Morphopathological changes induced by the Obstetrical Antiphospholipid Antibody Syndrome in fetal adnexa and uterus.

The Obstetrical Antiphospholipid Antibody Syndrome (OAAS) is representing a separate entity of the global Antiphospholipid Antibody Syndrome (APS), focusing the pregnancy morbidity. OAAS is generating morphopathological changes in almost all components of the gestational biologic transitory system (GBTS): placenta, umbilical cord or uterine wall. The most important, serious and lengthened anomalies are occuring in placenta. Our research has been developed on a group of 68 patients diagnosed with OAAS, initially using the Sapporo criteria and later using the "Sydney" ones. There have been morphopathologically examined: placenta, umbilical cord and myometrium. Histological examination revealed on one hand macroscopic modifications: fibrinoid deposits, white or red placental infarctions, intervillous thrombosis, marginal or basal decidual hematoma, calcareous deposits, umbilical cord thrombosis, and on the other hand microscopic findings: placental infarction, fibrinoid necrosis, myometrial thrombosis, degenerative myometrial disorders, focal myometrial necrosis, villous stasis and necrosis, umbilical cord thrombosis. Because of the increased prothrombotic background, in APS, any vessel or organ could be involved, with no exception for GBTS elements. The basis of the pregnancy morbidity from the obstetrical APS is represented by the morphopathological changes occurring in fetal adnexa and uterine structures.

Distribution of lactate dehydrogenase isoenzymes in coelomic fluid and fetal adnexae.

The objective of this study was to evaluate the distribution of lactate dehydrogenase isoenzymes in the human gestational sac. Total lactate dehydrogenase and its isoenzymes were measured in matched coelomic fluid and samples of villous and decidual tissues collected at the time of pregnancy termination in a group of 16 healthy women who were between 7 and 12 weeks of gestation. In addition intact secondary yolk sacs (n = 2) and fragments of fetal liver (n = 3) were collected. For comparison, samples of placental tissue, amniotic membrane and chorion obtained at term, were also investigated. In early pregnancy, H-type lactate dehydrogenase isoenzymes predominate in placental villous tissue and coelomic fluid, whereas M-type lactate dehydrogenase isoenzymes predominate in extracts of decidua, secondary yolk sac and fetal liver. These results highlight the important contribution of placental bioproducts to the constitution of the coelomic fluid. We observed also that placental patterns of lactate dehydrogenase isoenzymes change between the first and the third trimester of gestation, from the H-type to the M-type lactate dehydrogenase isoenzymes. We suggest that the lactate dehydrogenase pattern might be an indicator of proliferative or differentiative potential of the trophoblastic cells throughout pregnancy.