Calprotectin, a marker of inflammation, is elevated in the maternal but not in the fetal circulation in preeclampsia

Brække, Kristin; Holthe, Mette R.; Harsem, Nina Kittelsen; Fagerhol, Magne K.; Staff, Anne Cathrine

doi:10.1016/j.ajog.2004.11.055

Cited by 58 publications

(35 citation statements)

References 21 publications

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“…This is also in accordance with our previous findings that in preeclampsia, elevated maternal levels of markers of inflammation and oxidative stress are generally not reflected in the fetal circulation (2,3).…”

Section: Discussionsupporting

confidence: 82%

“…Increased concentrations of biomarkers for preeclampsia in the maternal circulation are usually not reflected in the infant. Previously, our group has shown that newborns from preeclamptic pregnancies did not differ from those born after uncomplicated pregnancies with respect to circulating biomarkers of inflammation (CRP and calprotectin) (2), and oxidative stress (3), but newborns from preeclamptic pregnancies had elevated concentrations of homocysteine (4).…”

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confidence: 99%

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Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

et al. 2009

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Preeclampsia is a leading cause of intrauterine growth restriction and preterm birth. Endothelial dysfunction is the common final pathway leading to clinical signs of preeclampsia including hypertension and proteinuria. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from L-arginine. The purpose of this study was to investigate maternal and fetal concentrations of ADMA, L-arginine, and symmetric dimethylarginine (SDMA). Women with preeclampsia (n ϭ 47) and controls (n ϭ 51) who gave birth by cesarean section were included in the study. We analyzed the maternal plasma and umbilical vein and artery plasma. We found that not only maternal concentrations of ADMA and SDMA but also L-arginine were significantly higher in women with preeclampsia than in controls. In fetal samples, only SDMA concentrations were higher in the preeclampsia group than in controls. The median ADMA concentration was three times higher in the fetal circulation than in the maternal circulation, but there was no difference between the preeclampsia group and the control group, and the veno-arterious gradient indicated that the placenta was the source of ADMA. (Pediatr Res 66: 411-415, 2009) P reeclampsia is a common pregnancy complication associated with increased risk of preterm birth and fetal growth restriction (1). The exact etiology of preeclampsia is not known, and hence no definitive preventative measures or treatments are available.Endothelial dysfunction is the common final pathway leading to the clinical signs of preeclampsia including hypertension and proteinuria. It is not known to what extent endothelial dysfunction also affects the infant. Increased concentrations of biomarkers for preeclampsia in the maternal circulation are usually not reflected in the infant. Previously, our group has shown that newborns from preeclamptic pregnancies did not differ from those born after uncomplicated pregnancies with respect to circulating biomarkers of inflammation (CRP and calprotectin) (2), and oxidative stress (3), but newborns from preeclamptic pregnancies had elevated concentrations of homocysteine (4).In women with previous preeclampsia, there is an increased risk for cardiovascular disease later in life (5) and an increased risk of hypertension has also been found for their offspring (6,7).It is not clear whether the increased risk in the offspring is caused by the intrauterine environment, shared genes, or impaired intrauterine growth. In epidemiologic and animal studies, low birth weight by itself is associated with an increased risk of cardiovascular disease and metabolic syndrome (8).NO is essential for vascular tone and endothelial function, and elevated circulating concentrations of asymmetric dimethylarginine (ADMA) are associated with reduced vasodilation and endothelial dysfunction (9). ADMA is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from L-arginine. The ratio...

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Section: Discussionsupporting

confidence: 82%

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confidence: 99%

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

et al. 2009

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“…Thirty‐two studies in total reported on C‐reactive protein levels,21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52 of which 17 were applicable for meta‐analysis 21, 22, 23, 29, 30, 31, 32, 33, 34, 37, 38, 39, 41, 42, 47, 49, 50. A significantly higher C‐reactive protein was found in women with pre‐eclampsia than in non‐hypertensive controls ( Figure 2), and this correlation was stronger in severe than in mild pre‐eclampsia ( Figure 3).…”

