title: Fetuses from preeclamptic mothers show reduced hepatic erythropoiesis.
abstract: The fetal liver is the main hematopoietic organ during intrauterine life. Morphometrical studies were performed on liver sections to detect changes occurring with intrauterine growth retardation and preeclampsia. Compared with the controls (n = 10), fetuses from preeclamptic mothers showed a severe reduction of erythroid cells by 60% on average (n = 18). Closer examination revealed that the erythroid cells at early stages of differentiation were more affected (80% reduction) than at later stages (55%). Seven out of 18 fetuses from preeclamptic mothers did not show growth retardation but exhibited severely reduced hepatic erythropoiesis. We suggest that the prime factor for impaired red blood cell production is preeclampsia itself rather than intrauterine growth retardation. Regulation of erythropoiesis in utero might depend on the interaction of many hematopoietic growth factors, and preeclampsia might alter the balance. To test this notion, we quantitated erythropoietin in fetal blood and various cytokines in the amniotic fluid. An elevation of erythropoietin and interleukin (IL)-3 levels was seen in babies born under the conditions of preeclampsia, whereas the concentrations of granulocyte/macrophage-colony-stimulating factor (CSF), granulocyte-CSF, and IL-1 beta were reduced, and the levels of IL-6 and IL-8 remained constant. With preeclampsia, a discrepancy between elevation of erythrocyte numbers in peripheral blood and depression of hematopoiesis at the main production site, the fetal liver, is seen. Concomitantly, there is elevation of some but reduction of other hematopoietic cytokines. We envision that during the course of preeclampsia quantitation of hematopoietic growth factors might allow to predict the deterioration of in utero life conditions.
authors.affiliation: Department of Pathology, University Hospital Zurich, Switzerland.
authors.forename: T
authors.initials: T
authors.lastname: Stallmach
authors.forename: L
authors.initials: L
authors.lastname: Karolyi
authors.forename: P
authors.initials: P
authors.lastname: Lichtlen
authors.forename: M
authors.initials: M
authors.lastname: Maurer
authors.forename: G
authors.initials: G
authors.lastname: Hebisch
authors.forename: H
authors.initials: H
authors.lastname: Joller
authors.forename: H H
authors.initials: HH
authors.lastname: Marti
authors.forename: M
authors.initials: M
authors.lastname: Gassmann
mesh_terms: D000653:Amniotic Fluid / Q000378:metabolism; D016022:Case-Control Studies; D016207:Cytokines / Q000378:metabolism; D004920:Erythropoiesis / Q000502:physiology; D004921:Erythropoietin / Q000097:blood; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005317:Fetal Growth Retardation / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D005333:Fetus / Q000473:pathology* / Q000503:physiopathology; D016298:Hematopoietic Cell Growth Factors / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000473:pathology* / Q000503:physiopathology; D008431:Maternal-Fetal Exchange; D011225:Pre-Eclampsia / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D011247:Pregnancy
chemical_list: D016207:Cytokines; D016298:Hematopoietic Cell Growth Factors; D004921:Erythropoietin