scholarly journals Pregnancy Per- and Polyfluoroalkyl Substance Concentrations and Postpartum Health in Project Viva: A Prospective Cohort

2020 ◽  
Vol 105 (9) ◽  
pp. e3415-e3426
Author(s):  
Susanna D Mitro ◽  
Sharon K Sagiv ◽  
Abby F Fleisch ◽  
Lindsay M Jaacks ◽  
Paige L Williams ◽  
...  

Abstract Context Per- and polyfluoroalkyl substances (PFAS) are environmental chemicals linked to weight gain and type 2 diabetes. Objective We examined the extent to which PFAS plasma concentrations during pregnancy were associated with postpartum anthropometry and biomarkers. Design, Patients, and Measures We studied women recruited between 1999 and 2002 in the Project Viva prospective cohort with pregnancy plasma concentrations of PFAS, including perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and 2-(N-ethyl-perfluorooctane sulfonamide) acetic acid (EtFOSAA). Three-year postpartum anthropometry measurements were available from 786 to 801 women, blood pressure from 761 women, and blood biomarkers from 450 to 454 women. We used multivariable regression to evaluate the association of log2-transformed PFAS with postpartum anthropometry, blood pressure, and blood biomarkers (leptin, adiponectin, sex hormone binding globulin [SHBG], hemoglobin A1c, interleukin-6 [IL-6], C-reactive protein), adjusting for age, prepregnancy body mass index, marital status, race/ethnicity, education, income, smoking, parity, and breastfeeding history. Results Pregnancy concentrations of certain PFAS were associated with greater adiposity (eg, 0.4 cm [95% confidence interval [95%CI]: −0.1, 0.9] greater waist circumference per doubling in EtFOSAA; 0.2 cm [95%CI: −0.1, 0.5] greater mid-upper arm circumference per doubling in PFOA; 1.2 mm [95%CI: 0.1, 2.2] thicker sum of subscapular and triceps skinfolds per doubling in PFOS) and higher systolic blood pressure (eg, 1.2 mm Hg [95%CI: 0.3, 2.2] per doubling in PFOS) at 3 years postpartum. Higher EtFOSAA concentrations were also associated with 10.8% higher IL-6 (95%CI: 3.3, 18.9) and 6.1% lower SHBG (95%CI: 0.7, 11.2) per doubling. Conclusions Pregnancy concentrations of EtFOSAA, PFOS, and PFOA were associated with adverse postpartum cardiometabolic markers.

2007 ◽  
Vol 97 (01) ◽  
pp. 15-20 ◽  
Author(s):  
Angela Silveira ◽  
Stella Thomassen ◽  
Lars-Olof Hansson ◽  
Jan Rosing ◽  
Anders Hamsten ◽  
...  

SummaryHormonal emergency contraception (EC) is a well established contraceptive method, recommended to all women, although the effects on haemostais are not fully evaluated. The aim of this study was to evaluate whether exposure to EC has effects on well established cardiovascular risk factors, and also to examine whether differences exist between two EC treatments. In a prospective randomized cross over design 11 women used two different EC methods, one with estrogen and levonorgestrel (EE-EC) and one with levonorgestrel only (LNG-EC). Plasma concentrations of haemostatic factors (APC resistance, antithrombin, fibrinogen, prothrombin fragment 1+2, free protein S, factor VII and PAI-1), sex-hormone-binding globulin (SHBG), the apolipoprotein (apo)B/apoA1 ratio and C-reactive protein (CRP) were followed frequently during the following 48 h A rapid haemostatic activation was induced with both treatments, although more pronounced with EE-EC. Already two hours after EC, the plasma concentrations of haemostatic parameters and SHBG were significantly different from baseline concentrations. An ETP-based APC-resistance method showed increased APC resistance with EE-EC and decreased APC resistance with LNG-EC. The ApoB/ApoA1 ratio was affected in a favourable direction with EE-EC.CRP increased slightly regardless of treatment. Even a very short exposure to exogenous sex hormones causes prompt effects on hepatic protein synthesis and the coagulation system. This must be taken into consideration whenever exogenous steroid hormones are administered, especially to individuals with a genetic predisposition to thrombosis or transiently disturbed haemostasis.


