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Serum Inflammatory Markers and Preeclampsia in Type 1 Diabetes:: A prospective study

  • Autores: Mei Du, Arpita Basu, Dongxu Fu, Mingyuan Wu, Michael Centola, Alicia J. Jenkins, Kristian Hanssen, S.K. Garg, Samar M. Hammad, James A. Scardo, Christopher E. Aston, Timothy Lyons
  • Localización: Diabetes care, ISSN-e 0149-5992, Vol. 36, Nº. 7, 2013, págs. 2054-2061
  • Idioma: inglés
  • Texto completo no disponible (Saber más ...)
  • Resumen
    • Inflammation and endothelial dysfunction have been associated with the immunobiology of preeclampsia (PE), a significant cause of adverse pregnancy outcomes. The prevalence of PE is elevated several fold in the presence of maternal type 1 diabetes mellitus (T1DM). Although cross-sectional studies of pregnancies among women without diabetes have shown altered inflammatory markers in the presence of PE, longitudinal studies of diabetic women are lacking. In maternal serum samples, we examined the temporal associations of markers of inflammation with the subsequent development of PE in women with T1DM. We conducted longitudinal analyses of serum C-reactive protein (CRP), adhesion molecules, and cytokines during the first (mean ± SD, 12.2 ± 1.9 weeks), second (21.6 ± 1.5 weeks), and third (31.5 ± 1.7 weeks) trimesters of pregnancy (visits 1-3, respectively). All study visits took place before the onset of PE. Covariates were BMI, HbA^sub 1c^, age of onset, duration of diabetes, and mean arterial pressure. In women with T1DM who developed PE versus those who remained normotensive, CRP tended to be higher at visits 1 (P = 0.07) and 2 (P = 0.06) and was significantly higher at visit 3 (P < 0.05); soluble E-selectin and interferon-γ-inducible protein-10 (IP-10) were significantly higher at visit 3; interleukin-1 receptor antagonist (IL-1ra) and eotaxin were higher and lower, respectively, at visit 2 (all P < 0.05). These conclusions persisted following adjustment for covariates. In pregnant women with T1DM, elevated CRP, soluble E-selectin, IL-1ra, and IP-10 and lower eotaxin were associated with subsequent PE. The role of inflammatory factors as markers and potential mechanisms of the high prevalence of PE in T1DM merits further investigation.


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