Soluble C-Type Lectin-Like Receptor 2 Is a Biomarker for Disseminated Intravascular Coagulation.

DIC platelet activation poor outcome sCLEC-2

Journal

Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588

Informations de publication

Date de publication:
28 Jun 2021
Historique:
received: 19 05 2021
revised: 23 06 2021
accepted: 24 06 2021
entrez: 2 7 2021
pubmed: 3 7 2021
medline: 3 7 2021
Statut: epublish

Résumé

Disseminated intravascular coagulation (DIC) is induced by excess activation coagulation, and activated platelets are also involved in pathogenesis. Therefore, plasma levels of soluble C-type lectin-like receptor 2 (sCLEC-2), a new marker for platelet activation, can be expected as a marker of DIC in critically ill patients. Plasma levels of sCLEC-2 and D-dimer were measured using the STACIA system. Plasma sCLEC-2 and D-dimer levels were significantly higher in patients with underlying diseases of DIC than in those with unidentified clinical syndrome (UCS). Plasma sCLEC-2 levels were significantly higher in the patients with DIC and Pre-DIC than in those without DIC or Pre-DIC. Similarly, plasma D-dimer levels were also significantly higher in patients with DIC and Pre-DIC than in those without DIC or Pre-DIC. The plasma sCLEC-2 levels in all patients and those with a DIC score ≤ 4 were significantly higher in non-survivors than survivors. The plasma D-dimer levels in all patients, those with a DIC score ≥ 5 and those with a DIC score ≤ 4, were significantly higher in non-survivors than in survivors. The plasma sCLEC-2 is expected as a marker for DIC/Pre-DIC as well as the prognostic marker in critically ill patients.

Identifiants

pubmed: 34203210
pii: jcm10132860
doi: 10.3390/jcm10132860
pmc: PMC8269023
pii:
doi:

Types de publication

Journal Article

Langues

eng

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Auteurs

Akitaka Yamamoto (A)

Department of Emergency and Critical Care Center, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.

Hideo Wada (H)

Department of Central Laboratory, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.
Department of General Medicine, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.

Yuhuko Ichkawa (Y)

Department of Central Laboratory, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.

Motoko Tanaka (M)

Department of Central Laboratory, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.

Haruhiko Tashiro (H)

Department of Emergency and Critical Care Center, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.

Katsuya Shiraki (K)

Department of Central Laboratory, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.
Department of General Medicine, Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.

Hideto Shimpo (H)

Mie Prefectural General Medical Center, Yokkaichi 510-0885, Japan.

Yoshiki Yamashita (Y)

Department of Hematology and Oncology, Mie University Hospital, Mie University Graduate School of Medicine, Tsu 514-8507, Japan.

Takeshi Mastumoto (T)

Department of Blood Transfusion and Cell Therapy, Mie University Hospital, Mie University Graduate School of Medicine, Tsu 514-8507, Japan.

Motomu Shimaoka (M)

Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, Tsu 514-8507, Japan.

Toshiaki Iba (T)

Department of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.

Katsue Suzuki-Inoue (K)

Department of Clinical and Laboratory Medicine, Yamanashi Medical University, Yamanashi 400-8510, Japan.

Classifications MeSH