Serum keratin 19 (CYFRA21-1) links ductular reaction with portal hypertension and outcome of various advanced liver diseases.


Journal

BMC medicine
ISSN: 1741-7015
Titre abrégé: BMC Med
Pays: England
ID NLM: 101190723

Informations de publication

Date de publication:
12 11 2020
Historique:
received: 18 02 2020
accepted: 16 09 2020
entrez: 12 11 2020
pubmed: 13 11 2020
medline: 23 2 2021
Statut: epublish

Résumé

Keratins (Ks) represent tissue-specific proteins. K18 is produced in hepatocytes while K19, the most widely used ductular reaction (DR) marker, is found in cholangiocytes and hepatic progenitor cells. K18-based serum fragments are commonly used liver disease predictors, while K19-based serum fragments detected through CYFRA21-1 are established tumor but not liver disease markers yet. Since DR reflects the severity of the underlying liver disease, we systematically evaluated the usefulness of CYFRA21-1 in different liver disease severities and etiologies. Hepatic expression of ductular keratins (K7/K19/K23) was analyzed in 57 patients with chronic liver disease (cohort i). Serum CYFRA21-1 levels were measured in 333 Austrians with advanced chronic liver disease (ACLD) of various etiologies undergoing hepatic venous pressure gradient (HVPG) measurement (cohort ii), 231 French patients with alcoholic cirrhosis (cohort iii), and 280 hospitalized Germans with decompensated cirrhosis of various etiologies (cohort iv). (i) Hepatic K19 levels were comparable among F0-F3 fibrosis stages, but increased in cirrhosis. Hepatic K19 mRNA strongly correlated with the levels of other DR-specific keratins. (ii) In ACLD, increased serum CYFRA21-1 associated with the presence of clinically significant portal hypertension (CSPH; HVPG ≥ 10 mmHg) (OR = 5.87 [2.95-11.68]) and mortality (HR = 3.02 [1.78-5.13]; median follow-up 22 months). (iii) In alcoholic cirrhosis, elevated serum CYFRA21-1 indicated increased risk of death/liver transplantation (HR = 2.59 [1.64-4.09]) and of HCC (HR = 1.74 [1.02-2.96]) over the long term (median follow-up 73 months). (iv) In decompensated cirrhosis, higher serum CYFRA21-1 predicted 90-day mortality (HR = 2.97 [1.92-4.60]) with a moderate accuracy (AUROC 0.64), independently from established prognostic scores. Hepatic K19 mRNA and serum CYFRA21-1 levels rise in cirrhosis. Increased CYFRA21-1 levels associate with the presence of CSPH and reliably indicate mortality in the short and long term independently of conventional liver biochemistry markers or scoring systems. Hence, the widely available serum CYFRA21-1 constitutes a novel, DR-related marker with prognostic implications in patients with different settings of advanced liver disease.

Sections du résumé

BACKGROUND
Keratins (Ks) represent tissue-specific proteins. K18 is produced in hepatocytes while K19, the most widely used ductular reaction (DR) marker, is found in cholangiocytes and hepatic progenitor cells. K18-based serum fragments are commonly used liver disease predictors, while K19-based serum fragments detected through CYFRA21-1 are established tumor but not liver disease markers yet. Since DR reflects the severity of the underlying liver disease, we systematically evaluated the usefulness of CYFRA21-1 in different liver disease severities and etiologies.
METHODS
Hepatic expression of ductular keratins (K7/K19/K23) was analyzed in 57 patients with chronic liver disease (cohort i). Serum CYFRA21-1 levels were measured in 333 Austrians with advanced chronic liver disease (ACLD) of various etiologies undergoing hepatic venous pressure gradient (HVPG) measurement (cohort ii), 231 French patients with alcoholic cirrhosis (cohort iii), and 280 hospitalized Germans with decompensated cirrhosis of various etiologies (cohort iv).
RESULTS
(i) Hepatic K19 levels were comparable among F0-F3 fibrosis stages, but increased in cirrhosis. Hepatic K19 mRNA strongly correlated with the levels of other DR-specific keratins. (ii) In ACLD, increased serum CYFRA21-1 associated with the presence of clinically significant portal hypertension (CSPH; HVPG ≥ 10 mmHg) (OR = 5.87 [2.95-11.68]) and mortality (HR = 3.02 [1.78-5.13]; median follow-up 22 months). (iii) In alcoholic cirrhosis, elevated serum CYFRA21-1 indicated increased risk of death/liver transplantation (HR = 2.59 [1.64-4.09]) and of HCC (HR = 1.74 [1.02-2.96]) over the long term (median follow-up 73 months). (iv) In decompensated cirrhosis, higher serum CYFRA21-1 predicted 90-day mortality (HR = 2.97 [1.92-4.60]) with a moderate accuracy (AUROC 0.64), independently from established prognostic scores.
CONCLUSIONS
Hepatic K19 mRNA and serum CYFRA21-1 levels rise in cirrhosis. Increased CYFRA21-1 levels associate with the presence of CSPH and reliably indicate mortality in the short and long term independently of conventional liver biochemistry markers or scoring systems. Hence, the widely available serum CYFRA21-1 constitutes a novel, DR-related marker with prognostic implications in patients with different settings of advanced liver disease.

