Smoking and the correlation between birth weight and placental weight. Evidence of interaction with maternal haptoglobin phenotype

Gloria‐Bottini, F.; Bottini, E

doi:10.1016/j.ejogrb.2014.12.019

Cited by 6 publications

(4 citation statements)

References 25 publications

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“…They reported a positive staining with Hp in cases with histological chorioamnionitis and a strong correlation with cord blood Hp and IL-6 levels and concluded that Hp had a role in triggering preterm birth by enhancing placental PGE 2 . Another study among pregnant women by Gloria-Bottini et al evaluated the maternal haptoglobin phenotype among smoking mothers and found a correlation with preserved placental weight and the Hp * 2 allele [22]. In our small sample size study, there were no smoking mothers and hence smoking was not taken as a variable.…”

Section: Discussionmentioning

confidence: 61%

Maternal Serum Haptoglobin Levels as a Marker of Preterm Premature Rupture of Membranes

Buyuk

Oskovi-Kaplan

Durukan

2020

Z Geburtshilfe Neonatol

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Objective We aimed to investigate the prognostic value of maternal serum haptoglobin levels in patients presenting with preterm premature rupture of fetal membranes (PPROM) during the second and the third trimesters of pregnancy. Methods In this case control study, 60 patients were recruited (30 pregnant women with PPROM between 26–34 weeks of gestation and 30 healthy, gestational-age-matched pregnant women without PPROM). White blood cell count (WBC), interleukin 6 (IL-6), C-reactive protein (CRP), sedimentation rate, and haptoglobin levels were measured. Results The mean age, gestational week, gravida, and parity of the 2 groups were statistically comparable (P>0.001). There was a statistically significant difference between the 2 groups in terms of haptoglobin values (p<0.001). The mean haptoglobin level was 115.5+33.1(mg/dl) in the PPROM group and 66.5+42.6 (mg/dl) in the control group. ROC curve analysis was performed to determine whether the level of haptoglobin alone could diagnose PPROM as an independent marker. It was shown that the level of 94.5 mg/dL for haptoglobin could indicate the diagnosis of PPROM with 80% sensitivity and specificity Conclusion Maternal serum haptoglobin levels may be a diagnostic marker for suspected PPROM cases when membrane rupture diagnosis is not accurate based on physical examination and other diagnostic tests.

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Section: Discussionmentioning

confidence: 61%

Maternal Serum Haptoglobin Levels as a Marker of Preterm Premature Rupture of Membranes

Buyuk

Oskovi-Kaplan

Durukan

2020

Z Geburtshilfe Neonatol

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“…The types of environmental and lifestyle-related chemicals assessed were diverse. Twenty-seven studies used questionnaires to investigate the type of maternal smoking during pregnancy (also see Tables 1 to 5 ), including maternal active smoking, passive smoking, or secondhand smoking [ 20 , 23 , 25 , 27 , 31 , 34 , 36 , 38 – 40 , 46 , 56 , 60 – 62 , 68 , 70 , 73 , 74 , 79 , 80 , 82 – 87 ]. Three studies examined the biomarker levels related to maternal smoking including cotinine levels [ 47 , 49 , 51 ].…”

Section: Gene-environment Interaction Studiesmentioning

confidence: 99%

“…Nineteen studies found significantly decreased birth size or observed gene-environment interactions on birth size [ 18 , 23 , 36 , 39 , 40 , 46 , 49 , 51 , 56 , 61 , 62 , 70 , 74 , 79 , 80 , 83 – 86 ]. Eleven studies found significantly increased risks or observed gene-environment interactions related to PB, SGA fetuses, and IUGR [ 20 , 25 , 27 , 31 , 33 , 34 , 38 , 47 , 60 , 82 , 87 ].…”

