Efficacy of nicotine replacement therapy in pregnancy

Coleman, Tim; Chamberlain, Catherine; Ma, Davey; Cooper, Sue; Leonardi‐Bee, Jo

doi:10.1111/1471-0528.12064

Cited by 3 publications

(3 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite the deleterious effects of DNE on brain development and cardiorespiratory control in animal models discussed above, obstetricians routinely prescribe nicotine patches in pregnant, nicotine‐addicted mothers (Coleman et al, ), with the intention of avoiding the other chemicals in tobacco smoke. However, whether or not nicotine patches increase smoking cessation in pregnancy or improve birth outcomes is unclear (Coleman et al, ; Coleman et al, ; Coleman et al, ). Moreover, there are no data on the effects of nicotine patches on cardiorespiratory control in human neonates.…”

Section: Discussionmentioning

confidence: 99%

Developmental nicotine exposure alters cholinergic control of respiratory frequency in neonatal rats

Wollman

Haggerty

Pilarski

et al. 2016

Developmental Neurobiology

View full text Add to dashboard Cite

Prenatal nicotine exposure with continued exposure through breast milk over the first week of life (developmental nicotine exposure, DNE) alters the development of brainstem circuits that control breathing. Here, we test the hypothesis that DNE alters the respiratory motor response to endogenous and exogenous acetylcholine (ACh) in neonatal rats. We used the brainstem-spinal cord preparation in the split-bath configuration, and applied drugs to the brainstem compartment while measuring the frequency and amplitude of the fourth cervical ventral nerve roots (C4VR), which contain the axons of phrenic motoneurons. We applied ACh alone; the nicotinic acetylcholine receptor (nAChR) antagonist curare, either alone or in the presence of ACh; and the muscarinic acetylcholine receptor (mAChR) antagonist atropine, either alone or in the presence of ACh. The main findings include: 1) atropine reduced frequency similarly in controls and DNE animals, while curare caused modest slowing in controls but no consistent change in DNE animals; 2) DNE greatly attenuated the increase in C4VR frequency mediated by exogenous ACh; 4) stimulation of nAChRs with ACh in the presence of atropine increased frequency markedly in controls, but not DNE animals; 5) stimulation of mAChRs with ACh in the presence of curare caused a modest increase in frequency, with no treatment group differences. DNE blunts the response of the respiratory central pattern generator to exogenous ACh, consistent with reduced availability of functionally competent nAChRs; DNE did not alter the muscarinic control of respiratory motor output.

show abstract

Section: Discussionmentioning

confidence: 99%

Developmental nicotine exposure alters cholinergic control of respiratory frequency in neonatal rats

Wollman

Haggerty

Pilarski

et al. 2016

Developmental Neurobiology

View full text Add to dashboard Cite

show abstract

“…We appreciate the letter of Coleman et al 1 in response to our report in BJOG. 2 First, we are very sorry that we did not include in our review Coleman et al's review, 3 which was published in early 2011.…”

Section: Sirmentioning

confidence: 88%

“…

We appreciate the letter of Coleman et al 1 in response to our report in BJOG.2 First, we are very sorry that we did not include in our review Coleman et al's review, 3 which was published in early 2011. We should have searched and reviewed previous literature on this issue more thoroughly.

Second, we agree with them that there is 'insufficient' evidence to support the use of pharmacotherapy for smoking cessation in pregnant smokers because no significant efficacy was found in the three placebo-controlled trials, whereas a significant efficacy was found only in the four non placebocontrolled trials.

…”

mentioning

confidence: 99%

Authors' response to: Efficacy of nicotine replacement therapy in pregnancy

Myung¹,

Hg²

2013

BJOG

View full text Add to dashboard Cite

We appreciate the letter of Coleman et al. 1 in response to our report in BJOG.2 First, we are very sorry that we did not include in our review Coleman et al.'s review, 3 which was published in early 2011. We should have searched and reviewed previous literature on this issue more thoroughly.Second, we agree with them that there is 'insufficient' evidence to support the use of pharmacotherapy for smoking cessation in pregnant smokers because no significant efficacy was found in the three placebo-controlled trials, whereas a significant efficacy was found only in the four non placebocontrolled trials. We already described this in the limitations section of the Discussion. We concluded that there 'may' be clinical evidence to support the use of pharmacotherapy for smoking cessation among pregnant smokers.Third, when we reviewed their previous meta-analysis and then compared it with ours, we found that Coleman et al. used a random-effects model in all the analyses, whereas we used both fixed-effects and random-effects models according to the results of the heterogeneity test (i.e. fixed-effects model for data showing less heterogeneity and random-effects model for data showing heterogeneity). Coleman et al. reported the pooled risk ratio (RR) and 95% confidence interval (95% CI) for smoking cessation in later pregnancy after using nicotine replacement therapy (NRT) was 1.63 (0.85-3.14) using a random-effects model. When we performed a 'fixed-effects' meta-analysis using data shown in Figure 2 of Coleman et al.'s review (I 2 = 45%; in our review, when I 2 is <50%, we used a fixed-effects model), NRT was efficacious (pooled RR, 1.47; 95% CI 1.05-2.05; I 2 = 44.9%). Hence, the main reason why the findings and conclusions are not consistent between the two metaanalyses, although similar data were used, is that different models were used, respectively. If Coleman et al. applied a fixed-effects model when I 2 is <50%, their conclusion would also be that NRT is efficacious, as in our review.Last, the remaining issue would be that we should present more conservative findings when the pooled effect sizes are different in the meta-analyses by using between fixed-effects and random-effects models in case of less heterogeneity. We, basically, think that using a fixed-effects model is reasonable although the findings are different between the two models if the heterogeneity test shows less heterogeneity (i.e. I 2 < 50%). However, we want to hear other experts' opinions on this issue. &

show abstract