Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome

Participation of blood platelets in the development of sepsis is clearly illustrated by hemocoagulation disorders and frequently observed thrombocytopenia. In the patients with sepsis, thrombocytopenia develops rapidly, with minimal platelet counts registered on the fourth day of observation, after...

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Autores principales:	N. B. Serebryanaya, P. P. Yakutseni
Formato:	article
Lenguaje:	RU
Publicado:	SPb RAACI 2021
Materias:	sepsis multiple organ failure syndrome thrombocytopenia platelets neutrophils serotonin Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/349d158801db47568211f9f353a03a4c
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spelling	oai:doaj.org-article:349d158801db47568211f9f353a03a4c2021-11-18T08:03:50ZBlood platelets in the development of sepsis, septic shock and multiple organ failure syndrome1563-06252313-741X10.15789/1563-0625-BPI-2090https://doaj.org/article/349d158801db47568211f9f353a03a4c2021-01-01T00:00:00Zhttps://www.mimmun.ru/mimmun/article/view/2090https://doaj.org/toc/1563-0625https://doaj.org/toc/2313-741XParticipation of blood platelets in the development of sepsis is clearly illustrated by hemocoagulation disorders and frequently observed thrombocytopenia. In the patients with sepsis, thrombocytopenia develops rapidly, with minimal platelet counts registered on the fourth day of observation, after which the platelet counts usually rise. Continuous thrombocytopenia and absence of a relative increase in platelets are considered predictors of patient death. The mechanisms of thrombocytopenia developing in sepsis are quite diverse, but the processes in periphery are prevailing, e.g., the so-called “platelet consumption” which is determined by their activation, chemotaxis and isolation in the microvasculature. Recently, a mechanism has been identified for the accelerated removal of platelets with desialized surface glycoproteins from the circulation. Sialidases, also known as neuraminidases, are widely present in viruses and bacteria, and pharmacological inhibition of sialidases is able to withstand thrombocytopenia in the infectious process. The key role of platelets in the development of septic shock was revealed. Sequestration of platelets in the microvessels of the lungs and brain (manifesting as thrombocytopenia) is accompanied by rapid serotonin release, thus underlying the main clinical manifestations, e.g., decreased blood pressure, heart rate and increased capillary permeability. To counteract sharp release of this mediator, pharmacological attempts are made to inhibit the SERT transporter by means of selective serotonin reuptake inhibitors. Blood platelets are key participants in the pathogenesis of multiple organ failure syndromes, such as acute renal damage, acute respiratory distress syndrome, myocardial dysfunction, and sepsis-associated encephalopathy. To restore impaired vascular permeability in these conditions, in particular, sepsis-associated encephalopathy, a pharmacological S1P receptor mimetic is under study. The review specifies possible pathogenetically significant targets that can be used to perform pharmacological correction of conditions associated with sepsis and concomitant thrombocytopenia.N. B. SerebryanayaP. P. YakutseniSPb RAACIarticlesepsismultiple organ failure syndromethrombocytopeniaplateletsneutrophilsserotoninImmunologic diseases. AllergyRC581-607RUMedicinskaâ Immunologiâ, Vol 22, Iss 6, Pp 1085-1096 (2021)
institution	DOAJ
collection	DOAJ
language	RU
topic	sepsis multiple organ failure syndrome thrombocytopenia platelets neutrophils serotonin Immunologic diseases. Allergy RC581-607
spellingShingle	sepsis multiple organ failure syndrome thrombocytopenia platelets neutrophils serotonin Immunologic diseases. Allergy RC581-607 N. B. Serebryanaya P. P. Yakutseni Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome
description	Participation of blood platelets in the development of sepsis is clearly illustrated by hemocoagulation disorders and frequently observed thrombocytopenia. In the patients with sepsis, thrombocytopenia develops rapidly, with minimal platelet counts registered on the fourth day of observation, after which the platelet counts usually rise. Continuous thrombocytopenia and absence of a relative increase in platelets are considered predictors of patient death. The mechanisms of thrombocytopenia developing in sepsis are quite diverse, but the processes in periphery are prevailing, e.g., the so-called “platelet consumption” which is determined by their activation, chemotaxis and isolation in the microvasculature. Recently, a mechanism has been identified for the accelerated removal of platelets with desialized surface glycoproteins from the circulation. Sialidases, also known as neuraminidases, are widely present in viruses and bacteria, and pharmacological inhibition of sialidases is able to withstand thrombocytopenia in the infectious process. The key role of platelets in the development of septic shock was revealed. Sequestration of platelets in the microvessels of the lungs and brain (manifesting as thrombocytopenia) is accompanied by rapid serotonin release, thus underlying the main clinical manifestations, e.g., decreased blood pressure, heart rate and increased capillary permeability. To counteract sharp release of this mediator, pharmacological attempts are made to inhibit the SERT transporter by means of selective serotonin reuptake inhibitors. Blood platelets are key participants in the pathogenesis of multiple organ failure syndromes, such as acute renal damage, acute respiratory distress syndrome, myocardial dysfunction, and sepsis-associated encephalopathy. To restore impaired vascular permeability in these conditions, in particular, sepsis-associated encephalopathy, a pharmacological S1P receptor mimetic is under study. The review specifies possible pathogenetically significant targets that can be used to perform pharmacological correction of conditions associated with sepsis and concomitant thrombocytopenia.
format	article
author	N. B. Serebryanaya P. P. Yakutseni
author_facet	N. B. Serebryanaya P. P. Yakutseni
author_sort	N. B. Serebryanaya
title	Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome
title_short	Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome
title_full	Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome
title_fullStr	Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome
title_full_unstemmed	Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome
title_sort	blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome
publisher	SPb RAACI
publishDate	2021
url	https://doaj.org/article/349d158801db47568211f9f353a03a4c
work_keys_str_mv	AT nbserebryanaya bloodplateletsinthedevelopmentofsepsissepticshockandmultipleorganfailuresyndrome AT ppyakutseni bloodplateletsinthedevelopmentofsepsissepticshockandmultipleorganfailuresyndrome
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Blood platelets in the development of sepsis, septic shock and multiple organ failure syndrome

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