Inflammatory pathways in transfusion-associated circulatory overload
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 phen...
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| Format: | Article |
| Language: | English |
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Elsevier
2025-08-01
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| Series: | Blood Vessels, Thrombosis & Hemostasis |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2950327225000373 |
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| author | RoseAnn E. Vik Esther B. Bulle Wilmore C. Webley Paul Visintainer Samantha Ramirez Peter St. Marie Theresa Stec Lynne O’Hearn Chester Andrzejewski, Jr. Alexander P. J. Vlaar |
| author_facet | RoseAnn E. Vik Esther B. Bulle Wilmore C. Webley Paul Visintainer Samantha Ramirez Peter St. Marie Theresa Stec Lynne O’Hearn Chester Andrzejewski, Jr. Alexander P. J. Vlaar |
| author_sort | RoseAnn E. Vik |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-7ed89e1c84854d16a8974cd7fa7f8f75 |
| institution | Kabale University |
| issn | 2950-3272 |
| language | English |
| publishDate | 2025-08-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Blood Vessels, Thrombosis & Hemostasis |
| spelling | doaj-art-7ed89e1c84854d16a8974cd7fa7f8f752025-08-20T05:08:35ZengElsevierBlood Vessels, Thrombosis & Hemostasis2950-32722025-08-012310008010.1016/j.bvth.2025.100080Inflammatory pathways in transfusion-associated circulatory overloadRoseAnn E. Vik0Esther B. Bulle1Wilmore C. Webley2Paul Visintainer3Samantha Ramirez4Peter St. Marie5Theresa Stec6Lynne O’Hearn7Chester Andrzejewski, Jr.8Alexander P. J. Vlaar9Department of Microbiology, University of Massachusetts Amherst, Amherst, MADepartment of Intensive Care, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Laboratory of Experimental Intensive Care and Anesthesiology, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The NetherlandsDepartment of Microbiology, University of Massachusetts Amherst, Amherst, MA; Correspondence: Wilmore C. Webley, Department of Microbiology, University of Massachusetts Amherst, 639 North Pleasant St, N418 Morrill IV, Amherst, MA 01003;Office of Research, University of Massachusetts Chan Medical School-Baystate, Springfield, MADepartment of Pathology, Baystate Medical Center, Springfield, MAOffice of Research, University of Massachusetts Chan Medical School-Baystate, Springfield, MADepartment of Surgical Services, Baystate Medical Center, Springfield, MADepartment of Pathology, Blood Banking and Transfusion Medicine Services, Baystate Medical Center, Springfield, MADepartment of Pathology, Blood Banking and Transfusion Medicine Services, Baystate Medical Center, Springfield, MADepartment of Intensive Care, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Laboratory of Experimental Intensive Care and Anesthesiology, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, The NetherlandsAbstract: 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.http://www.sciencedirect.com/science/article/pii/S2950327225000373 |
| spellingShingle | RoseAnn E. Vik Esther B. Bulle Wilmore C. Webley Paul Visintainer Samantha Ramirez Peter St. Marie Theresa Stec Lynne O’Hearn Chester Andrzejewski, Jr. Alexander P. J. Vlaar Inflammatory pathways in transfusion-associated circulatory overload Blood Vessels, Thrombosis & Hemostasis |
| title | Inflammatory pathways in transfusion-associated circulatory overload |
| title_full | Inflammatory pathways in transfusion-associated circulatory overload |
| title_fullStr | Inflammatory pathways in transfusion-associated circulatory overload |
| title_full_unstemmed | Inflammatory pathways in transfusion-associated circulatory overload |
| title_short | Inflammatory pathways in transfusion-associated circulatory overload |
| title_sort | inflammatory pathways in transfusion associated circulatory overload |
| url | http://www.sciencedirect.com/science/article/pii/S2950327225000373 |
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