Systemic levels of the endothelium-derived soluble adhesion molecules endocan and E-selectin in patients with suspected deep vein thrombosis

Mosevoll, Knut Anders; Lindås, Roald; Wendelbo, Øystein; Bruserud, Øystein; Reikvam, Håkon

doi:10.1186/2193-1801-3-571

Cited by 21 publications

(14 citation statements)

References 24 publications

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“…We also showed that elevated sE-selectin levels were associated with PTS grade. Two previous studies evaluated sEselectin levels during the acute phase of DVT and showed no association between DVT and increased sE-selectin levels [20,38]. Our findings are interesting considering that we demonstrated endothelial dysfunction even a long time after the acute DVT episode, and this seems to be associated with PTS severity.…”

Section: Discussionsupporting

confidence: 51%

Increased inflammation and endothelial markers in patients with late severe post-thrombotic syndrome

Bittar¹,

Silva²,

Orsi³

et al. 2020

PLoS ONE

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IntroductionPost-thrombotic syndrome (PTS) is a limiting long-term complication present in 20-50% of patients with deep venous thrombosis (DVT) of the lower limbs. A panel of biomarkers with potential relevance to enhance knowledge on the pathophysiology of PTS was investigated. MethodsThis case-control study included 93 patients with DVT in the lower limbs, 31 with severe PTS (cases) and 62 with mild/no PTS (controls), over 24 months after an acute episode. Thirty-one healthy individuals (HI) with no history of DVT were included as a reference to the population. FVIII activity, D-dimer, inflammatory cytokines, endothelial dysfunction markers, matrix metalloproteinases, and their inhibitors, tissue remodeling and growth factor levels were evaluated. The classification of PTS was, by the Villalta scale. ResultsPatients with severe PTS showed elevated levels of CRP, sICAM-1, sE-selectin, and decreased MMP-9 and MCP-1 levels when compared to patients with mild/no PTS. Moreover, DVT patients presented higher levels of FVIII and D-dimer when compared to HI. ConclusionsDVT patients present an inflammatory status, endothelial dysfunction and altered proteolysis MMPs activity, even a long time after the acute thrombotic episode, which is more significant in severe PTS. These results suggest a possible role of these mediators in the maintenance and worsening of PTS severity.

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Section: Discussionsupporting

confidence: 51%

Increased inflammation and endothelial markers in patients with late severe post-thrombotic syndrome

Bittar¹,

Silva²,

Orsi³

et al. 2020

PLoS ONE

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“…A study [42] investigated plasma levels of the endocan and E-selectin; the combined analysis of these biomarkers (either the two markers alone or together with D-dimer and CRP) could be used to identify patient subsets with different frequencies of DVT in a group of consecutive/unselected 120 patients admitted to hospital with suspected DVT.…”

Section: Other Inflammatory Diseases and Endocanmentioning

confidence: 99%

Endocan: A novel inflammatory indicator in cardiovascular disease?

et al. 2015

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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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Systemic levels of the endothelium-derived soluble adhesion molecules endocan and E-selectin in patients with suspected deep vein thrombosis

Cited by 21 publications

References 24 publications

Increased inflammation and endothelial markers in patients with late severe post-thrombotic syndrome

Increased inflammation and endothelial markers in patients with late severe post-thrombotic syndrome

Endocan: A novel inflammatory indicator in cardiovascular disease?

A Dormant Microbial Component in the Development of Preeclampsia

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