Pasman Suzanne A, Meerman Robertjan H, Vandenbussche Frank P H A, Oepkes Dick
Department of Obstetrics, Leiden University Medical Centre, Leiden, The Netherlands.
Am J Obstet Gynecol. 2006 Apr;194(4):972-5. doi: 10.1016/j.ajog.2006.02.028.
The pathophysiology of fetal hydrops is still unclear. One factor that is believed to contribute to hydrops is hypoalbuminemia. Our research question was whether hypoalbuminemia in immune hydrops is causative or a secondary effect.
Between 1987 and 2005, fetal blood samples were taken at the first fetal blood transfusion in 224 Rh-D alloimmunized pregnancies. We measured hemoglobin concentration and albumin concentration and assessed the severity of hydrops.
A decrease in albumin concentration occurred only below a hemoglobin deficit of >8 SDs in 27 fetuses. In 161 nonhydropic, 44 mildly hydropic, and 19 severely hydropic fetuses, albumin concentrations were >2 SDs below the mean for gestational age in 6%, 14%, and 63%, respectively.
Our finding that most fetuses with immune hydrops have an albumin concentration within the normal range (71%) suggests that hypoalbuminemia is unlikely to cause the initial development of immune hydrops.
胎儿水肿的病理生理学仍不清楚。低白蛋白血症被认为是导致水肿的一个因素。我们的研究问题是免疫性水肿中的低白蛋白血症是病因还是继发效应。
1987年至2005年期间，在224例Rh - D同种免疫妊娠的首次胎儿输血时采集胎儿血样。我们测量了血红蛋白浓度和白蛋白浓度，并评估了水肿的严重程度。
仅在27例胎儿血红蛋白缺乏>8标准差以下时白蛋白浓度才下降。在161例非水肿、44例轻度水肿和19例重度水肿胎儿中，白蛋白浓度分别在6%、14%和63%的胎儿中低于胎龄均值2标准差以上。
我们的研究发现，大多数免疫性水肿胎儿的白蛋白浓度在正常范围内（71%），这表明低白蛋白血症不太可能导致免疫性水肿的初始发展。
