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      Serum and urine vitamin D metabolite analysis in early preeclampsia

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          Abstract

          Vitamin D deficiency is common in pregnant women and may contribute to adverse events in pregnancy such as preeclampsia (PET). To date, studies of vitamin D and PET have focused primarily on serum concentrations vitamin D, 25-hydroxyvitamin D3 (25(OH)D3) later in pregnancy. The aim here was to determine whether a more comprehensive analysis of vitamin D metabolites earlier in pregnancy could provide predictors of PET. Using samples from the SCOPE pregnancy cohort, multiple vitamin D metabolites were quantified by liquid chromatography–tandem mass spectrometry in paired serum and urine prior to the onset of PET symptoms. Samples from 50 women at pregnancy week 15 were analysed, with 25 (50%) developing PET by the end of the pregnancy and 25 continuing with uncomplicated pregnancy. Paired serum and urine from non-pregnant women ( n = 9) of reproductive age were also used as a control. Serum concentrations of 25(OH)D3, 25(OH)D2, 1,25(OH) 2D3, 24,25(OH) 2D3 and 3-epi-25(OH)D3 were measured and showed no significant difference between women with uncomplicated pregnancies and those developing PET. As previously reported, serum 1,25(OH) 2D3 was higher in all pregnant women (in the second trimester), but serum 25(OH)D2 was also higher compared to non-pregnant women. In urine, 25(OH)D3 and 24,25(OH) 2D3 were quantifiable, with both metabolites demonstrating significantly lower ( P < 0.05) concentrations of both of these metabolites in those destined to develop PET. These data indicate that analysis of urinary metabolites provides an additional insight into vitamin D and the kidney, with lower urinary 25(OH)D3 and 24,25(OH) 2D3 excretion being an early indicator of a predisposition towards developing PET.

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          Incidence of preeclampsia: risk factors and outcomes associated with early- versus late-onset disease.

          Sarka Lisonkova, K Joseph (2013)
          The population-based incidence of early-onset (<34 weeks) and late-onset preeclampsia (≥34 weeks) has not been adequately studied. We examined the gestational age-specific incidence of preeclampsia onset and identified the associated risk factors and birth outcomes. All singleton deliveries in Washington State, 2003-2008 (n = 456,668), were included, and preeclampsia onset was determined from hospital records linked to birth certificates. Cox and logistic regression models were used to obtain adjusted hazard ratios and odds ratios (AORs) for risk factors and birth outcomes, respectively. The overall preeclampsia rate was 3.1% and the incidence increased sharply with gestation; early- and late-onset preeclampsia rates were 0.38% and 2.72%, respectively. Among women with early-onset preeclampsia, 12% delivered at a gestation of 34 weeks or longer. Risk/protective factors common to both diseases included older maternal age, Hispanic and Native-American race, smoking, unmarried status, and male fetus. African-American race, chronic hypertension, and congenital anomalies were more strongly associated with early-onset preeclampsia, whereas younger maternal age, nulliparity, and diabetes mellitus were more strongly associated with late-onset disease. Early- but not late-onset preeclampsia conferred a high risk of fetal death (AOR, 5.8; 95% confidence interval [CI], 4.0-8.3 vs AOR, 1.3; 95% CI, 0.8-2.0, respectively). The AOR for perinatal death/severe neonatal morbidity was 16.4 (95% CI, 14.5-18.6) in early-onset and 2.0 (95% CI, 1.8-2.3) in late-onset preeclampsia. Early- and late-onset preeclampsia shares some etiological features, differ with regard to several risk factors, and lead to different outcomes. The 2 preeclampsia types should be treated as distinct entities from an etiological and prognostic standpoint. Copyright © 2013 Mosby, Inc. All rights reserved.
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            An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3.

            A Nykjaer, D Dragun, D. Walther … (1999)
            Steroid hormones may enter cells by diffusion through the plasma membrane. However, we demonstrate here that some steroid hormones are taken up by receptor-mediated endocytosis of steroid-carrier complexes. We show that 25-(OH) vitamin D3 in complex with its plasma carrier, the vitamin D-binding protein, is filtered through the glomerulus and reabsorbed in the proximal tubules by the endocytic receptor megalin. Endocytosis is required to preserve 25-(OH) vitamin D3 and to deliver to the cells the precursor for generation of 1,25-(OH)2 vitamin D3, a regulator of the calcium metabolism. Megalin-/- mice are unable to retrieve the steroid from the glomerular filtrate and develop vitamin D deficiency and bone disease.
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              Why is placentation abnormal in preeclampsia?

