# ABO Blood Group and Biomarker-Based Risk in Acute Pulmonary Embolism: A Retrospective Cohort Study

**Authors:** Abdulkader Jamal Eddin, Stefan Iulian Stanciugelu, Arnaldo Dario Damian, Bogdan Petru Miutescu, Oana Elena Tunea, Ioana Monica Mozos

PMC · DOI: 10.3390/jcm15041432 · 2026-02-12

## TL;DR

This study found that ABO blood group does not affect baseline biomarker levels or their ability to predict outcomes in patients with acute pulmonary embolism.

## Contribution

The study is the first to show that ABO blood group does not modify the prognostic value of biomarkers in acute pulmonary embolism.

## Key findings

- Non-O ABO blood groups did not independently associate with baseline biomarker levels.
- ABO type did not significantly modify the relationship between biomarkers and clinical outcomes.
- Biomarkers like NT-proBNP and CRP were strong predictors of mortality and complications.

## Abstract

Background. Non-O ABO blood groups are known to confer an increased risk of venous thromboembolism, primarily through higher circulating levels of von Willebrand factor and factor VIII. However, it remains unclear whether ABO type affects biochemical profiles at the time of presentation or alters the prognostic value of commonly used biomarkers in acute pulmonary embolism (PE). This study examined the relationship between ABO blood group, baseline biomarkers, and short-term clinical outcomes in patients with confirmed acute PE. Methods. We performed a retrospective cohort study of adults admitted with computed tomography pulmonary angiography-verified PE at a single tertiary center. Associations between biomarkers and clinical outcomes were assessed using logistic regression adjusted for age, sex, active cancer, chronic kidney disease, obesity, and ABO group. Interaction terms tested whether ABO type modified biomarker–outcome relationships. Results. Among 317 included patients (median age 69 years), in-hospital mortality was 11.0%; 29.6% experienced severe PE, 48.3% developed infection, and 11.7% developed sepsis. Baseline biomarker distributions were similar across ABO groups, and multivariable models showed no independent association between non-O type and biomarker levels. NT-proBNP, CRP, and procalcitonin predicted in-hospital mortality, while NT-proBNP, procalcitonin, and CK-MB predicted severe PE. CRP, procalcitonin, D-dimer, creatinine, and leukocyte count were associated with infectious and septic complications. ABO type did not meaningfully modify biomarker–outcome relationships, aside from one exploratory interaction for infection. Sensitivity analyses confirmed the robustness of these findings. Conclusions. ABO blood group did not influence baseline biomarker profiles or the prognostic performance of key biomarkers in acute PE. Early outcomes were instead driven by indicators of right ventricular strain, inflammation, and renal dysfunction.

## Linked entities

- **Proteins:** CRP (C-reactive protein), ckmb (creatine kinase, muscle b)
- **Diseases:** venous thromboembolism (MONDO:0005399), infection (MONDO:0005550)

## Full-text entities

- **Genes:** SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, GGTLC5P (gamma-glutamyltransferase light chain 5 pseudogene) [NCBI Gene 653590] {aka GGT}, ABO (ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase) [NCBI Gene 28] {aka A3GALNT, A3GALT1, GTA, GTB, NAGAT}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}
- **Diseases:** pulmonary infarction (MESH:D054060), hypertension (MESH:D006973), hematologic disease (MESH:D006402), death (MESH:D003643), VTE (MESH:D054556), injury (MESH:D014947), septic complications (MESH:D008107), acute inflammation (MESH:D007249), pressure overload (MESH:D019190), thrombotic (MESH:D013927), deep vein thrombosis (MESH:D020246), leukocytosis (MESH:D007964), chronic kidney disease (MESH:D051436), asthma (MESH:D001249), RV failure (MESH:D051437), myocardial infarction (MESH:D009203), RV overload (MESH:D018497), inflammatory complications (MESH:D018746), chronic venous insufficiency (MESH:D014689), infection (MESH:D007239), diabetes mellitus (MESH:D003920), atrial fibrillation (MESH:D001281), endothelial dysfunction (MESH:D014652), ischemic stroke (MESH:D002544), cancer (MESH:D009369), chronic obstructive pulmonary disease (MESH:D029424), dementia (MESH:D003704), systemic (MESH:D015619), Stroke (MESH:D020521), dysfunction (MESH:D006331), Cardiac strain (MESH:D013180), embolic event (MESH:D004617), respiratory failure (MESH:D012131), bacterial infections (MESH:D001424), heart failure (MESH:D006333), bleeding (MESH:D006470), obesity (MESH:D009765), renal dysfunction (MESH:D007674), tissue injury (MESH:D017695), sepsis (MESH:D018805), pulmonary hypertension (MESH:D006976), infectious (MESH:D003141), acute (MESH:D000208), Acute Pulmonary Embolism (MESH:D011655)
- **Chemicals:** potassium (MESH:D011188), sodium (MESH:D012964), triglycerides (MESH:D014280), bilirubin (MESH:D001663), Lipid (MESH:D008055), glucose (MESH:D005947), Creatinine (MESH:D003404), cholesterol (MESH:D002784), calcium (MESH:D002118)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12942291/full.md

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Source: https://tomesphere.com/paper/PMC12942291