Prognostic role of the preoperative neutrophil-to-lymphocyte ratio and albumin for 30-day mortality in patients with postoperative acute pulmonary embolism

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Abstract

Background

This retrospective study aimed to investigate the prognostic value of the neutrophil-to-lymphocyte ratio (NLR) and albumin for 30-day mortality in patients with postoperative acute pulmonary embolism (PAPE).

Methods

We retrospectively reviewed the medical records of 101 patients with PAPE admitted from September 1, 2012, to March 31, 2019. The characteristics, surgical information, admission examination data and mortality within 30 days after PAPE were obtained from our electronic medical recording system and follow-up. The associations between the NLR, PLR, and other predictors and 30-day mortality were analyzed with univariate and multivariate analyses. Then, the nomogram including the independent predictors was established and evaluated.

Results

Twenty-four patients died within 30 days, corresponding to a 30-day mortality rate of 23.8%. The results of the multivariate analysis indicated that both the NLR and albumin were independent predictors for 30-day mortality in patients with PAPE. The probability of death increased by approximately 17.1% (OR = 1.171, 95% CI: 1.073–1.277, P = 0.000) with a one-unit increase in the NLR, and the probability of death decreased by approximately 15.4% (OR = 0.846, 95% CI: 0.762c–0.939, P = 0.002) with a one-unit increase in albumin. The area under the curve of the nomogram was 0.888 (95% CI: 0.812–0.964).

Conclusion

Our findings showed that an elevated NLR and decreased albumin were related to poor prognosis in patients with PAPE. The NLR and albumin were independent prognostic factors for PAPE.

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Most cited references 27

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Human serum albumin, systemic inflammation, and cirrhosis.

Vicente Arroyo, Rita García-Martínez, Xavier Salvatella (2014)

Human serum albumin (HSA) is one of the most frequent treatments in patients with decompensated cirrhosis. Prevention of paracentesis-induced circulatory dysfunction, prevention of type-1 HRS associated with bacterial infections, and treatment of type-1 hepatorenal syndrome are the main indications. In these indications treatment with HSA is associated with improvement in survival. Albumin is a stable and very flexible molecule with a heart shape, 585 residues, and three domains of similar size, each one containing two sub-domains. Many of the physiological functions of HSA rely on its ability to bind an extremely wide range of endogenous and exogenous ligands, to increase their solubility in plasma, to transport them to specific tissues and organs, or to dispose of them when they are toxic. The chemical structure of albumin can be altered by some specific processes (oxidation, glycation) leading to rapid clearance and catabolism. An outstanding feature of HSA is its capacity to bind lipopolysaccharide and other bacterial products (lipoteichoic acid and peptidoglycan), reactive oxygen species, nitric oxide and other nitrogen reactive species, and prostaglandins. Binding to NO and prostaglandins are reversible, so they can be transferred to other molecules at different sites from their synthesis. Through these functions, HSA modulates the inflammatory reaction. Decompensated cirrhosis is a disease associated systemic inflammation, which plays an important role in the pathogenesis of organ or system dysfunction/failure. Although, the beneficial effects of HAS have been traditionally attributed to plasma volume expansion, they could also relate to its effects modulating systemic and organ inflammation.

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The Role of Inflammation in Venous Thromboembolism

Brian Branchford, Shannon Carpenter (2018)

Venous thromboembolism (VTE), comprising deep vein thrombosis (DVT), and pulmonary embolism (PE), is becoming increasingly recognized as a cause of morbidity and mortality in pediatrics, particularly among hospitalized children. Furthermore, evidence is accumulating that suggests the inflammatory response may be a cause, as well as consequence, of VTE, but current anticoagulation treatment regimens are not designed to inhibit inflammation. In fact, many established clinical VTE risk factors such as surgery, obesity, cystic fibrosis, sepsis, systemic infection, cancer, inflammatory bowel disease, and lupus likely modulate thrombosis through inflammatory mediators. Unlike other traumatic mechanisms of thrombosis involving vascular transection and subsequent exposure of subendothelial collagen and other procoagulant extracellular matrix materials, inflammation of the vessel wall may initiate thrombosis on an intact vein. Activation of endothelial cells, platelets, and leukocytes with subsequent formation of microparticles can trigger the coagulation system through the induction of tissue factor (TF). Identification of biomarkers to evaluate VTE risk could be of great use to the clinician caring for a patient with inflammatory disease to guide decisions regarding the risk:benefit ratio of various types of potential thromboprophylaxis strategies, or suggest a role for anti-inflammatory therapy. Unfortunately, no such validated inflammatory scoring system yet exists, though research in this area is ongoing. Elevation of C-reactive protein, IL-6, IL-8, and TNF-alpha during a response to systemic inflammation have been associated with increased VTE risk. Consequent platelet activation enhances the prothrombotic state, leading to VTE development, particularly in patients with other risk factors, most notably central venous catheters.

