Impact of prothrombin and factor V Leiden mutations on the progression of fibrosis in patients with chronic hepatitis C.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2022
2022
Historique:
received:
23
06
2021
accepted:
11
10
2022
entrez:
10
11
2022
pubmed:
11
11
2022
medline:
15
11
2022
Statut:
epublish
Résumé
The role of thrombotic factors in the pathogenesis and progression of liver fibrosis remains obscure. We aimed to study the relationship between prothrombin G20210A (PT20210) and factor V Leiden (FVL) mutations and the progression of fibrosis and liver function in chronic HCV patients. The study included 100 subjects, 88 patients with HCV-related cirrhosis (compensated: 38, decompensated: 50), and 12 controls. Patients with other viral hepatitis or coinfection, inherited metabolic disease, autoimmune hepatitis, hepatic or extrahepatic malignancy, in addition to patients with causes of hypoalbuminemia, elevated bilirubin or prolonged INR not related to cirrhosis were excluded from the study. Relevant clinical data were collected and basic laboratory tests were performed. Liver fibrosis was assessed using APRI and FIB-4 scores. FVL and PT20210 mutations were analyzed. FVL and PT20210 mutations were significantly higher in decompensated vs. compensated patients (32% vs. 5.3%, P = 0.001; 20% vs. 5.3%, 0.043, respectively) and absent in controls. Both mutations significantly correlated to the duration of infection, platelet count and fibrosis scores. PT20210 mutation significantly correlated to serum albumin and INR. Both mutations significantly predicted fibrosis scores, especially PT20210 (AUROC: 0.833 for APRI and 0.895 for FIB-4). Both mutations are significantly correlated to fibrosis progression and liver profile and could be considered as markers predicting the need for early and different intervention.
Sections du résumé
BACKGROUND
The role of thrombotic factors in the pathogenesis and progression of liver fibrosis remains obscure. We aimed to study the relationship between prothrombin G20210A (PT20210) and factor V Leiden (FVL) mutations and the progression of fibrosis and liver function in chronic HCV patients.
METHODS
The study included 100 subjects, 88 patients with HCV-related cirrhosis (compensated: 38, decompensated: 50), and 12 controls. Patients with other viral hepatitis or coinfection, inherited metabolic disease, autoimmune hepatitis, hepatic or extrahepatic malignancy, in addition to patients with causes of hypoalbuminemia, elevated bilirubin or prolonged INR not related to cirrhosis were excluded from the study. Relevant clinical data were collected and basic laboratory tests were performed. Liver fibrosis was assessed using APRI and FIB-4 scores. FVL and PT20210 mutations were analyzed.
RESULTS
FVL and PT20210 mutations were significantly higher in decompensated vs. compensated patients (32% vs. 5.3%, P = 0.001; 20% vs. 5.3%, 0.043, respectively) and absent in controls. Both mutations significantly correlated to the duration of infection, platelet count and fibrosis scores. PT20210 mutation significantly correlated to serum albumin and INR. Both mutations significantly predicted fibrosis scores, especially PT20210 (AUROC: 0.833 for APRI and 0.895 for FIB-4).
CONCLUSIONS
Both mutations are significantly correlated to fibrosis progression and liver profile and could be considered as markers predicting the need for early and different intervention.
Identifiants
pubmed: 36355755
doi: 10.1371/journal.pone.0276592
pii: PONE-D-21-20660
pmc: PMC9648710
doi:
Substances chimiques
Prothrombin
9001-26-7
factor V Leiden
0
Biomarkers
0
Aspartate Aminotransferases
EC 2.6.1.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0276592Informations de copyright
Copyright: © 2022 Naguib et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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