Hayashi Masatoshi
Department of Obstetrics and Gynecology, Koshigaya Hospital, Dokkyo University School of Medicine, 2-1-50, Minami-Koshigaya, Koshigaya-shi, Saitama 343-8555, Japan.
Clin Sci (Lond). 2003 Sep;105(3):269-71. doi: 10.1042/CS20030181.
Schlembach and co-workers in this issue of Clinical Science have studied the association of maternal and/or fetal factor V Leiden (FVL) and prothrombin G20210A gene mutation with HELLP syndrome and intrauterine growth restriction (IUGR) to confirm whether these genetic mutations are important risk factors for the pathogenesis of the HELLP syndrome, leading to an inadequate maternal-fetal circulation. Results showed that fetal FVL and prothrombin G20210A gene mutation were significantly associated with IUGR. The authors speculated that fetal thrombophilic mutations resulted in placental microthrombosis, leading to a disturbed fetoplacental blood flow. This study represents another important step in our understanding of the pathophysiological action of fetal thrombophilic mutations on fetal development. Regarding the aetiology of pre-eclampsia, one possible speculation is that systemic immune maladaptation, including systemic cytokine imbalance, contributes to placental ischaemia and systemic vessel abnormalities leading to pre-eclampsia.
施伦巴赫及其同事在本期《临床科学》中研究了母体和/或胎儿因子V莱顿（FVL）及凝血酶原G20210A基因突变与HELLP综合征和宫内生长受限（IUGR）的关联，以确认这些基因突变是否为HELLP综合征发病机制中的重要危险因素，进而导致母婴循环不足。结果显示，胎儿FVL和凝血酶原G20210A基因突变与IUGR显著相关。作者推测，胎儿血栓形成倾向突变导致胎盘微血栓形成，进而导致胎盘血流紊乱。这项研究是我们在理解胎儿血栓形成倾向突变对胎儿发育的病理生理作用方面迈出的又一重要一步。关于子痫前期的病因，一种可能的推测是，包括全身细胞因子失衡在内的全身免疫适应不良会导致胎盘缺血和全身血管异常，进而引发子痫前期。
