Serum endocan concentration in women with pre-eclampsia

Yüksel, Mehmet Aytaç; Tüten, Abdullah; Öncül, Mahmut; Açıkgöz, Aydan; Yüksel, İlkbal Temel; Toprak, Muhammet Sait; Ekmekçi, Hakan; Ekmekçi, Özlem Balcı; Madazli, Rıza

doi:10.1007/s00404-014-3605-x

Cited by 18 publications

(19 citation statements)

References 21 publications

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“…Studies have shown an increase in CEC number and other markers of EC damage such as soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin and endocan in PE compared with Norm-Preg women (Canbakan et al, 2007; Adekola et al, 2015; Tuzcu et al, 2015; Cakmak et al, 2016), although some studies reported no difference in serum endocan levels (Yuksel et al, 2015). Other studies have shown a decrease in circulating endothelial progenitor cells as a marker of endothelial damage in PE women (Sakashita et al, 2014) (Table 1).…”

Section: Endothelial Dysfunction In Preeclampsiamentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

191

117

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Preeclampsia is a pregnancy-related disorder characterized by hypertension, and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

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Section: Endothelial Dysfunction In Preeclampsiamentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

191

117

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“…It has been suggested to be a new biomarker for endothelial dysfunction and PE (751, 752). It would appear, however, to be a rather less specific inflammatory biomarker (753, 754) and is associated with a variety of diseases, including chronic kidney disease (755, 756) and cardiovascular disease (755). Most pertinently from our perspective, it is also raised strongly during sepsis (757–760).…”

Section: Proteomic and Similar Biomarkers – Circulating And Placentalmentioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one.

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“…These results suggest that endocan may be a functional protein rather than a simple biomarker. Interestingly, it has also been suggested that change of circulating endocan may be a marker of women with preeclampsia [18][19][20][21][22][23][24][25]. However, results of previous pilot studies are inconsistent [18][19][20][21][22][23][24][25].…”

Section: Introductionmentioning

confidence: 99%

“…Interestingly, it has also been suggested that change of circulating endocan may be a marker of women with preeclampsia [18][19][20][21][22][23][24][25]. However, results of previous pilot studies are inconsistent [18][19][20][21][22][23][24][25]. Some studies showed that circulating endocan may be higher in women with preeclampsia than those with normal pregnancy [18,20,22,24], while others did not find a significant difference regarding the circulating endocan between pregnant women with and without preeclampsia [19,21,23,25].…”

Section: Introductionmentioning

confidence: 99%

“…However, results of previous pilot studies are inconsistent [18][19][20][21][22][23][24][25]. Some studies showed that circulating endocan may be higher in women with preeclampsia than those with normal pregnancy [18,20,22,24], while others did not find a significant difference regarding the circulating endocan between pregnant women with and without preeclampsia [19,21,23,25]. Since the sample sizes of these studies are generally small, some studies may be statistically underpowered to detect a significant difference of circulating endocan between women with preeclampsia and those with normal pregnancy.…”

Section: Introductionmentioning

confidence: 99%

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Circulating endocan and preeclampsia: a meta-analysis

Lan

Liu

2020

Bioscience Reports

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Background: Endocan, a novel protein involved in inflammation and endothelial dysfunction, has been suggested to be related to preeclampsia, although the results of previous studies were not consistent. The aim of the study was to evaluate the potential difference of circulating endocan in women with preeclampsia and those with normal pregnancy. Methods: Matched case–control studies evaluating the difference of circulating endocan between women with preeclampsia and those with normal pregnancy were identified via systematic search of PubMed and Embase databases. A random-effect model or a fixed-effect model was used to pool the results according to the heterogeneity. Subgroup analysis was performed to evaluate whether the timing of preeclampsia onset affected the outcome. Results: Overall, eight matched case–control studies, including 451 women with preeclampsia and 442 women with normal pregnancy were included. Significant heterogeneity was detected among the included studies (P for Cochrane’s Q test = 0.006, I2 = 65%). Meta-analysis with a random-effect model showed that women with preeclampsia had significantly higher circulating level of endocan compared with women with normal pregnancy (standardized mean difference = 0.37, 95% confidence interval: 0.13–0.62, P = 0.003). Subsequent subgroup analyses showed that the difference of circulating endocan between women with early onset preeclampsia and those with normal pregnancy was not statistically different from that between women with late-onset preeclampsia and those with normal pregnancy (P for subgroup difference = 0.81). Conclusions: Women with preeclampsia have higher circulating endocan than those with normal pregnancy.

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Serum endocan concentration in women with pre-eclampsia

Abstract: These findings suggest that the role of endocan in the pathogenesis of pre-eclampsia was not related to pre-eclampsia; hence, further studies are needed to investigate the role of endocan in the pathogenesis of pre-eclampsia.

Cited by 18 publications

References 21 publications

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

A Dormant Microbial Component in the Development of Preeclampsia

Circulating endocan and preeclampsia: a meta-analysis

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