Section: Resultsmentioning

confidence: 99%

Shared biomarkers between female diastolic heart failure and pre‐eclampsia: a systematic review and meta‐analysis

et al. 2017

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Evidence accumulates for associations between hypertensive pregnancy disorders and increased cardiovascular risk later. The main goal of this study was to explore shared biomarkers representing common pathogenic pathways between heart failure with preserved ejection fraction (HFpEF) and pre‐eclampsia where these biomarkers might be potentially eligible for cardiovascular risk stratification in women after hypertensive pregnancy disorders. We sought for blood markers in women with diastolic dysfunction in a first literature search, and through a second search, we investigated whether these same biochemical markers were present in pre‐eclampsia.This systematic review and meta‐analysis presents two subsequent systematic searches in PubMed and EMBASE. Search I yielded 3014 studies on biomarkers discriminating women with HFpEF from female controls, of which 13 studies on 11 biochemical markers were included. Cases had HFpEF, and controls had no heart failure. The second search was for studies discriminating women with pre‐eclampsia from women with non‐hypertensive pregnancies with at least one of the biomarkers found in Search I. Search II yielded 1869 studies, of which 51 studies on seven biomarkers were included in meta‐analyses and 79 studies on 12 biomarkers in systematic review.Eleven biological markers differentiated women with diastolic dysfunction from controls, of which the following 10 markers differentiated women with pre‐eclampsia from controls as well: C‐reactive protein, HDL, insulin, fatty acid‐binding protein 4, brain natriuretic peptide, N terminal pro brain natriuretic peptide, adrenomedullin, mid‐region pro adrenomedullin, cardiac troponin I, and cancer antigen 125.Our study supports the hypothesis that HFpEF in women shares a common pathogenic background with pre‐eclampsia. The biomarkers representing inflammatory state, disturbances in myocardial function/structure, and unfavourable lipid metabolism may possibly be eligible for future prognostic tools.

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“…All of the blood samples were prepared and stored as described previously. 10,13 mRNA Isolation and Gene Array…”

Section: Samplesmentioning

confidence: 99%

Dysregulation of the Circulating and Tissue-Based Renin-Angiotensin System in Preeclampsia

et al. 2007

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Abstract-The renin-angiotensin system (RAS) participates in preeclampsia; however, the relative contributions from the circulating RAS and the tissue-based, uteroplacental RAS are unknown. We hypothesized that the tissue-based uteroplacental RAS is dysregulated in preeclampsia. We performed microarray and gene expression studies and confirmed the findings on the protein level by immunohistochemistry in ureteroplacental units from 10 preeclamptic women and 10 women with uneventful pregnancies. All of the women were delivered by cesarean section. We also analyzed plasma renin activity and circulating agonistic angiotensin II type 1 (AT 1 ) receptor autoantibodies. In preeclampsia, we found that the angiotensin II AT 1 receptor gene was 5-fold upregulated in decidua (maternal origin). We also found AT 1 autoantibodies in preeclamptic women and in their offspring by neonatal cardiomyocyte bioassay compared with women with normal pregnancies and their infants (mother: 17.5Ϯ2.2 versus 0.05Ϯ0.4; fetus: 14.5Ϯ1.8 versus 0.5Ϯ0.5 ⌬bpm). Gene expressions for renin (35.0-fold), angiotensin-converting enzyme (2.9-fold), and angiotensinogen (8.9-fold) were higher in decidua than placenta (fetal origin) in both control and preeclamptic women, whereas the AT 1 receptor was expressed 10-fold higher in placenta than in decidua in both groups. Our findings elucidate the ureteroplacental unit RAS in preeclamptic and normal pregnancies. We found that, in preeclampsia, the AT 1 receptor expression is particularly high in decidua, combined with pregnancy-specific tissue RAS involving decidual angiotensin II production and AT 1 autoantibodies. We also showed that AT 1 autoantibodies cross the ureteroplacental barrier. These components could participate in the pathophysiology of preeclampsia.

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Calprotectin, a marker of inflammation, is elevated in the maternal but not in the fetal circulation in preeclampsia

Cited by 58 publications

References 21 publications

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

Asymmetric Dimethylarginine in the Maternal and Fetal Circulation in Preeclampsia

Shared biomarkers between female diastolic heart failure and pre‐eclampsia: a systematic review and meta‐analysis

Dysregulation of the Circulating and Tissue-Based Renin-Angiotensin System in Preeclampsia

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