Stallmach T, Karolyi L, Lichtlen P, Maurer M, Hebisch G, Joller H, Marti H H, Gassmann M
Department of Pathology, University Hospital Zurich, Switzerland.
Pediatr Res. 1998 Mar;43(3):349-54. doi: 10.1203/00006450-199803000-00007.
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.
胎儿肝脏是子宫内生命期间的主要造血器官。对肝脏切片进行形态计量学研究，以检测宫内生长受限和先兆子痫时发生的变化。与对照组（n = 10）相比，先兆子痫母亲所生胎儿的红系细胞平均严重减少60%（n = 18）。进一步检查发现，分化早期的红系细胞比晚期受影响更大（减少80%）（减少55%）。18例先兆子痫母亲所生胎儿中有7例未出现生长受限，但肝脏红细胞生成严重减少。我们认为，红细胞生成受损的主要因素是先兆子痫本身，而非宫内生长受限。子宫内红细胞生成的调节可能取决于多种造血生长因子的相互作用，而先兆子痫可能会改变这种平衡。为验证这一观点，我们对胎儿血液中的促红细胞生成素和羊水中的各种细胞因子进行了定量分析。在先兆子痫情况下出生的婴儿中，促红细胞生成素和白细胞介素（IL）-3水平升高，而粒细胞/巨噬细胞集落刺激因子（CSF）、粒细胞集落刺激因子和IL-1β的浓度降低，IL-6和IL-8水平保持不变。先兆子痫时，外周血红细胞数量增加与主要造血部位胎儿肝脏造血抑制之间存在差异。同时，一些造血细胞因子升高，而另一些则降低。我们设想，在先兆子痫过程中，对造血生长因子进行定量分析可能有助于预测子宫内生命状况的恶化。