Section: Gene-environment Interaction Studiesmentioning

confidence: 99%

“…Eleven studies found significantly increased risks or observed gene-environment interactions related to PB, SGA fetuses, and IUGR [ 20 , 25 , 27 , 31 , 33 , 34 , 38 , 47 , 60 , 82 , 87 ]. The significant maternal genotypes detected were cytochrome P450 (CYP) 1A1 ( CYP1A1 ; MspI) m1/m2 and m2/m2 [ 28 , 34 , 36 , 61 ], CYP1A1 (Ile462Val) AG/GG [ 49 ], glutathione S-transferase (GST) mu 1 ( GSTM1 ) null [ 25 , 36 , 47 , 61 ], GST theta 1 ( GSTT1 ) null [ 25 , 40 , 47 , 60 ], GST theta 2 ( GSTT2 ) null [ 39 ], aryl hydrocarbon receptor ( AHR ) (Arg554Lys) Arg/Arg or GG [ 49 , 61 ], NAD[P]H quinone dehydrogenase 1 ( NQO1 ; Pro185Ser) Pro/Pro [ 62 ], CYP2E1*5 [ 62 ], 8-oxoguanine glycosylase 1 ( OGG1 ; Ser326Cys) CG/GG [ 80 ], methylenetetrahydrofolate reductase ( MTHFR ; A1298C) AA [ 70 ], X-ray repair cross-complementing protein 1 ( XRCC1 ; Arg194Trp) CT/TT [ 49 ], XRCC1 (Gln399Trp) GA/AA [ 49 ], murine double minute 4 ( MDM4 ; rs1090595) AC [ 87 ], tumor protein p53 ( TP53 ) CT [ 87 ], haptoglobin 2 ( Hp2 ) *2 [ 79 ], DNA [cytosine-5-]-methyltransferase 3 beta ( DNMT3B ; rs1569686) TT [ 20 ], epoxide hydrolase 1 ( EPHX1 ; Tyr113His) His/His [ 68 ], CYP2A6*1/*4 and CYP2A6*4/*4 [ 38 ]. The significant infant genotypes detected were GSTT1 null [ 40 ] and NQO1 (Pro187Ser) Pro/Pro [ 82 ].…”

Section: Gene-environment Interaction Studiesmentioning

confidence: 99%

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Gene-environment interactions related to maternal exposure to environmental and lifestyle-related chemicals during pregnancy and the resulting adverse fetal growth: a review

Kobayashi

Sata

Kishi

2022

Environ Health Prev Med

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Background There are only limited numbers of reviews on the association of maternal-child genetic polymorphisms and environmental and lifestyle-related chemical exposure during pregnancy with adverse fetal growth. Thus, this article aims to review: (1) the effect of associations between the above highlighted factors on adverse fetal growth and (2) recent birth cohort studies regarding environmental health risks. Methods Based on a search of the PubMed database through August 2021, 68 epidemiological studies on gene-environment interactions, focusing on the association between environmental and lifestyle-related chemical exposure and adverse fetal growth was identified. Moreover, we also reviewed recent worldwide birth cohort studies regarding environmental health risks. Results Thirty studies examined gene-smoking associations with adverse fetal growth. Sixteen maternal genes significantly modified the association between maternal smoking and adverse fetal growth. Two genes significantly related with this association were detected in infants. Moreover, the maternal genes that significantly interacted with maternal smoking during pregnancy were cytochrome P450 1A1 ( CYP1A1 ), X-ray repair cross-complementing protein 3 ( XRCC3 ), interleukin 6 ( IL6 ), interleukin 1 beta ( IL1B ), human leukocyte antigen (HLA) DQ alpha 1 ( HLA-DQA1 ), HLA DQ beta 1 ( HLA-DQB1 ), and nicotinic acetylcholine receptor. Fetal genes that had significant interactions with maternal smoking during pregnancy were glutathione S-transferase theta 1 ( GSTT1 ) and fat mass and obesity-associated protein ( FTO ). Thirty-eight studies examined the association between chemical exposures and adverse fetal growth. In 62 of the 68 epidemiological studies (91.2%), a significant association was found with adverse fetal growth. Across the studies, there was a wide variation in the analytical methods used, especially with respect to the genetic polymorphisms of interest, environmental and lifestyle-related chemicals examined, and the study design used to estimate the gene-environment interactions. It was also found that a consistently increasing number of European and worldwide large-scale birth cohort studies on environmental health risks have been conducted since approximately 1996. Conclusion There is some evidence to suggest the importance of gene-environment interactions on adverse fetal growth. The current knowledge on gene-environment interactions will help guide future studies on the combined effects of maternal-child genetic polymorphisms and exposure to environmental and lifestyle-related chemicals during pregnancy. Supplementary information The online version contains supplementary material available ...

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Intrauterine Development of Sex Differences—Fetal Programming * *For easier reading, I will be using throughout this chapter the term “fetus” whenever I refer to the embryo or the fetus and I will use the term “mother” for the pregnant woman. Moreover, whenever I use throughout this chapter the terms “increased risk” for a certain type of pathology, I mean just that, namely that a preexisting risk may increase, but still leave the majority of children unaffected.

Glezerman

2017

Principles of Gender-Specific Medicine

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Smoking and the correlation between birth weight and placental weight. Evidence of interaction with maternal haptoglobin phenotype

Cited by 6 publications

References 25 publications

Maternal Serum Haptoglobin Levels as a Marker of Preterm Premature Rupture of Membranes

Maternal Serum Haptoglobin Levels as a Marker of Preterm Premature Rupture of Membranes

Gene-environment interactions related to maternal exposure to environmental and lifestyle-related chemicals during pregnancy and the resulting adverse fetal growth: a review

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