Berle Jan Øystein, Steen Vidar M, Aamo Trond Oskar, Breilid Harald, Zahlsen Kolbjørn, Spigset Olav
Centre for Child and Adolescent Mental Health, University of Bergen, Bergen, Norway.
J Clin Psychiatry. 2004 Sep;65(9):1228-34. doi: 10.4088/jcp.v65n0911.
The aims of the study were to quantify the drug exposure in breastfed infants of antidepressant-treated mothers, to identify possible adverse events, and to correlate these variables to maternal and infant drug metabolism-relevant genotypes and milk triglyceride content.
The study included 25 lactating women treated with citalopram (N = 9), sertraline (N = 6), paroxetine (N = 6), fluoxetine (N = 1), or venlafaxine (N = 3) and their 26 breastfed infants. Drug concentrations in maternal and infant serum and milk were analyzed using liquid chromotography mass spectrometry methods; milk triglyceride levels were measured with a commercial kit. Cytochrome P450 (CYP) 2D6 and CYP2C19 activity was determined by polymerase chain reaction-based genotyping of the mothers and infants. An infant adverse event questionnaire was completed by the medication-treated mothers as well as by a control group of medication-free breastfeeding mothers of 68 infants.
Sertraline and paroxetine were not detected in any of the drug-exposed infants. The infant serum level of citalopram was either undetectable (N = 4) or low (N = 6). All venlafaxine-exposed infants had measurable drug concentrations. We identified a paroxetine-treated mother and her infant who were both CYP2D6 poor metabolizers, as well as a citalopram-treated mother with CYP2C19 poor metabolizer status, but the serum drug levels of their infants were still either undetectable (paroxetine) or low (citalopram). There was no evidence of adverse events in the drug-exposed infants.
Serum drug levels in breastfed infants of antidepressant-treated mothers were undetectable or low. This study adds further evidence to previously published data indicating that breastfeeding should not be generally discouraged in women using serotonin reuptake inhibitor anti-depressants.
本研究的目的是量化接受抗抑郁药物治疗的母亲所哺乳婴儿的药物暴露量,识别可能的不良事件,并将这些变量与母亲和婴儿与药物代谢相关的基因型以及乳汁甘油三酯含量相关联。
该研究纳入了25名接受西酞普兰(N = 9)、舍曲林(N = 6)、帕罗西汀(N = 6)、氟西汀(N = 1)或文拉法辛(N = 3)治疗的哺乳期妇女及其26名母乳喂养的婴儿。采用液相色谱质谱法分析母婴血清和乳汁中的药物浓度;使用商用试剂盒测量乳汁甘油三酯水平。通过基于聚合酶链反应的母亲和婴儿基因分型来确定细胞色素P450(CYP)2D6和CYP2C19活性。接受药物治疗的母亲以及68名未用药的母乳喂养母亲组成的对照组完成了婴儿不良事件问卷。
在任何药物暴露婴儿中均未检测到舍曲林和帕罗西汀。婴儿血清中的西酞普兰水平要么无法检测到(N = 4),要么很低(N = 6)。所有暴露于文拉法辛的婴儿都有可测量的药物浓度。我们识别出一名接受帕罗西汀治疗的母亲及其婴儿均为CYP2D6慢代谢者,以及一名接受西酞普兰治疗且母亲为CYP2C19慢代谢者,但他们婴儿的血清药物水平仍然要么无法检测到(帕罗西汀),要么很低(西酞普兰)。没有证据表明药物暴露婴儿出现不良事件。
接受抗抑郁药物治疗的母亲所哺乳婴儿的血清药物水平无法检测到或很低。本研究为先前发表的数据增添了进一步的证据,表明一般不应劝阻使用5-羟色胺再摄取抑制剂抗抑郁药的女性进行母乳喂养。