Hepatic erythropoietin response in cirrhosis

Louise M Risør; Mogens Fenger; Niels V Olsen; Søren Møller

doi:10.3109/00365513.2015.1137351

Hepatic erythropoietin response in cirrhosis

Louise M Risør, Mogens Fenger, Niels V Olsen, Søren Møller

1 Citation (Scopus)

Abstract

BACKGROUND: Erythropoietin (EPO) is produced in the liver during fetal life, but after birth the production shifts to the kidneys. The liver maintains a production capacity of 10% of the total EPO-production, but can be up-regulated to 100%. Previous studies have demonstrated both elevated and reduced concentrations of EPO in cirrhosis. Increased EPO concentrations could be expected due to anemia, hypoxia, renal hypoperfusion, or EPO-mediated hepatoprotective mechanisms. In contrast, poor hepatic production capacity may cause reduced EPO concentrations in cirrhosis. In the present paper we aimed to study hepatic and renal venous concentrations of EPO in relation to the severity of the disease.

MATERIALS AND METHODS: We included 24 patients with alcoholic cirrhosis and eight age-matched healthy controls. All had a full catheterization performed with the determination of EPO concentrations in the hepatic, renal and femoral veins and artery. All patients were clinically, biochemically, and hemodynamically characterized.

RESULTS: The median arterial EPO concentrations in the cirrhotic patients and controls were 7.1 mIU/mL (range 3.5-179) and 7.2 mIU/mL (range 3.8-15.3), respectively. In the patient group we found no significant correlations to stage of disease of hemodynamic derangement.

CONCLUSION: We found no significant differences in EPO concentrations across the liver, kidney, or peripheral circulation in the patient or control groups; and no significant correlations to clinical, biochemical, or hemodynamic characteristics. This suggests that hepatic EPO synthesis is not enhanced in cirrhosis, but larger scale studies are needed to clarify this question.

Original language	English
Journal	Scandinavian Journal of Clinical & Laboratory Investigation
Volume	76
Issue number	3
Pages (from-to)	234-9
Number of pages	6
ISSN	0036-5513
DOIs	https://doi.org/10.3109/00365513.2015.1137351
Publication status	Published - 2 Apr 2016

Keywords

Adult
Aged
Aged, 80 and over
Biomarkers
Case-Control Studies
Erythropoietin
Female
Femoral Artery
Femoral Vein
Hepatic Artery
Humans
Liver
Liver Cirrhosis, Alcoholic
Male
Middle Aged
Renal Artery
Journal Article

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10.3109/00365513.2015.1137351

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title = "Hepatic erythropoietin response in cirrhosis",

abstract = "BACKGROUND: Erythropoietin (EPO) is produced in the liver during fetal life, but after birth the production shifts to the kidneys. The liver maintains a production capacity of 10% of the total EPO-production, but can be up-regulated to 100%. Previous studies have demonstrated both elevated and reduced concentrations of EPO in cirrhosis. Increased EPO concentrations could be expected due to anemia, hypoxia, renal hypoperfusion, or EPO-mediated hepatoprotective mechanisms. In contrast, poor hepatic production capacity may cause reduced EPO concentrations in cirrhosis. In the present paper we aimed to study hepatic and renal venous concentrations of EPO in relation to the severity of the disease.MATERIALS AND METHODS: We included 24 patients with alcoholic cirrhosis and eight age-matched healthy controls. All had a full catheterization performed with the determination of EPO concentrations in the hepatic, renal and femoral veins and artery. All patients were clinically, biochemically, and hemodynamically characterized.RESULTS: The median arterial EPO concentrations in the cirrhotic patients and controls were 7.1 mIU/mL (range 3.5-179) and 7.2 mIU/mL (range 3.8-15.3), respectively. In the patient group we found no significant correlations to stage of disease of hemodynamic derangement.CONCLUSION: We found no significant differences in EPO concentrations across the liver, kidney, or peripheral circulation in the patient or control groups; and no significant correlations to clinical, biochemical, or hemodynamic characteristics. This suggests that hepatic EPO synthesis is not enhanced in cirrhosis, but larger scale studies are needed to clarify this question.",

keywords = "Adult, Aged, Aged, 80 and over, Biomarkers, Case-Control Studies, Erythropoietin, Female, Femoral Artery, Femoral Vein, Hepatic Artery, Humans, Liver, Liver Cirrhosis, Alcoholic, Male, Middle Aged, Renal Artery, Journal Article",

