Plasma Nogo-A and placental growth factor levels are associated with portal hypertension in patients with liver cirrhosis.


Journal

World journal of gastroenterology
ISSN: 2219-2840
Titre abrégé: World J Gastroenterol
Pays: United States
ID NLM: 100883448

Informations de publication

Date de publication:
21 Jun 2019
Historique:
received: 23 03 2019
revised: 18 04 2019
accepted: 29 04 2019
entrez: 29 6 2019
pubmed: 30 6 2019
medline: 1 1 2020
Statut: ppublish

Résumé

Clinically significant portal hypertension (CSPH) and severe portal hypertension (SPH) increase the risk for decompensation and life-threatening complications in liver cirrhosis. Pathologic angiogenesis might contribute to the formation of these conditions. Placental growth factor (PlGF) and Nogo-A protein are biomarkers of pathological angiogenesis, but data on their role in liver cirrhosis and portal hypertension is scarce. To determine plasma levels of PlGF and Nogo-A in patients with liver cirrhosis, CSPH, SPH and potential to predict portal hypertension. A cohort of 122 patients with hepatitis C virus and/or alcohol-induced liver cirrhosis with characterized hepatic venous pressure gradient (HVPG) were included in the study. Demographic data, medical history, Child-Turcotte-Pugh and Model of End Stage liver disease score, clinical chemistry, liver stiffness values were recorded on the day of the procedure prior HVPG measurement. The degree of portal hypertension was determined by the invasive HVPG measurement. Nogo-A and PlGF plasma levels were evaluated using enzyme linked immunosorbent assay. The control group consisted of 30 healthy age- and sex- matched individuals. Peripheral PlGF levels were higher and Nogo-A levels were lower in patients with liver cirrhosis (23.20 Plasma PlGF levels were higher while Nogo-A levels were lower in patients with liver cirrhosis and portal hypertension. Biomarkers showed moderate predictive value in determining CSPH and SPH.

Sections du résumé

BACKGROUND BACKGROUND
Clinically significant portal hypertension (CSPH) and severe portal hypertension (SPH) increase the risk for decompensation and life-threatening complications in liver cirrhosis. Pathologic angiogenesis might contribute to the formation of these conditions. Placental growth factor (PlGF) and Nogo-A protein are biomarkers of pathological angiogenesis, but data on their role in liver cirrhosis and portal hypertension is scarce.
AIM OBJECTIVE
To determine plasma levels of PlGF and Nogo-A in patients with liver cirrhosis, CSPH, SPH and potential to predict portal hypertension.
METHODS METHODS
A cohort of 122 patients with hepatitis C virus and/or alcohol-induced liver cirrhosis with characterized hepatic venous pressure gradient (HVPG) were included in the study. Demographic data, medical history, Child-Turcotte-Pugh and Model of End Stage liver disease score, clinical chemistry, liver stiffness values were recorded on the day of the procedure prior HVPG measurement. The degree of portal hypertension was determined by the invasive HVPG measurement. Nogo-A and PlGF plasma levels were evaluated using enzyme linked immunosorbent assay. The control group consisted of 30 healthy age- and sex- matched individuals.
RESULTS RESULTS
Peripheral PlGF levels were higher and Nogo-A levels were lower in patients with liver cirrhosis (23.20
CONCLUSION CONCLUSIONS
Plasma PlGF levels were higher while Nogo-A levels were lower in patients with liver cirrhosis and portal hypertension. Biomarkers showed moderate predictive value in determining CSPH and SPH.

Identifiants

pubmed: 31249451
doi: 10.3748/wjg.v25.i23.2935
pmc: PMC6589742
doi:

Substances chimiques

Biomarkers 0
Nogo Proteins 0
PGF protein, human 0
RTN4 protein, human 0
Placenta Growth Factor 144589-93-5

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2935-2946

Déclaration de conflit d'intérêts

Conflict-of-interest statement: The authors have declared no conflicts of interest.

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Auteurs

Sigita Gelman (S)

Department of Gastroenterology, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania.

Violeta Salteniene (V)

Institute for Digestive Research, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania.

Andrius Pranculis (A)

Department of Radiology, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania.

Jurgita Skieceviciene (J)

Institute for Digestive Research, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania.

Romanas Zykus (R)

Department of Gastroenterology, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania.

Dalius Petrauskas (D)

Department of Gastroenterology, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania.

Limas Kupcinskas (L)

Institute for Digestive Research and Department of Gastroenterology, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania.

Ali Canbay (A)

Department of Gastroenterology, Hepatology and Infectious Diseases Otto-von-Guericke University, Magdeburg 39106, Germany.

Alexander Link (A)

Department of Gastroenterology, Hepatology and Infectious Diseases Otto-von-Guericke University, Magdeburg 39106, Germany.

Juozas Kupcinskas (J)

Institute for Digestive Research and Department of Gastroenterology, Medical Academy, Lithuanian University of Health Sciences, Kaunas 44307, Lithuania. juozas.kupcinskas@lsmuni.lt.

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Classifications MeSH