The diagnostic and prognostic value of serum endocan in patients with cirrhotic cardiomyopathy

Voiosu, Andrei; Bălănescu, Paul; Daha, I.; Smarandache, Bianca; Rădoi, Aurelia; Mateescu, Bogdan; Băicuș, Cristian; Voiosu, Theodor

doi:10.2478/rjim-2018-0007

Cited by 9 publications

(8 citation statements)

References 30 publications

(29 reference statements)

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“…Also, there are reports that observed decreased Endocan levels in adult NAFLD [ 27 ]. Decreased Endocan levels were also associated with cardiac complications in adult cirrhotic patients [ 28 ]. All these previous data suggest that a decrease in Endocan levels could be linked with an increase in cardiac complications in chronic hepatic diseases.…”

Section: Resultsmentioning

confidence: 99%

Endocan and Lumican in Relation to Cardiometabolic Risk in a Pediatric Overweight and Obese Cohort: A Cross-Sectional Study

Balanescu

Codreanu

Comanici

et al. 2020

BioMed Research International

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The aim of the study was to evaluate serum Endocan and Lumican levels as biomarkers for pediatric Nonalcoholic Fatty Liver Disease (NAFLD) and to explore their associations with pediatric cardiometabolic risk factors. We conducted a cross-sectional study on 68 pediatric obese and overweight (O&O) patients. Ten healthy controls were recruited. Serum Lumican and Endocan levels were analyzed using ELISA kits. O&O patients had lower levels of Endocan compared to healthy controls (p<0.001). There were no differences between serum Endocan levels in O&O patients with NAFLD and those without (p=0.53). Patients considered having Nonalcoholic Steatohepatitis (NASH) had lower Endocan levels compared to O&O patients without NASH (p=0.026). Patients with metabolic syndrome had lower levels of Endocan (p=0.003). There were no significant differences between serum Lumican levels in O&O children compared to healthy controls. Lumican levels were higher in patients with hypertension (p=0.04). In O&O patients, Lumican levels were negatively correlated with Endocan levels (r=−0.37, p=0.002). Endocan seems a promising biomarker for the evaluation of pediatric NASH. Lumican was not confirmed as a biomarker for NAFLD in our cohort but was associated with higher arterial pressure. Low Endocan levels are accompanied by high serum Lumican levels, and this could be an early signature of cardiometabolic risk.

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Section: Resultsmentioning

confidence: 99%

Endocan and Lumican in Relation to Cardiometabolic Risk in a Pediatric Overweight and Obese Cohort: A Cross-Sectional Study

Balanescu

Codreanu

Comanici

et al. 2020

BioMed Research International

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“…In non-dialysis chronic kidney disease patients (stage 5), circadian heart rate variability correlates positively with serum ESM1 concentration [ 27 ]. Toshikuni et al showed that liver cirrhosis patients have high levels of serum ESM1 and that this protein may be a survival marker of liver cirrhosis [ 28 ] and cirrhotic cardiomyopathy [ 29 ]. ESM1 overexpression was reported to increase the expression of tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein-1, which are involved in liver inflammation and fibrosis [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis

Hung

Chu

et al. 2020

Toxins

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The endothelial-to-mesenchymal transition (EndoMT) is involved in the complex pathogenesis of renal fibrosis. The soluble proteoglycan endothelial cell-specific molecule 1 (ESM1) is significantly upregulated in many tumor cells and cirrhosis-related disease. The role of ESM1 in renal fibrosis is unknown. This study investigates the role of ESM1 in renal fibrosis, using an in vivo unilateral ureteral obstruction (UUO) mouse model of renal fibrosis and in vitro mouse kidney MES 13 cells overexpressing ESM1. We observed that ESM1 overexpression significantly increased the motility and migration of MES 13 cells, independent of cell viability. In ESM1-overexpressing MES 13 cells, we also observed elevated expression of mesenchymal markers (N-cadherin, vimentin, matrix metallopeptidase 9 (MMP9)) and the fibrosis marker α-smooth muscle actin (α-SMA) and decreased expression of the endothelial marker vascular endothelial cadherin (VE-cadherin) and CD31. In a mouse model of fibrosis induced by unilateral ureter obstruction, we observed time-dependent increases in ESM1, α-SMA, and vimentin expression and renal interstitial collagen fibers in kidney tissue samples. These results suggest that ESM1 may serve as an EndoMT marker of renal fibrosis progression.

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“…These patients already face a challenging transplantation journey from a significant pretransplant disease burden [50]. Unsurprisingly, a significant number of cardiac complications has been observed in transplant patients, with the most common being refractory hypotension [51]. The current literature suggests that transesophageal echocardiography should be done immediately post-transplant as standard of care, because it provides invaluable information relevant to the required level of post-transplant cardiac support [46] (see Figure 4).…”

Section: Liver Transplantationmentioning

confidence: 99%

Cirrhotic Cardiomyopathy

Longley

Tran

2021

Gastroenterology Insights

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Cirrhotic cardiomyopathy (CCM), cardiac dysfunction in end-stage liver disease in the absence of prior heart disease, is an important clinical entity that contributes significantly to morbidity and mortality. The original definition for CCM, established in 2005 at the World Congress of Gastroenterology (WCG), was based upon known echocardiographic parameters to identify subclinical cardiac dysfunction in the absence of overt structural abnormalities. Subsequent advances in cardiovascular imaging and in particular myocardial deformation imaging have rendered the WCG criteria outdated. A number of investigations have explored other factors relevant to CCM, including serum markers, electrocardiography, and magnetic resonance imaging. CCM characteristics include a hyperdynamic circulatory state, impaired contractility, altered diastolic relaxation, and electrophysiological abnormalities, particularly QT interval prolongation. It is now known that cardiac dysfunction worsens with the progression of cirrhosis. Treatment for CCM has traditionally been limited to supportive efforts, but new pharmacological studies appear promising. Left ventricular diastolic dysfunction in CCM can be improved by targeted heart rate reduction. Ivabradine combined with carvedilol improves left ventricular diastolic dysfunction through targeted heart rate reduction, and this regimen can improve survival in patients with cirrhosis. Orthotopic liver transplantation also appears to improve CCM. Here, we canvass diagnostic challenges associated with CCM, introduce cardiac physiology principles and the application of echocardiographic techniques, and discuss the evidence behind therapeutic interventions in CCM.

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The diagnostic and prognostic value of serum endocan in patients with cirrhotic cardiomyopathy

Abstract: Endocan is a promising biomarker of severity of cirrhosis and may help in the diagnosis of cardiac dysfunction in this population.

Cited by 9 publications

References 30 publications

Endocan and Lumican in Relation to Cardiometabolic Risk in a Pediatric Overweight and Obese Cohort: A Cross-Sectional Study

Endocan and Lumican in Relation to Cardiometabolic Risk in a Pediatric Overweight and Obese Cohort: A Cross-Sectional Study

Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis

Cirrhotic Cardiomyopathy

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