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Contact system revisited: an interface between inflammation, coagulation, and innate immunity.

A T Long, E Kenne, R Jung … (2016)

The contact system is a plasma protease cascade initiated by factor XII (FXII) that activates the proinflammatory kallikrein-kinin system and the procoagulant intrinsic coagulation pathway. Anionic surfaces induce FXII zymogen activation to form proteolytically active FXIIa. Bacterial surfaces also have the ability to activate contact system proteins, indicating an important role for host defense using the cooperation of the inflammatory and coagulation pathways. Recent research has shown that inorganic polyphosphate found in platelets activates FXII in vivo and can induce coagulation in pathological thrombus formation. Experimental studies have shown that interference with FXII provides thromboprotection without a therapy-associated increase in bleeding, renewing interest in the FXIIa-driven intrinsic pathway of coagulation as a therapeutic target. This review summarizes how the contact system acts as the cross-road of inflammation, coagulation, and innate immunity.

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Author and article information

Contributors

Cheng-Liang Zhao: 38221965@qq.com

Gui-Yun Ma: maguiyun3778@163.com

Journal

Journal ID (nlm-ta): BMC Pulm Med

Journal ID (iso-abbrev): BMC Pulm Med

Title: BMC Pulmonary Medicine

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2466

Publication date (Electronic): 24 June 2020

Publication date PMC-release: 24 June 2020

Publication date Collection: 2020

Volume: 20

Electronic Location Identifier: 180

Affiliations

[1 ]GRID grid.413851.a, ISNI 0000 0000 8977 8425, Department of Orthopedic, , Affiliated Hospital of Chengde Medical University, ; Chengde, China

[2 ]GRID grid.412449.e, ISNI 0000 0000 9678 1884, Graduate School of China Medical University, ; Shenyang, China

[3 ]GRID grid.268099.c, ISNI 0000 0001 0348 3990, School and Hospital of Stomatology, , Wenzhou Medical University, ; Wenzhou, China

[4 ]GRID grid.410645.2, ISNI 0000 0001 0455 0905, Qingdao University medical college, ; Qingdao, China

[5 ]GRID grid.268099.c, ISNI 0000 0001 0348 3990, Second Clinical Medical College of Wenzhou Medical University, ; Wenzhou, China

Article

Publisher ID: 1216

DOI: 10.1186/s12890-020-01216-5

PMC ID: 7315518

PubMed ID: 32580706

SO-VID: 148a9c5f-be94-41b7-bab2-ff65a5cdc298

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 4 January 2020

Date accepted : 15 June 2020

Custom metadata

ScienceOpen disciplines: Respiratory medicine

Keywords: neutrophil-to-lymphocyte ratio,albumin,mortality,postoperative acute pulmonary embolism

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ScienceOpen disciplines: Respiratory medicine

Keywords: neutrophil-to-lymphocyte ratio, albumin, mortality, postoperative acute pulmonary embolism

Prognostic role of the preoperative neutrophil-to-lymphocyte ratio and albumin for 30-day mortality in patients with postoperative acute pulmonary embolism

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Abstract

Background

Methods

Results

Conclusion

Related collections

Inflamed lung in vitro co-culture models

Most cited references 27

Human serum albumin, systemic inflammation, and cirrhosis.

The Role of Inflammation in Venous Thromboembolism

Contact system revisited: an interface between inflammation, coagulation, and innate immunity.

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Contributors

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