Pregnancy induced TMA in severe preeclampsia results from complement-mediated thromboinflammation

Autor: Jenni Heikkinen-Eloranta, A. Inkeri Lokki
Přispěvatelé: HUS Gynecology and Obstetrics, TRIMM - Translational Immunology Research Program, Department of Bacteriology and Immunology, University of Helsinki, Helsinki University Hospital Area, Department of Obstetrics and Gynecology
Rok vydání: 2020
Předmět:
MATERNAL KIR
Placenta
Disease
030204 cardiovascular system & hematology
ACTIVATION
0302 clinical medicine
Pre-Eclampsia
3123 Gynaecology and paediatrics
Pregnancy
Immunology and Allergy
Medicine
Endothelial dysfunction
Complement Activation
Atypical Hemolytic Uremic Syndrome
RISK
0303 health sciences
Thromboinflammation
General Medicine
CIRCULATING ANTIANGIOGENIC FACTORS
female genital diseases and pregnancy complications
3. Good health
ADAMTS13 ACTIVITY
THROMBOTIC MICROANGIOPATHY
Female
Blood Platelets
FACTOR-H
Thrombotic microangiopathy
Complement system
Immunology
Thrombotic thrombocytopenic purpura
Preeclampsia
TROPHOBLAST INVASION
03 medical and health sciences
Atypical hemolytic uremic syndrome
Animals
Humans
030304 developmental biology
business.industry
Vascular disease
Thrombotic Microangiopathies
Models
Immunological
Complement System Proteins
medicine.disease
ANGIOGENIC FACTORS
ENDOTHELIAL GROWTH-FACTOR
Endothelium
Vascular
business
Zdroj: Human immunology. 82(5)
ISSN: 1879-1166
Popis: Preeclampsia is a multifactorial vascular disease unique to human pregnancy. While genetic and antiangiogenic factors are important contributors to preeclampsia susceptibility, recent studies have shown that dysregulation and/or over-activation of the complement system has an integral role in dis-ease etiology. Furthermore, the role of the coagulation cascade may be underappreciated in the develop-ment of the disease. Traditionally, for research purposes, the pool of preeclampsia cases has been divided into non-severe and severe disease depending on the onset and severity of the symptoms. However, of particular interest are a small but important minority of cases that present with symptoms likening to those of hemolysis, elevated liver enzymes and low platelets syndrome, atypical hemolytic uremic syn-drome, or thrombotic thrombocytopenic purpura, all thrombotic microangiopathy (TMA) diseases, with the hallmark mechanisms of endothelial dysfunction and aberrant activation of complement and coagu-lation cascades. We therefore propose a third class, severe TMA-like preeclampsia to be included in the categorization of preeclampsia patients. Identifying these patients would target research, diagnostic dif-ferentiation, and novel treatment options to the subclass of patients with life-threatening disease that are most likely to benefit from next-generation drug development. (c) 2021 The Authors. Published by Elsevier Inc. on behalf of American Society for Histocompatibility and Immunogenetics. This is an open access article under the CC BY-NC-ND license (http://creativecommons. org/licenses/by-nc-nd/4.0/).
Databáze: OpenAIRE
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