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Letters to the Editor

Re: Cudihy D, Lee RV. 2009. The pathophysiology of pre-eclampsia: current clinical concepts. Journal of Obstetrics and Gynaecology 29(7):576–582

Pages 426-427 | Published online: 12 May 2010

Dear Sir,

In this paper, the authors summarised the reasons for the observation that smoking reduces the incidence of pre-eclampsia as the following: (1) smoking decreases anti-angiogenic soluble fms-like tyrosine kinase 1 (sFlt-1); (2) nicotine in the cigarette smoke enhances angiogenesis; and (3) smokers have much larger placentas with increased capillary density compared with non-smokers, which is interpreted by the authors as ‘a response designed to increase the surface area available for oxygen exchange in order to compensate for impaired oxygen transport caused by carbon monoxide in cigarette smoke’.

The authors pointed out the ‘evil side’ of carbon monoxide (CO) and fully ignored its beneficial effects, which might explain why smokers have a decreased risk of pre-eclampsia.

Mounting evidence now speaks loudly and clearly for the vital importance of CO (Wu and Wang Citation2005). Both endogenous and exogenous CO can promote angiogenesis (Li Volti et al. Citation2005; Dulak et al. Citation2008) and suppress sFlt-1 release (Cudmore et al. Citation2007). In addition, CO suppresses inflammation (Mazzola et al. Citation2005; Chora et al. Citation2007) and relaxes blood vessels (Vedernikov et al. Citation1989; Lyall et al. Citation2000). Thus, CO could protect against pre-eclampsia, which is associated with an angiostatic, over-inflamed (Redman et al. Citation1999) and vasoconstrictive status.

The authors stated that smokers produce much larger placenta. However, this is not true. Smoking has no effect on placental weight (Williams et al. Citation1997). The authors confused placental weight with relative placental weight (placental to birth weight ratio). Smoking is associated with relative placental weight which, however, is solely due to the decreased birth weight by smoking.

The observation of increased capillary density in smokers (Pfarrer et al. Citation1999) is consistent with the pro-angiogenic effect of CO. It has been reported that exhaled CO is significantly lower in pre-eclamptic patients compared with healthy pregnant women (Baum et al. Citation2000), further supporting an important role of CO in the pathogenesis of pre-eclampsia.

Thus, CO in the cigarette smoke might explain why smokers have a decreased risk of pre-eclampsia.

Declaration of interest: The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.

References

  • Baum M, Schiff E, Kreiser D, Dennery PA, Stevenson DK, Rosenthal T et al 2000. End-tidal carbon monoxide measurements in women with pregnancy-induced hypertension and preeclampsia. American Journal of Obstetrics and Gynecology 183:900–903.
  • Chora AA, Fontoura P, Cunha A, Pais TF, Cardoso S, Ho PP et al 2007. Heme oxygenase-1 and carbon monoxide suppress autoimmune neuroinflammation. Journal of Clinical Investigation 117:438–447.
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  • Pfarrer C, Macara L, Leiser R, Kingdom J. 1999. Adaptive angiogenesis in placentas of heavy smokers. Lancet 354:303.
  • Redman CW, Sacks GP, Sargent IL. 1999. Preeclampsia: an excessive maternal inflammatory response to pregnancy. American Journal of Obstetrics and Gynecology 180:499–506.
  • Vedernikov YP, Graser T, Vanin AF. 1989. Similar endothelium-independent arterial relaxation by carbon monoxide and nitric oxide. Biomedica Biochimica Acta 48:601–603.
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