2013 ◽  
Vol 141 (1-2) ◽  
pp. 41-47 ◽  
Author(s):  
Aleksandra Simoncig-Netjasov ◽  
Svetlana Vujovic ◽  
Miomira Ivovic ◽  
Milina Tancic-Gajic ◽  
Ljiljana Marina ◽  
...  

Introduction. Menopause leads to the development of central adiposity, a more atherogenic lipid profile and increased incidence of metabolic syndrome independent of age and other factors. Objective. The aim of the study was to investigate the relationships between anthropometric characteristics, sex hormones, lipids and fasting glucose in menopausal women. Methods. The study included 87 menopausal women, who where divided into groups according to two criteria: BMI?26.7 kg/m2 and BMI?25 kg/m2. Anthropometric characteristics and blood pressure were measured. Blood was taken at 08.00 h for fasting glucose, triglycerides, cholesterol, HDL, LDL, apolipoprotein A, apolipoprotein B, lipoprotein(a) (Lp(a)), C-reactive protein, fibrinogen, follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), estradiol, progesterone, testosterone and sex hormone binding globulin (SHBG). Results. Significant differences between groups were found for weight, BMI, waist, hips circumference, waist/hip ratio (WHR), systolic and diastolic blood pressure, Lp(a), FSH, LH, PRL (for systolic blood pressure p<0.05, for the rest p<0.01) and fasting glucose (p<0.05). In obese and overweight women with BMI?26.7kg/m2 significant negative correlations were found for FSH and glucose, SHBG and LDL, SHBG and total cholesterol, SHBG and glucose, BMI and HDL, WC and HDL. In obese and overweight women with BMI?25kg/m2 significant negative correlations were found for BMI and HDL, waist circumference (WC) and HDL, WHR and HDL, FSH and glucose, SHBG and glucose; significant positive correlations were between BMI and glucose, WC and glucose and WHR with triglycerides. Conclusion. Gaining weight and decreased SHBG are related to dyslipidemia and increased fasting glucose confirming increased incidence of metabolic abnormalities in the menopause.


2020 ◽  
Vol 15 (3) ◽  
pp. 227-239 ◽  
Author(s):  
Hader I. Sakr ◽  
Akef A. Khowailed ◽  
Reham S. Al-Fakharany ◽  
Dina S. Abdel-Fattah ◽  
Ahmed A. Taha

Background: Pre-eclampsia poses a significant potential risk of hypertensive disorders during pregnancy, a leading cause of maternal deaths. Hyperuricemia is associated with adverse effects on endothelial function, normal cellular metabolism, and platelet aggregation and adhesion. This study was designed to compare serum urate levels in normotensive pregnant women to those with pregnancy-induced hypertension, and to evaluate its value as a potential predictive marker of hypertension severity during pregnancy. Methods: A prospective, observational, case-control study conducted on 100 pregnant women in their third trimester. Pregnant women were classified into two groups (n=50) according to arterial blood pressure measurements: group I had normal blood pressure, and group II had a blood pressure of ≥ 140/90, which was further subdivided according to hypertension severity into IIa (pregnancy- induced hypertension, IIb (mild pre-eclampsia), and IIc (severe pre-eclampsia). Blood samples were obtained on admission. Serum urate, high sensitive C-reactive protein, and interleukin-1β levels, and lipid profile were compared among the groups. Results: A significant increase in the mean values of serum urate, C-reactive protein, and interleukin- 1β levels was detected in gestational hypertensives. In addition, there was a positive correlation between serum urate levels and C-reactive protein and interleukin-1β, as well as between serum urate levels and hypertension severity. Conclusion: Hyperuricemia and increased C-reactive protein and interleukin-1β serum levels correlate with the severity of pregnancy-induced hypertension, and these biomarkers may play a role in the pathogenesis of pre-eclampsia. Serum urate measurement is sensitive, reliable markers that correlate well with the severity of hypertension in pregnant females with pre-eclampsia.


