Rasmussen Svein, Irgens Lorentz M
Community Medicine Department, Faculty of Medicine, Urmia University of Medical Sciences,, Urmia, Iran.
BMC Pregnancy Childbirth. 2006 Apr 21;6:16. doi: 10.1186/1471-2393-6-16.
It is well known that smoking and pregnancy induced hypertension (PIH) are associated with decreased fetal growth. It has been reported that in preeclampsia the fetal growth deficit attributable to smoking is higher, which has been contradicted in other studies. We therefore evaluated the effects on fetal growth of early- and late onset PIH and chronic hypertension and how cigarette smoking modify these effects. We also quantified the proportion of small for gestational age (SGA) cases attributable to PIH, chronic hypertension, and smoking.
Population-based study based on record of 215598 singleton pregnancies from the Medical Birth Registry of Norway.
In severe preeclampsia, mild preeclampsia, transient hypertension, and normotension in term birth, odds ratios (ORs) of SGA in smokers compared with non-smokers were 1.4 (95% confidence interval 0.9, 2.2), 1.6 (1.3, 1.9), 2.3 (1.8, 3.1), and 2.0 (1.9, 2.1), respectively. For preterm births, corresponding ORs were 1.3 (0.9, 2.0), 1.8 (1.1, 3.0), 4.1 (1.9, 9.0), and 1.7 (1.4, 2.0), respectively. The effect of early onset PIH was stronger than that in term births, while the effect of smoking was equal in preterm and term newborns. Only in non-smokers who delivered at term, the rates of SGA significantly increased with the severity of PIH (ORs = 1.3 (1.1, 1.5), 1.8 (1.7, 2.0), and 2.5 (2.2, 3.0) for transient hypertension, mild-, and severe preeclampsia, respectively). The combined effects of smoking and hypertension were generally not synergistic. The effect of smoking was not stronger in women who had chronic hypertension. Nor were the effects of chronic hypertension stronger in smokers. PIH explained 21.9 and 2.5% of preterm and term cases of SGA, respectively, while smoking explained 12% of SGA cases.
The effects of hypertensive disorder and smoking were generally not synergistic, which suggest that they may exert their main actions on separate sites or work through separate mechanisms within or outside the placenta. If smoking were eliminated in pregnant women, the number of SGA cases would be reduced by 12%.
众所周知，吸烟与妊娠高血压（PIH）均与胎儿生长发育迟缓有关。据报道，子痫前期中由吸烟导致的胎儿生长发育不足更为严重，但其他研究对此提出了反驳。因此，我们评估了早发型和晚发型PIH以及慢性高血压对胎儿生长发育的影响，以及吸烟如何改变这些影响。我们还量化了因PIH、慢性高血压和吸烟导致的小于胎龄儿（SGA）病例的比例。
基于挪威医学出生登记处215598例单胎妊娠记录进行的人群研究。
在重度子痫前期、轻度子痫前期、短暂性高血压和足月分娩的血压正常者中，吸烟者发生SGA的比值比（OR）与非吸烟者相比分别为1.4（95%置信区间0.9，2.2）、1.6（1.3，1.9）、2.3（1.8，3.1）和2.0（1.9，2.1）。对于早产，相应的OR分别为1.3（0.9，2.0）、1.8（1.1，3.0）、4.1（1.9，9.0）和1.7（1.4，2.0）。早发型PIH的影响在早产中比足月分娩时更强，而吸烟在早产和足月新生儿中的影响相同。仅在足月分娩的非吸烟者中，SGA的发生率随PIH严重程度显著增加（短暂性高血压、轻度和重度子痫前期的OR分别为1.3（1.1，1.5）、1.8（1.7，2.0）和2.5（2.2，3.0））。吸烟与高血压的联合作用通常不存在协同效应。吸烟对患有慢性高血压的女性影响并不更强。慢性高血压对吸烟者的影响也不更强。PIH分别解释了21.9%的早产SGA病例和2.5%的足月SGA病例，而吸烟解释了12%的SGA病例。
高血压疾病和吸烟的影响通常不存在协同效应，这表明它们可能在不同部位发挥主要作用，或通过胎盘内外不同机制起作用。如果孕妇戒烟，SGA病例数将减少12%。
