Comparison of liver biopsies before and after direct-acting antiviral therapy for hepatitis C and correlation with clinical outcome.
Adult
Alkaline Phosphatase
/ blood
Antiviral Agents
/ therapeutic use
Biopsy
Carcinoma, Hepatocellular
/ pathology
Fatty Liver
/ pathology
Female
Hepatitis C
/ drug therapy
Humans
Liver
/ drug effects
Liver Cirrhosis
/ pathology
Liver Neoplasms
/ pathology
Male
Middle Aged
Retrospective Studies
Treatment Outcome
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
15 07 2021
15 07 2021
Historique:
received:
11
03
2021
accepted:
18
06
2021
entrez:
16
7
2021
pubmed:
17
7
2021
medline:
18
11
2021
Statut:
epublish
Résumé
Direct-acting antivirals (DAA) have replaced interferon (IFN)-based therapies for hepatitis C virus. In this retrospective clinical study, we examined differences in histopathologic features in paired liver biopsies collected from the same patient before and after DAA and correlated these findings with clinical outcome. Biopsies (n = 19) were evaluated by quantitative imaging analysis to measure steatosis and fibrosis. Most patients had decreased steatosis in their post-treatment, follow-up biopsies. However, one patient had a striking increase in steatosis (from 0.86 to 6.32%) and later developed decompensated cirrhosis and hepatocellular carcinoma (HCC). This patient had a marked increase in fibrosis between biopsies, with a CPA of 6.74 to 32.02. Another patient, who already had bridging fibrosis at the time of her pre-treatment biopsy, developed cholangiocarcinoma after DAA. Even though the overall inflammatory activity in the post-treatment biopsies significantly decreased after treatment, 60% of patients had persistent portal lymphocytic inflammation. In summary, DAAs decreased steatosis and hepatic inflammation in most patients, although some may have persistence of lymphocytic portal inflammation. Patients known to have advanced fibrosis at treatment initiation and who have other risk factors for ongoing liver injury, such as steatosis, should be followed closely for the development of adverse outcomes, such as portal hypertension and primary liver cancers.
Identifiants
pubmed: 34267267
doi: 10.1038/s41598-021-93881-7
pii: 10.1038/s41598-021-93881-7
pmc: PMC8282660
doi:
Substances chimiques
Antiviral Agents
0
Alkaline Phosphatase
EC 3.1.3.1
Types de publication
Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
14506Subventions
Organisme : NCATS NIH HHS
ID : KL2 TR001441
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA217674
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK125730
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK007639
Pays : United States
Informations de copyright
© 2021. The Author(s).
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