              Susan J. Fisher (2015)
              The causes of preeclampsia remain one of the great medical mysteries of our time. This syndrome is thought to occur in 2 stages with abnormal placentation leading to a maternal inflammatory response. Specific regions of the placenta have distinct pathologic features. During normal pregnancy, cytotrophoblasts emigrate from the chorionic villi and invade the uterus, reaching the inner third of the myometrium. This unusual process is made even more exceptional by the fact that the placental cells are hemiallogeneic, coexpressing maternal and paternal genomes. Within the uterine wall, cytotrophoblasts deeply invade the spiral arteries. Cytotrophoblasts migrate up these vessels and replace, in a retrograde fashion, the maternal endothelial lining. They also insert themselves among the smooth muscle cells that form the tunica media. As a result, the spiral arteries attain the physiologic properties that are required to perfuse the placenta adequately. In comparison, invasion of the venous side of the uterine circulation is minimal, sufficient to enable venous return. In preeclampsia, cytotrophoblast invasion of the interstitial uterine compartment is frequently shallow, although not consistently so. In many locations, spiral artery invasion is incomplete. There are many fewer endovascular cytotrophoblasts, and some vessels retain portions of their endothelial lining with relatively intact muscular coats, although others are not modified. Work from our group showed that these defects mirror deficits in the differentiation program that enables cytotrophoblast invasion of the uterine wall. During normal pregnancy, invasion is accompanied by the down-regulation of epithelial-like molecules that are indicative of their ectodermal origin and up-regulation of numerous receptors and ligands that typically are expressed by endothelial or vascular smooth muscle cells. For example, the expression of epithelial-cadherin (the cell-cell adhesion molecule that many ectodermal derivatives use to adhere to one another) becomes nearly undetectable, replaced by vascular-endothelial cadherin, which serves the same purpose in blood vessels. Invading cytotrophoblasts also modulate vascular endothelial growth factor ligands and receptors, at some point in the differentiation process expressing every (mammalian) family member. Molecules in this family play crucial roles in vascular and trophoblast biology, including the prevention of apoptosis. In preeclampsia, this process of vascular mimicry is incomplete, which we theorize hinders the cells interactions with spiral arterioles. What causes these aberrations? Given what is known from animal models and human risk factors, reduced placental perfusion and/or certain disease states (metabolic, immune and cardiovascular) lie upstream. Recent evidence suggests the surprising conclusion that isolation and culture of cytotrophoblasts from the placentas of pregnancies complicated by preeclampsia enables normalization of their gene expression. The affected molecules include SEMA3B, which down-regulates vascular endothelial growth factor signaling through the PI3K/AKT and GSK3 pathways. Thus, some aspects of the aberrant differentiation of cytotrophoblasts within the uterine wall that is observed in situ may be reversible. The next challenge is asking what the instigating causes are. There is added urgency to finding the answers, because these pathways could be valuable therapeutic targets for reversing abnormal placental function in patients.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocr Connect
                Journal ID (iso-abbrev): Endocr Connect
                Journal ID (hwp): EC
                Title: Endocrine Connections
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Electronic): 2049-3614
                Publication date Collection: January 2018
                Publication date (Electronic): 07 December 2017
                Volume: 7
                Issue: 1
                Pages: 199-210
                Affiliations
                [1 ]Institute of Metabolism and Systems Research (IMSR) College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
                [2 ]Birmingham Women’s Foundation Hospital Edgbaston, Birmingham, UK
                [3 ]Centre for Endocrinology Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
                Author notes
                Correspondence should be addressed to M Hewison: m.hewison@ 123456bham.ac.uk

                *(M Hewison and M D Kilby co-senior authors)

                Article
                Publisher ID: EC170308
                DOI: 10.1530/EC-17-0308
                PMC ID: 5793806
                PubMed ID: 29217650
                SO-VID: cfebec6c-c6c2-4d36-a1f0-8af4678dcdb2
                Copyright © © 2018 The authors
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                Date received : 22 November 2017
                Date accepted : 07 December 2017
                Categories
                Subject: Research

                Keywords: pregnancy,preeclampsia,vitamin d,biomarker,serum and urine
                Data availability:
                Keywords: pregnancy, preeclampsia, vitamin d, biomarker, serum and urine

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