArticleBlood vessels, thrombosis & hemostasis2025

Inflammatory pathways in transfusion-associated circulatory overload.

RoseAnn E Vik, Esther B Bulle, Wilmore C Webley, Paul Visintainer, Samantha Ramirez, Peter St Marie, Theresa Stec, Lynne O'Hearn, Chester Andrzejewski, Alexander P J Vlaar

Abstract read
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Article in Blood vessels, thrombosis & hemostasis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

RoseAnn E VikDepartment of Microbiology, University of Massachusetts Amherst, Amherst, MA.
Esther B BulleDepartment of Intensive Care, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Wilmore C WebleyDepartment of Microbiology, University of Massachusetts Amherst, Amherst, MA.
Paul VisintainerOffice of Research, University of Massachusetts Chan Medical School-Baystate, Springfield, MA.
Samantha RamirezDepartment of Pathology, Baystate Medical Center, Springfield, MA.
Peter St MarieOffice of Research, University of Massachusetts Chan Medical School-Baystate, Springfield, MA.
Theresa StecDepartment of Surgical Services, Baystate Medical Center, Springfield, MA.
Lynne O'HearnDepartment of Pathology, Blood Banking and Transfusion Medicine Services, Baystate Medical Center, Springfield, MA.
Chester AndrzejewskiDepartment of Pathology, Blood Banking and Transfusion Medicine Services, Baystate Medical Center, Springfield, MA.
Alexander P J VlaarDepartment of Intensive Care, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transfusion-associated circulatory overload (TACO) is a leading cause of transfusion-associated mortality. TACO is thought to result from hydrostatic forces in the vascular space, leading to transudative pulmonary edema. Recent studies suggest that TACO is not solely a volume overload phenomenon, but may involve inflammatory processes. This study aimed to further explore the presence of inflammation in patients with TACO. We conducted a retrospective study with 3 cohorts receiving red blood cell transfusion: (1) patients having TACO as defined by a national hemovigilance case surveillance classification (conventional TACO [cTACO], n = 33); (2) patients having symptoms consistent with TACO but not completely meeting reporting criteria (institutional TACO [iTACO], n = 33); and (3) a patient cohort who experienced uncomplicated transfusions (n = 6). Samples from before transfusion, after transfusion, and 8 to 36 hours after transfusion were examined. Samples were analyzed for levels of tumor necrosis factor α, interleukin-1α (IL-1α), IL-6, IL-8, IL-10, C-reactive protein, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1, atrial natriuretic peptide, cardiac troponin, and N-terminal pro-B-type natriuretic peptide. Patients with cTACO and iTACO had an elevated body temperature, higher heart rate, and lower oxygen saturation after transfusion, whereas only patients with cTACO had higher blood pressures. Levels of key proinflammatory cytokines, IL-6, and IL-8 were elevated in patients with cTACO and iTACO after transfusion, whereas ICAM-1 was elevated only in patients with iTACO after transfusion. Our results suggest that inflammatory pathways may be invoked in patients with TACO. Patients with iTACO showed a more distinctive inflammatory profile, suggesting a gray area between transfusion-related acute lung injury and TACO.

Identifiers

PMID40896543
PMCPMC12395531

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.