Hypertensive disorders in pregnancy and timing of pubertal development in daughters and sons

2020 ◽  
Vol 35 (9) ◽  
pp. 2124-2133 ◽  
Author(s):  
Lea Lykke Harrits Lunddorf ◽  
Nis Brix ◽  
Andreas Ernst ◽  
Linn H Arendt ◽  
Henrik Støvring ◽  
...  

Abstract STUDY QUESTION Do maternal hypertensive disorders affect pubertal development in daughters and sons? SUMMARY ANSWER Pubertal development tended to occur earlier in daughters of mothers with ‘preeclampsia, eclampsia or HELLP syndrome’ (hemolysis, elevated liver enzymes and low blood platelets) or hypertension in pregnancy compared to daughters born of normotensive mothers. WHAT IS KNOWN ALREADY The existing literature suggests some or no association between preeclampsia and pubertal development in daughters, but not in sons. None of the previous studies has investigated the possible association between other types of hypertensive disorders (hypertension, eclampsia or HELLP syndrome) and pubertal timing in children. STUDY DESIGN, SIZE, DURATION Longitudinal cohort study consisting of 15 819 mother–child pairs with information on maternal hypertensive disorders collected during pregnancy and information on pubertal development collected half-yearly from the age of 11 years and until fully developed or 18 years of age. PARTICIPANTS/MATERIALS, SETTING, METHODS Participants are children from the Puberty Cohort nested within the Danish National Birth Cohort. The exposure was register-based and self-reported information on maternal hypertensive disorders during pregnancy. The outcomes were children’s self-reported information on pubertal development, including Tanner stage 1–5 (pubic hair (both daughters and sons) and breast development (daughters) or genital development (sons)), first menstrual bleeding (daughters) or first ejaculation (sons), voice break episode (sons), axillary hair development and acne occurrence (both daughters and sons). The main outcome was mean difference in age at attaining each pubertal milestone and a combined pubertal marker in children of mothers with hypertensive disorders in pregnancy (either hypertension (n = 490), ‘preeclampsia, eclampsia or HELLP syndrome’ (n = 419) or ‘unspecific hypertensive disorders’ (n = 334) with unexposed children as reference (n = 14 576)). MAIN RESULTS AND THE ROLE OF CHANCE In daughters of mothers with ‘preeclampsia, eclampsia or HELLP syndrome’, we observed tendencies of earlier pubertal timing (combined marker: −2.0 (95% CI: −3.9; 0.0) months). In daughters of mothers with hypertension, several pubertal milestones tended to occur earlier than in daughters of normotensive mothers; however, all 95% CIs overlapped the null resulting in a combined pubertal marker of −1.0 (95% CI: −3.2; 1.1) months. In sons of mothers with any of the hypertensive disorders, we observed no difference in pubertal timing (combined markers: ‘preeclampsia, eclampsia or HELLP syndrome’: 0.1 (95% CI: −2.0; 2.1) months; hypertension: −0.6 (95% CI: −2.3; 1.1) months; ‘unspecific hypertensive disorders’: 0.2 (95% CI: −1.9; 2.2) months). LIMITATIONS, REASONS FOR CAUTION The study is subject to non-differential misclassification of self-reported information on maternal hypertensive disorders in pregnancy and current pubertal status; possibly causing bias toward the null. WIDER IMPLICATIONS OF THE FINDINGS Hypertensive disorders in pregnancy might accelerate pubertal timing in daughters; however, more studies are needed for causal conclusions. STUDY FUNDING/COMPETING INTEREST(S) The study was funded by the Faculty of Health at Aarhus University. The authors have no financial relationships or competing interests to disclose. TRIAL REGISTRATION NUMBER N/A.

2020 ◽  
pp. 1-22
Author(s):  
Charlotte Frise ◽  
Sally Collins

This chapter covers physiology and blood pressure in the pregnant patient, followed by hypertensive disorders in pregnancy. This includes pre-existing hypertension, and hypertension induced by pregnancy. It also describes the background, investigations, management, and counselling of pre-eclampsia, HELLP syndrome, and eclampsia. Postnatal management is also covered, and the uses of antihypertensives in the pregnant patient are indicated, along with contraindications and possible side effects.


Author(s):  
Jasmine A McDonald ◽  
Sinaida Cherubin ◽  
Mandy Goldberg ◽  
Ying Wei ◽  
Wendy K Chung ◽  
...  

