Smoking, Hemoglobin Concentration and Pregnancy-Induced Hypertension

Rasmussen, Svein; Øian, Pål

doi:10.1159/000010039

Cited by 13 publications

(10 citation statements)

References 29 publications

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“…25 Our database holds information on maternal smoking, which is a strong and common risk factor for fetal growth restriction and seems to be negatively associated with PIH. 26 As expected, adjustment for smoking increased the association of SGA with later PIH (data not shown). The Medical Birth Registry also holds data on conditions like chronic renal disease, chronic hearth disease, rheumatoid arthritis, diabetes mellitus type 1 and 2, and gestational diabetes.…”

Section: Rasmussen and Irgens Pregnancy-induced Hypertension In Womensupporting

confidence: 71%

Pregnancy-Induced Hypertension in Women Who Were Born Small

Rasmussen

Irgens

2007

Hypertension

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Abstract-We assessed whether a pregnant woman who was born small for gestational age has increased risk of pregnancy-induced hypertension (PIH), and whether the same applies to a pregnant partner of a man who was born small for gestational age. We linked generational data from the medical birth registry of Norway (1967Norway ( -2005. Female and male newborns were identified as parents with 197 716 and 131 959 first or second pregnancies from 1998 to 2005, respectively. In the first pregnancy in women who were born with birth weight Ͻ2.5, 2.5 to 4.9, and 5 to 9.9 birth weight percentiles, odds ratios of PIH in general adjusted for smoking and maternal age were 1.5, 1.4, and 1.1, respectively, compared with percentile 25 to 75. In the second pregnancy, corresponding odds ratios were 1.5, 1.3, and 1.2, respectively. A similar trend was found in all of the subgroups of PIH. Women who were born below the 5th birth weight percentile were 2 to 3 times more likely to have preeclampsia with onset before 34 weeks of gestation than those with birth weight between the 25th and 75th percentiles (adjusted odds ratios: 1.8 to 2.8). Father's birth weight for gestational age was not associated with mother's development of PIH. In conclusion, women who were born growth restricted after normotensive pregnancies were more likely to develop PIH later in life. The lack of association with the father's size at birth agrees with the hypothesis of fetal environmental origin of PIH, although maternal genetic transmission of susceptibility for PIH cannot be ruled out.

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Section: Rasmussen and Irgens Pregnancy-induced Hypertension In Womensupporting

confidence: 71%

Pregnancy-Induced Hypertension in Women Who Were Born Small

Rasmussen

Irgens

2007

Hypertension

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“…In addition, although obesity has become more prevalent in Norway, the pregnancy population is still relatively lean. 22 Our database holds data on maternal smoking, which seems to be negatively associated with PIH, 23 although a risk factor for fetal growth restriction. As expected, adjustment for smoking increased rather than decreased the association of SGA with later PIH (data not shown).…”

Section: Strengths and Weaknesses: Possible Sources Of Confoundingmentioning

confidence: 99%

History of Fetal Growth Restriction Is More Strongly Associated With Severe Rather Than Milder Pregnancy-Induced Hypertension

Rasmussen

Irgens

2008

Hypertension

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Abstract-We assessed whether fetal growth restriction without pregnancy-induced hypertension (PIH) is associated with the different clinical subgroups of PIH in the subsequent pregnancy. We also assessed the maternal and paternal contributions to this effect. Pairs of first and second, second and third, third and fourth, and fourth and fifth births were identified among all of the births in Norway: 137 375 pairs with same mother and father, 18 376 pairs with same mother and different fathers, and 18 916 pairs with same father and different mothers. Second births in each pair were restricted to those that occurred in 1998 -2005. Odds ratios to predict early onset, severe, and mild preeclampsia and transient hypertension in the second birth from birth weight Ͻ1500 g in the first compared with 3500 to 3999 g were 13.8, 7.1, 3.5, and 2.2, respectively. Odds ratios to predict early onset, severe, and mild preeclampsia and transient hypertension from birth weight below the 2.5th percentile compared with percentiles 10.0 to 89.9 were 4.2, 2.5, 2.1, and 1.7, respectively. Men who fathered a child with low birth weight in 1 woman were not more likely to later father a PIH pregnancy in another woman. The results indicate that placental dysfunction and PIH share a genetic factor that can be expressed as fetal growth restriction in 1 pregnancy and PIH in a subsequent pregnancy. Future genetic study is needed to confirm whether the association is caused by delayed genetic expression of endothelial dysfunction and whether the clinical subgroups of PIH have different genetic backgrounds. (Hypertension. 2008;51:1231-1238.)