Identifiants

pubmed: 33176798
doi: 10.1186/s12916-020-01784-7
pii: 10.1186/s12916-020-01784-7
pmc: PMC7661160
doi:

Substances chimiques

Biomarkers 0
KRT19 protein, human 0
Keratin-19 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

336

Subventions

Organisme : German Research Foundation
ID : STR 1095/4-2
Pays : International
Organisme : German Research Foundation
ID : MU 1373/9-1
Pays : International
Organisme : German Research Foundation
ID : BR 4182/3-1
Pays : International

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Auteurs

Karim Hamesch (K)

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Nurdan Guldiken (N)

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Mahmoud Aly (M)

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.
Department of Medicine and Infectious Diseases, Faculty of Veterinary Medicine, University of Sadat City, Sadat City, Egypt.

Norbert Hüser (N)

Department of Surgery, Technical University of Munich, School of Medicine, Klinikum rechts der Isar, 81675, Munich, Germany.

Daniel Hartmann (D)

Department of Surgery, Technical University of Munich, School of Medicine, Klinikum rechts der Isar, 81675, Munich, Germany.

Pierre Rufat (P)

AP-HP, Service d'Biostatistic Hopital Jean Verdier, Bondy, France.

Marianne Ziol (M)

Unité de Formation et de Recherche Santé Médecine et Biologie Humaine, Université Paris 13, Communauté d'Universités et Etablissements Sorbonne Paris Cité, Paris, France.
Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, USPC, Université Paris Descartes, Université Paris Diderot, F-75006, Paris, France.
Centre de ressources biologiques du groupe hospitalier Paris-Seine-Saint-Denis, BB0033-00027, Hôpitaux Universitaires Paris-Seine-Saint-Denis, Assistance Publique Hôpitaux de Paris, Bondy, France.

Katharina Remih (K)

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Georg Lurje (G)

Department of Surgery and Transplantation, University Hospital Aachen, Aachen, Germany.
Department of Surgery, Campus Charité Mitte | Campus Virchow-Klinikum-Charité-Universitätsmedizin Berlin, Berlin, Germany.

Bernhard Scheiner (B)

Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology und Hepatology, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria.

Christian Trautwein (C)

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.

Mattias Mandorfer (M)

Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology und Hepatology, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria.

Thomas Reiberger (T)

Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology und Hepatology, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria.

Sebastian Mueller (S)

Salem Medical Center and Center for Alcohol Research, University of Heidelberg, Heidelberg, Germany.

Tony Bruns (T)

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.
Department of Internal Medicine IV, Gastroenterology, Hepatology and Infectious Diseases, Jena University Hospital, Jena, Germany.
Integrated Research and Treatment Center, Center for Sepsis Control and Care (CSCC), Jena University Hospital, Jena, Germany.

Pierre Nahon (P)

AP-HP, Service d'Hépatologie, Hopital Jean Verdier, Bondy, France.
Université Paris 13, Sorbonne Paris Cité, "Equipe labellisée Ligue Contre le Cancer", F-93206, Saint-Denis, France.
Inserm, UMR-1162, "Génomique fonctionnelle des tumeur solides", F-75000, Paris, France.

Pavel Strnad (P)

Medical Clinic III, Gastroenterology, Metabolic Diseases and Intensive Care, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany. pstrnad@ukaachen.de.

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