Abstract
Normal pregnancy is characterized by a mild systemic inflammatory response and progressive increase in serum inflammatory cytokines that peak in the third trimester. During pregnancy pre-existing inflammatory conditions, acquired oxidative stress arising from the placenta malfunction and nutritional deficiencies can trigger intense systemic responses that lead to endothelial activation, dysfunction and preeclampsia. We investigated the principal nutritional, oxidative and inflammatory pathways that trigger the clinical manifestation of preeclampsia.
 This case-control study included 250 women with preeclampsia and 150 normotensive pregnant women. Urinary Iodine concentration (IUC) and serum levels of Ferritin, Thyroid-stimulating Hormone (TSH), selenium, Nitric Oxide (NO) gamma glutamyl transferase (GGT), Rheumatoid factor, and high sense C-reactive protein (hs-CRP) of cases and controls were compared using the student’s t and the Mann-Whitney U tests. Principal component analysis was carried out to delineate the patterns of association between nutritional, inflammatory and oxidative markers and preeclampsia.
 The main pathophysiological pathways identified were the interactions between selenium/iodine deficiency and elevated serum TSH (endothelial dysfunction); serum ferritin, GGT, CRP and low urinary iodine concentration (inflammatory oxidative stress); elevated serum hs-CRP and Rheumatoid factor subclinical inflammation and immune cell activation) and high T3/T4 ratio (acute TSH stimulation of thyroid with low thyroid iodine stores)
 Combined selenium and iodine deficiency resulting into elevated TSH, low NO and preferential T3 secretion; acute inflammatory conditions associated with elevated serum GGT, CRP, and Ferritin; and subclinical inflammatory conditions characterized by autoimmunity are some of the major oxidant and inflammatory pathways associated with increased risk of preeclampsia.
Highlights
The normal physiological changes in pregnancy include mild systemic inflammatory response [1]
The four were: Iodine and selenium deficiency acting together with elevated Thyroid-stimulating Hormone (TSH) and low serum Nitric Oxide (NO), accounting for almost 34% of the observed variance among participants with preeclampsia. This matches perfectly with the pathophysiology of thyroid gland in states of combined iodine and selenium deficiency, which is endemic in Democratic Republic of Congo (DRC): iodine deficiency exacerbated by the physiological changes of pregnancy predisposing to low production of thyroxine (T4) and tri-iodothyronine (T3), diminished negative feedback on the pituitary and elevated TSH [6]–[8]
Elevated TSH with simultaneous selenium deficiency will result in excessive production of serum superoxide and hydrogen peroxide by the thyroid gland [9]
Summary
The normal physiological changes in pregnancy include mild systemic inflammatory response [1]. This is characterized by an elaboration of inflammatory leukocytes, endothelial activation, the acute phase response, and metabolic features of systemic inflammation, a decrease in plasma albumin levels and increased plasma fibrinogen levels. It is hypothesized that an oxidatively stressed placenta in a previously normal woman, or a normal systemic inflammatory response in a woman with a chronic inflammatory response due to pre-existing chronic infection such as Helicobacter pylori, obesity, essential hypertension, diabetes or other stimulus, can trigger an intense systemic response that leads to endothelial activation, dysfunction and preeclampsia [1].
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