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“…For Hb, the mechanisms that contribute to hypertensive disorders of pregnancy may be related with blood viscosity, which can be induced by elevation of hematocrit and Hb levels, since it has been suggested that increased blood viscosity may worsen cardiovascular function partly through an effect on blood pressure [31]. Given this finding regarding blood viscosity, it might probably explain the previous studies [7-9] that the positive associations between increased Hb and PIH were in agreement with elevated blood viscosity during pregnancy. Furthermore, free Hb is a scavenger of nitric oxide (NO), which can relax the muscle cells, increased free Hb levels may thus bind to NO and contribute to vasoconstriction and hypertension [32,33].…”

Section: Discussionmentioning

confidence: 97%

“…A recent system review including 13 trials, however, indicates that dietary intervention appears effective to reduce total and weekly gestational weight gain, but no significant effect on preventing preeclampsia and gestational diabetes [21]. For Hb, several observational studies found significantly increased Hb concentrations in women who developed PIH in the second or third trimester [7-9]. Also, a recent study showed that Hb level was positively associated with both SBP and DBP in a large cohort of healthy individuals [22].…”

Section: Discussionmentioning

confidence: 99%

“…Although the etiology of hypertensive disorders during pregnancy is not yet completely clear, maternal anthropometric measure such as high body mass index (BMI) in pregnancy has been reported to increase the risk of pregnancy-induced hypertension (PIH) or preeclampsia [3-6]. Similarly, several studies have shown that maternal hemoglobin (Hb) levels were positively associated with PIH [7-9]. Moreover, a review suggests that higher than normal hemoglobin concentrations should be regarded as an indicator of possible pregnancy complications [10].…”

Section: Introductionmentioning

confidence: 99%

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Interaction of body mass index and hemoglobin concentration on blood pressure among pregnant women in Guangxi, China

Zhong

Long

et al. 2014

BMC Public Health

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BackgroundBody mass index (BMI) and hemoglobin (Hb) are positively associated with hypertensive disorders among pregnant women. The aim of this study was to estimate a potential interaction between high BMI and high Hb concentrations on systolic blood pressure (SBP) and diastolic blood pressure (DBP) in pregnancy.MethodsWe recruited 4497 single-birth women aged 18–43 years who received routine antenatal care at three hospitals of Guigang, Guangxi, China, from December 2007 to January 2011. Of 4497 participants, 3472 women were in the first trimester, with following up, 2986 women and 2261 women were left in the second and third trimester, respectively. Clinical data were derived from medical records of each woman. We used multivariable linear regression, by trimesters of pregnancy, to evaluate the associations of high BMI and high Hb concentrations with SBP and DBP according to cross-sectional design.ResultsIn multivariable analyses, BMI was positively associated with SBP throughout all trimesters, but the corresponding association for Hb concentrations only in the first trimester, whereas both BMI and Hb concentrations were positively associated with DBP in the first and third trimesters. After full adjustment for confounding, the average differences in SBP and DBP comparing women with high BMI and high Hb to those with non-high BMI and non-high Hb were 2.9 mmHg (95% CI: 0.8 to 5.0 mmHg) and 3.9 mmHg (95% CI: 1.5 to 6.3 mmHg) in the first trimester, 2.6 mmHg (95% CI: 0.4 to 4.8 mmHg) and 1.5 mmHg (95% CI: -1.3 to 4.3 mmHg) in the second trimester, and 4.8 mmHg (95% CI: 2.3 to 7.4 mmHg) and 5.7 mmHg (95% CI: 3.2 to 8.3 mmHg) in the third trimester, respectively. With respect to the interaction, significant combined effects between high BMI and high Hb were confirmed on SBP (P = 0.02) and DBP (P = 0.004) in the third trimester, and the amount of interaction on SBP and DBP were 2.0 mmHg (95% CI: 0.1 to 3.9 mmHg) and 2.3 mmHg (95% CI: 0.4 to 4.3 mmHg), respectively.ConclusionOur findings suggest that high BMI and high Hb concentrations may have a synergistic effect on blood pressure in late stage of pregnancy.

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Smoking, Hemoglobin Concentration and Pregnancy-Induced Hypertension

Cited by 13 publications

References 29 publications

Pregnancy-Induced Hypertension in Women Who Were Born Small

Pregnancy-Induced Hypertension in Women Who Were Born Small

History of Fetal Growth Restriction Is More Strongly Associated With Severe Rather Than Milder Pregnancy-Induced Hypertension

Interaction of body mass index and hemoglobin concentration on blood pressure among pregnant women in Guangxi, China

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