1984 ◽  
Vol 62 (12) ◽  
pp. 1479-1486 ◽  
Author(s):  
Jean-Paul Clozel ◽  
Jacques Billette ◽  
Gilles Caillé ◽  
Pierre Théroux ◽  
Richard Cartier

Atrial and atrioventricular conduction variables were studied at control and at the end of each of six consecutive 45-min diltiazem administration periods in eight closed chest-anesthetized dogs. Diltiazem was given as a bolus (50 μg/kg, i.v.) followed by an infusion (0.5 μg∙kg−1∙min−1); doses were doubled in subsequent periods. The plasma concentrations, measured by gas–liquid chromatography, ranged from 8 to 1400 ng/mL and correlated strongly with the doses (r = 0.92; p < 0.01). The Wenckebach cycle length, basic conduction time, and functional refractory period of the atrioventricular (AV) node increased proportionally with plasma concentration (respective r = 0.90, 0.89, 0.80; p < 0.01). The minimum mean plasma concentrations affecting these variables significantly were 37, 83, and 175 ng/mL, respectively. Second or third degree AV blocks developed in all dogs for plasma concentrations between 379 and 1400 ng/mL. In four dogs which were given isoproterenol (0.2 μg∙kg−1∙min−1), these blocks disappeared within 1 min. Atrial conduction time and functional refractory period were slightly but significantly shortened by diltiazem with mean plasma concentrations of 175 ng/mL and over. His–Purkinje intervals were not significantly changed by diltiazem. Systolic and diastolic arterial pressures were decreased by diltiazem (r = −0.64, r = −0.79; p < 0.01) starting with a mean plasma concentration of 83 ng/mL. We conclude that AV nodal conduction variables are progressively prolonged with increasing plasma concentrations of diltiazem; plasma concentrations affecting blood pressure and AV nodal variables overlap; and the AV blocks produced by toxic concentrations of diltiazem can be corrected by isoproterenol.


2015 ◽  
Vol 309 (10) ◽  
pp. F836-F842 ◽  
Author(s):  
Lorena Rojas-Vega ◽  
Aldo R. Jiménez-Vega ◽  
Silvana Bazúa-Valenti ◽  
Isidora Arroyo-Garza ◽  
José Victor Jiménez ◽  
...  

Evidence in rodents suggests that tacrolimus-induced posttransplant hypertension is due to upregulation of the thiazide-sensitive Na+-Cl−cotransporter NCC. Here, we analyzed whether a similar mechanism is involved in posttransplant hypertension in humans. From January 2013 to June 2014, all adult kidney transplant recipients receiving a kidney allograft were enrolled in a prospective cohort study. All patients received tacrolimus as part of the immunosuppressive therapy. Six months after surgery, we assessed general clinical and laboratory variables, tacrolimus trough blood levels, and ambulatory 24-h blood pressure monitoring. Urinary exosomes were extracted to perform Western blot analysis using total and phospho-NCC antibodies. A total of 52 patients, including 17 women and 35 men, were followed. At 6 mo after transplantation, of the 35 men, 17 developed hypertension and 18 remained normotensive, while high blood pressure was observed in only 3 of 17 women. The hypertensive patients were significantly older than the normotensive group; however, there were no significant differences in body weight, history of acute rejection, renal function, and tacrolimus trough levels. In urinary exosomes, hypertensive patients showed higher NCC expression (1.7 ± 0.19) than normotensive (1 ± 0.13) ( P = 0.0096). Also, NCC phosphorylation levels were significantly higher in the hypertensive patients (1.57 ± 0.16 vs. 1 ± 0.07; P = 0.0049). Our data show that there is a positive correlation between NCC expression/phosphorylation in urinary exosomes and the development of hypertension in posttransplant male patients treated with tacrolimus. Our results are consistent with the hypothesis that NCC activation plays a major role in tacrolimus-induced hypertension.


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