author = "Ris{\o}r, {Louise M} and Mogens Fenger and Olsen, {Niels V} and S{\o}ren M{\o}ller",

year = "2016",

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doi = "10.3109/00365513.2015.1137351",

language = "English",

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TY - JOUR

T1 - Hepatic erythropoietin response in cirrhosis

AU - Risør, Louise M

AU - Fenger, Mogens

AU - Olsen, Niels V

AU - Møller, Søren

PY - 2016/4/2

Y1 - 2016/4/2

N2 - BACKGROUND: Erythropoietin (EPO) is produced in the liver during fetal life, but after birth the production shifts to the kidneys. The liver maintains a production capacity of 10% of the total EPO-production, but can be up-regulated to 100%. Previous studies have demonstrated both elevated and reduced concentrations of EPO in cirrhosis. Increased EPO concentrations could be expected due to anemia, hypoxia, renal hypoperfusion, or EPO-mediated hepatoprotective mechanisms. In contrast, poor hepatic production capacity may cause reduced EPO concentrations in cirrhosis. In the present paper we aimed to study hepatic and renal venous concentrations of EPO in relation to the severity of the disease.MATERIALS AND METHODS: We included 24 patients with alcoholic cirrhosis and eight age-matched healthy controls. All had a full catheterization performed with the determination of EPO concentrations in the hepatic, renal and femoral veins and artery. All patients were clinically, biochemically, and hemodynamically characterized.RESULTS: The median arterial EPO concentrations in the cirrhotic patients and controls were 7.1 mIU/mL (range 3.5-179) and 7.2 mIU/mL (range 3.8-15.3), respectively. In the patient group we found no significant correlations to stage of disease of hemodynamic derangement.CONCLUSION: We found no significant differences in EPO concentrations across the liver, kidney, or peripheral circulation in the patient or control groups; and no significant correlations to clinical, biochemical, or hemodynamic characteristics. This suggests that hepatic EPO synthesis is not enhanced in cirrhosis, but larger scale studies are needed to clarify this question.

AB - BACKGROUND: Erythropoietin (EPO) is produced in the liver during fetal life, but after birth the production shifts to the kidneys. The liver maintains a production capacity of 10% of the total EPO-production, but can be up-regulated to 100%. Previous studies have demonstrated both elevated and reduced concentrations of EPO in cirrhosis. Increased EPO concentrations could be expected due to anemia, hypoxia, renal hypoperfusion, or EPO-mediated hepatoprotective mechanisms. In contrast, poor hepatic production capacity may cause reduced EPO concentrations in cirrhosis. In the present paper we aimed to study hepatic and renal venous concentrations of EPO in relation to the severity of the disease.MATERIALS AND METHODS: We included 24 patients with alcoholic cirrhosis and eight age-matched healthy controls. All had a full catheterization performed with the determination of EPO concentrations in the hepatic, renal and femoral veins and artery. All patients were clinically, biochemically, and hemodynamically characterized.RESULTS: The median arterial EPO concentrations in the cirrhotic patients and controls were 7.1 mIU/mL (range 3.5-179) and 7.2 mIU/mL (range 3.8-15.3), respectively. In the patient group we found no significant correlations to stage of disease of hemodynamic derangement.CONCLUSION: We found no significant differences in EPO concentrations across the liver, kidney, or peripheral circulation in the patient or control groups; and no significant correlations to clinical, biochemical, or hemodynamic characteristics. This suggests that hepatic EPO synthesis is not enhanced in cirrhosis, but larger scale studies are needed to clarify this question.

KW - Adult

KW - Aged

KW - Aged, 80 and over

KW - Biomarkers

KW - Case-Control Studies

KW - Erythropoietin

KW - Female

KW - Femoral Artery

KW - Femoral Vein

KW - Hepatic Artery

KW - Humans

KW - Liver

KW - Liver Cirrhosis, Alcoholic

KW - Male

KW - Middle Aged

KW - Renal Artery

KW - Journal Article

U2 - 10.3109/00365513.2015.1137351

DO - 10.3109/00365513.2015.1137351

M3 - Journal article

C2 - 26924722

SN - 0036-5513

VL - 76

SP - 234

EP - 239

JO - Scandinavian Journal of Clinical & Laboratory Investigation

JF - Scandinavian Journal of Clinical & Laboratory Investigation

IS - 3

ER -

Hepatic erythropoietin response in cirrhosis

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