Abstract Earlier pubertal development is only partially explained by childhood body mass index (BMI); the role of other factors like childhood infections is less understood. Using data from the LEGACY Girls Study (2011 – 2016), we prospectively examined the associations between childhood viral infections (Cytomegalovirus (CMV), Epstein Barr Virus (EBV), Herpes Simplex Virus 1 (HSV1), HSV2 and pubertal timing. We measured exposures based on seropositivity in pre-menarcheal girls (n=490). Breast and pubic hair development were classified based on mother-reported Tanner Stage (TS: TS2+ compared with TS1), adjusting for age, BMI, and sociodemographic factors. The average age at first blood draw was 9.8 years (Stdev=1.9 years). The prevalences were 31% CMV+, 37% EBV+, 14% HSV1+, 0.4% HSV2+, and 16% for both CMV+/EBV+. CMV+ infection without co-infection was associated with developing breasts an average of 7 months earlier (Hazard Ratio (HR)=2.12, 95% CI 1.32, 3.40). CMV+ infection without co-infection and HSV1+ and/or HSV2+ infection were associated with developing pubic hair 9 months later (HR 0.41, 95% CI 0.24, 0.71, HR 0.42, 95% CI 0.22, 0.81, respectively). Infection was not associated with menarche. If replicated in larger cohorts with blood collection prior to any breast development, this study supports that childhood infections may play a role in altering pubertal timing.


2020 ◽  
Vol 03 (03) ◽  
Author(s):  
Nkem Ernest Njukang ◽  
Tah Aldof Yoah ◽  
Martin Sama ◽  
Thomas Obinchemti EGBE ◽  
Joseph Kamgno

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Salisu M. Ishaku ◽  
Timothy Olusegun Olanrewaju ◽  
Joyce L. Browne ◽  
Kerstin Klipstein-Grobusch ◽  
Gbenga A. Kayode ◽  
...  

Abstract Background Worldwide, hypertensive disorders in pregnancy (HDPs) complicate between 5 and 10% of pregnancies. Sub-Saharan Africa (SSA) is disproportionately affected by a high burden of HDPs and chronic kidney disease (CKD). Despite mounting evidence associating HDPs with the development of CKD, data from SSA are scarce. Methods Women with HDPs (n = 410) and normotensive women (n = 78) were recruited at delivery and prospectively followed-up at 9 weeks, 6 months and 1 year postpartum. Serum creatinine was measured at all time points and the estimated glomerular filtration rates (eGFR) using CKD-Epidemiology equation determined. CKD was defined as decreased eGFR< 60 mL/min/1.73m2 lasting for ≥ 3 months. Prevalence of CKD at 6 months and 1 year after delivery was estimated. Logistic regression analyses were conducted to evaluate risk factors for CKD at 6 months and 1 year postpartum. Results Within 24 h of delivery, 9 weeks, and 6 months postpartum, women with HDPs were more likely to have a decreased eGFR compared to normotensive women (12, 5.7, 4.3% versus 0, 2 and 2.4%, respectively). The prevalence of CKD in HDPs at 6 months and 1 year postpartum was 6.1 and 7.6%, respectively, as opposed to zero prevalence in the normotensive women for the corresponding periods. Proportions of decreased eGFR varied with HDP sub-types and intervening postpartum time since delivery, with pre-eclampsia/eclampsia showing higher prevalence than chronic and gestational hypertension. Only maternal age was independently shown to be a risk factor for decreased eGFR at 6 months postpartum (aOR = 1.18/year; 95%CI 1.04–1.34). Conclusion Prior HDP was associated with risk of future CKD, with prior HDPs being more likely to experience evidence of CKD over periods of postpartum follow-up. Routine screening of women following HDP-complicated pregnancies should be part of a postpartum monitoring program to identify women at higher risk. Future research should report on both the eGFR and total urinary albumin excretion to enable detection of women at risk of future deterioration of renal function.


2016 ◽  
Vol 34 (5) ◽  
pp. 914-919 ◽  
Author(s):  
I-Kuan Wang ◽  
Jiunn-Horng Chen ◽  
Chih-Hsin Muo ◽  
Che-Yi Chou ◽  
Yao-Lung Liu ◽  
...  

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