177-POS

• Published in: Pregnancy hypertension Vol. 5; no. 1; p. 91
• Main Authors: Verburg, Petra E, Tucker, Graeme, Scheil, Wendy, Erwich, Jan Jaap H, Roberts, Claire T, Dekker, Gus A
• Format: Journal Article
• Language: English
• Published: 01.01.2015
• Subjects: Cardiovascular; Obstetrics and Gynecology
• ISSN: 2210-7789; 2210-7797
• DOI: 10.1016/j.preghy.2014.10.183

Objectives To assess the seasonal variation of pregnancy induced hypertensive disorders (PIHD) in an Australian population. Methods Retrospective study of 59,993 South Australian singleton live born births, for whom a body mass index (BMI) of the mother and sex of the baby were recorded, during 2007–2011 in the South Australian Perinatal Statistics Collection. The incidence of PIHD in relation to birth date was assessed. Fourier series analysis was used to model seasonal trends. Results Of a total of 59,993 births recorded during the study period 4252 (7.1%) women were diagnosed with PIHD. Seasonal modelling showed a strong relation between PIHD and date of birth ( p < 0.000). When adjusted for confounders (age, BMI, race, smoking during second half of pregnancy, parity and gestational diabetes) the model still showed a strong relation between PIHD and date of birth ( p < 0.000). The peak prevalence occurred among births in Winter (Jun/Jul/Aug), with a trough in pregnancies with birth in (late-) Summer (Jan/Feb). Conclusions These epidemiological data support seasonal periodicity for PIHD in an Australian population. The highest incidence of PIHD was associated with birth in the Winter months (Jun/Jul/Aug). The etiology of PIHD is still elusive, but theories include genetic and immune mechanisms, abnormal placentation, and cardiovascular maladaptation to pregnancy, nutritional, hormonal and angiogenetic factors and enhanced systemic inflammatory response. Recent studies found a relation between both infection and low maternal vitamin D levels and pre-eclamspia. These conditions could explain the detected seasonality for PIHD. Further investigation into the biological mechanism(s) for this finding should be undertaken to identify additional risk factors, so PIHD can be prevented in the clinic. Disclosures P.E. Verburg: None. G. Tucker: None. W. Scheil: None. J.H. Erwich: None. C.T. Roberts: None. G.A. Dekker: None.