Fatores relacionados às microangiopatias trombóticas na gestação: revisão integrativa.

Abstract

Pregnancy can lead to the occurrence of Thrombotic Microangiopathy (TMA), chacterized by presence of microangiopathic hemolytic anemia and existence of thrombus in the microcirculation. Not very frequent conditions, but determine high maternal­fetal morbimortality, such as Hemolytic­Uremic Syndrome (HUS), Thrombotic Thrombocitopenic Purpura (TTP) and HELLP Syndrome. The present study intends to identify factors related to thrombotic microangiopathic in pregnant women, by analysis of scientific publications. The method was an integrative licterature review, using the descriptors thrombotic microangiopathy, pregnancy; consulted data base were PubMed, LILACS and SciELo, from August,2003 to September, 2014. Through detailed analysis of six selected articles the results of this review was possible, with elaboration of sinoptic boards of obtained data. Evidences point to an inappropriate cleavage of multimers of Von Willebrand factor (vWF), due to ADAMTS13 deficiency in TTP; endothelial activation as responsible for thrombotichemolytic state that occurs in gravidic diathesis of HELLP Syndrome; and the desregulation of alternative complement pathway involved in the atypical HUS, these are the main pathophysiologic mechanisms inveolved in TMAs, however, sometimes, differenciation among the three major microangiopathic syndromes metioned is a hard task, remaining in this context the obscurity of intersectional or undifferenciated states, thus, on many occasions, supportive therapy is the most effective management of such syndromes. The main factors related to TMAs seen were: alteration of the activity of ADAMTS13, complement regulatory gene mutation, pregnancy stage, maternal age, parity, laboratorial alterations, and abnormalities of the alternative complement pathway. We conclude the spectrum of thrombotic microangiopathic diseases during pregnancy have multifactorial characteristics and there is a lot to be discoverd about its real pathophysiological mechanism, as well as about the differentiation factors of TMAs, in order to provide a better clinical therapeutic management.