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2
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The diagnostic conundrum of maternal mirror syndrome progressing to pre-eclampsia - A case report.母源性镜像综合征进展为子痫前期的诊断难题——一例报告
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本文引用的文献

1
Clinical characteristics of mirror syndrome: a comparison of 10 cases of mirror syndrome with non-mirror syndrome fetal hydrops cases.镜像综合征的临床特征:10例镜像综合征与非镜像综合征胎儿水肿病例的比较
J Matern Fetal Neonatal Med. 2016;29(16):2630-4. doi: 10.3109/14767058.2015.1095880. Epub 2015 Oct 20.
2
Association of NT-proBNP with plasma renin activity and plasma aldosterone concentration in women with singleton pregnancy.在单胎妊娠的女性中,NT-proBNP 与血浆肾素活性和血浆醛固酮浓度的关系。
Pregnancy Hypertens. 2014 Jan;4(1):23-8. doi: 10.1016/j.preghy.2013.08.002. Epub 2013 Sep 4.
3
Reference ranges and determinants of total hCG levels during pregnancy: the Generation R Study.孕期总人绒毛膜促性腺激素水平的参考范围及决定因素:Generation R研究
Eur J Epidemiol. 2015 Sep;30(9):1057-66. doi: 10.1007/s10654-015-0039-0. Epub 2015 May 12.
4
Gestational weight gain according to number of fetuses in Japanese women.
J Perinat Med. 2014 Jul;42(4):523-8. doi: 10.1515/jpm-2013-0211.
5
Risk factors of eclampsia other than hypertension: pregnancy-induced antithrombin deficiency and extraordinary weight gain.子痫除高血压外的危险因素:妊娠诱导的抗凝血酶缺乏和体重异常增加。
Hypertens Pregnancy. 2012;31(2):268-77. doi: 10.3109/10641955.2011.638957. Epub 2011 Dec 9.
6
Mirror syndrome: a systematic review of fetal associated conditions, maternal presentation and perinatal outcome.镜像综合征:胎儿相关疾病、母体表现和围生期结局的系统评价。
Fetal Diagn Ther. 2010;27(4):191-203. doi: 10.1159/000305096. Epub 2010 Mar 27.
7
Role of aldosterone availability in preeclampsia.醛固酮可用性在子痫前期中的作用。
Mol Aspects Med. 2007 Apr;28(2):245-54. doi: 10.1016/j.mam.2007.03.002. Epub 2007 Apr 11.
8
Cytomegalovirus-induced mirror syndrome associated with elevated levels of angiogenic factors.巨细胞病毒诱导的镜像综合征与血管生成因子水平升高相关。
Obstet Gynecol. 2007 May;109(5):1205-6; author reply 1206. doi: 10.1097/01.AOG.0000263776.46071.d1.
9
Human adrenal cortex hyperfunction due to LH/hCG.由促黄体生成素/人绒毛膜促性腺激素引起的人类肾上腺皮质功能亢进。
Mol Cell Endocrinol. 2007 Apr 15;269(1-2):46-50. doi: 10.1016/j.mce.2006.06.014. Epub 2007 Feb 11.
10
Cytomegalovirus-induced mirror syndrome associated with elevated levels of circulating antiangiogenic factors.巨细胞病毒诱导的镜像综合征与循环抗血管生成因子水平升高相关。
Obstet Gynecol. 2007 Feb;109(2 Pt2):549-52. doi: 10.1097/01.AOG.0000248538.03280.cf.

巴兰坦综合征发生期间及之后超声心动图和血液变量的变化。

Changes in echocardiography and blood variables during and after development of Ballantyne syndrome.

作者信息

Umazume Takeshi, Morikawa Mamoru, Yamada Takahiro, Minakami Hisanori

机构信息

Hokkaido University Graduate School of Medicine, Sapporo, Japan.

出版信息

BMJ Case Rep. 2016 Jun 21;2016:bcr2016216012. doi: 10.1136/bcr-2016-216012.

DOI:10.1136/bcr-2016-216012
PMID:27329098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4932354/
Abstract

We report a pregnant woman who was monitored by echocardiography and determination of blood variables, including components of the renin-angiotensin-aldosterone system (RAAS), cardiac biomarkers and soluble fms-like tyrosine kinase-1 (sFlt-1), during and after the development of Ballantyne syndrome. Generalised maternal oedema with dyspnoea following fetal and placental hydrops necessitated a caesarean section at 33 weeks of gestation. Changes in blood variables and simultaneous echocardiography changes indicated acutely enhanced RAAS and hyperdynamic left ventricular function in response to excessive volume overload (as evidenced by brain-type natriuretic peptide level of 523 pg/mL) in the absence of increased systemic vascular resistance. Elevated sFlt-1 (15 600 pg/mL) and human chorionic gonadotrophin (404 000 IU/L) levels were also noted. The increased plasma aldosterone concentration (2070 pg/mL) may have been responsible for the increase in circulating plasma volume, and the increased sFlt-1 level was responsible for generalised maternal oedema. It remains unclear which factor(s) triggered RAAS activation.

摘要

我们报告了一名孕妇,在发生巴兰坦综合征期间及之后,通过超声心动图以及血液变量测定(包括肾素-血管紧张素-醛固酮系统(RAAS)的组成部分、心脏生物标志物和可溶性fms样酪氨酸激酶-1(sFlt-1))对其进行监测。胎儿和胎盘水肿后出现的全身性母体水肿伴呼吸困难,使得在妊娠33周时进行了剖宫产。血液变量的变化以及同步的超声心动图变化表明,在没有全身血管阻力增加的情况下,由于容量超负荷过大(脑钠肽水平为523 pg/mL可证明),RAAS急性增强且左心室功能亢进。还注意到sFlt-1(15 600 pg/mL)和人绒毛膜促性腺激素(404 000 IU/L)水平升高。血浆醛固酮浓度升高(2070 pg/mL)可能是循环血浆量增加的原因,而sFlt-1水平升高是全身性母体水肿的原因。尚不清楚是哪些因素触发了RAAS激活。