Non-classical and intermediate monocytes in patients following venous thromboembolism: Links with inflammation.


Journal

Advances in clinical and experimental medicine : official organ Wroclaw Medical University
ISSN: 1899-5276
Titre abrégé: Adv Clin Exp Med
Pays: Poland
ID NLM: 101138582

Informations de publication

Date de publication:
Jan 2019
Historique:
pubmed: 9 8 2018
medline: 27 8 2019
entrez: 9 8 2018
Statut: ppublish

Résumé

Monocyte subsets are involved in atherosclerotic vascular disease and its thromboembolic complications. Moreover, the role of monocytes has been suggested in the pathogenesis of venous thromboembolism (VTE). We hypothesized that pro-inflammatory non-classical and intermediate monocytes are increased in the first months following VTE. We enrolled 70 patients aged 18-65 years (mean age 41.6 ±11.6) with the firstever provoked (n = 32; 45.7%) or unprovoked (n = 38; 54.28%) VTE episode, and 46 healthy controls. The exclusion criteria were: acute infection, cancer, autoimmune disorders, previous myocardial infarction (MI), or stroke. Monocyte subsets were assessed 12 (8.5-21.5) months after VTE using flow cytometry and were defined as classical (CD14++CD16-), intermediate (CD14++CD16+) and non-classical (CD14+CD16++). Patients with VTE had higher intermediate and non-classical monocyte counts compared to the control group (16.8 ±9.3 vs 10.4 ±4.0 cells/μL, and 64.1 ±25.2 vs 44.1 ±19.2 cells/μL, respectively, both p < 0.001). Increased non-classical monocyte counts were observed in patients who experienced a VTE incident within 12 months prior to enrollment (71.5 ±27.4 vs 56.03 ±20.6 cells/μL; p = 0.01) and those with unprovoked VTE (70.2 ±4.1 vs 58.8 ±4.3 cells/μL; p = 0.06). There were no differences in monocyte subsets related to the current anticoagulation. Our data has shown for the first time that VTE is associated with an increased number of nonclassical and intermediate monocytes, which may indicate the involvement of monocyte-related mechanisms in the pathophysiology of this disease.

Sections du résumé

BACKGROUND BACKGROUND
Monocyte subsets are involved in atherosclerotic vascular disease and its thromboembolic complications. Moreover, the role of monocytes has been suggested in the pathogenesis of venous thromboembolism (VTE).
OBJECTIVES OBJECTIVE
We hypothesized that pro-inflammatory non-classical and intermediate monocytes are increased in the first months following VTE.
MATERIAL AND METHODS METHODS
We enrolled 70 patients aged 18-65 years (mean age 41.6 ±11.6) with the firstever provoked (n = 32; 45.7%) or unprovoked (n = 38; 54.28%) VTE episode, and 46 healthy controls. The exclusion criteria were: acute infection, cancer, autoimmune disorders, previous myocardial infarction (MI), or stroke. Monocyte subsets were assessed 12 (8.5-21.5) months after VTE using flow cytometry and were defined as classical (CD14++CD16-), intermediate (CD14++CD16+) and non-classical (CD14+CD16++).
RESULTS RESULTS
Patients with VTE had higher intermediate and non-classical monocyte counts compared to the control group (16.8 ±9.3 vs 10.4 ±4.0 cells/μL, and 64.1 ±25.2 vs 44.1 ±19.2 cells/μL, respectively, both p < 0.001). Increased non-classical monocyte counts were observed in patients who experienced a VTE incident within 12 months prior to enrollment (71.5 ±27.4 vs 56.03 ±20.6 cells/μL; p = 0.01) and those with unprovoked VTE (70.2 ±4.1 vs 58.8 ±4.3 cells/μL; p = 0.06). There were no differences in monocyte subsets related to the current anticoagulation.
CONCLUSIONS CONCLUSIONS
Our data has shown for the first time that VTE is associated with an increased number of nonclassical and intermediate monocytes, which may indicate the involvement of monocyte-related mechanisms in the pathophysiology of this disease.

Identifiants

pubmed: 30088349
doi: 10.17219/acem/76262
doi:

Types de publication

Journal Article

Langues

eng

Pagination

51-58

Auteurs

Ewa Wypasek (E)

Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland.
Department of Medicine, Jagiellonian University Medical College, Kraków, Poland.

Agnieszka Padjas (A)

Department of Medicine, Jagiellonian University Medical College, Kraków, Poland.

Magdalena Szymańska (M)

John Paul II Hospital, Kraków, Poland.

Krzysztof Plens (K)

Data Analysis Center, Cardiovascular Research Institute, Kraków, Poland.

Maciej Siedlar (M)

Department of Clinical Immunology, Chair of Clinical Immunology and Transplantation, Institute of Pediatrics, Jagiellonian University Medical College, Kraków, Poland.

Anetta Undas (A)

Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland.

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