Abstract
The article highlights the problem of fetal inflammatory response syndrome (FIRS) in modern conditions. This term has been introduced into the clinical practice to describe the systemic activation of the innate or acquired immune system of the fetus. FIRS can occur in response to infection or inflammation and is divided into two types depending on the type of immune response. FIRS I and II types are different clinical syndromes and correspond to acute and chronic inflammatory processes.The main pathophysiological mechanisms and clinical features of different variants of FIRS are described. Fetuses with this syndrome have signs of multiorgan damage. The consequences of FIRS are a high rate of complications in newborns: sepsis, congenital pneumonia, intraventricular hemorrhage, periventricular leukomalacia, cerebral palsy, neurosensory deafness, necrotic enterocolitis and others. The detailed description of fetal organs and systems damage by FIRS is presented. In further life, such children are at risk of long-term complications. This syndrome can also be the cause of unexplained antenatal fetal death.Laboratory diagnostic criteria for FIRS type I include elevated levels of interleukin-6 and acute phase reagents. Histologically there are the signs of funiculitis or chorionic vasculitis.The marker of FIRS type II is the chemotactic chemokine CXCL10, which simulates maternal antifetal rejection.The article presents the basic mechanisms of the immune response in FIRS. In this type of pathology there are chronic inflammatory lesions of the placenta which are determined by histological study (chronic chorioamnionitis, vilitis of unknown etiology, chronic deciduitis).
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