Comparison of liver biopsies before and after direct-acting antiviral therapy for hepatitis C and correlation with clinical 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
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

14506

Subventions

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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Auteurs

Omar A Saldarriaga (OA)

Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-0144, USA.

Bradley Dye (B)

School of Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-0144, USA.

Judy Pham (J)

School of Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-0144, USA.

Timothy G Wanninger (TG)

School of Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-0144, USA.

Daniel Millian (D)

School of Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-0144, USA.

Michael Kueht (M)

Dept. of Surgery, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-0144, USA.

Benjamin Freiberg (B)

Digital Pathology, Araceli Biosciences, 7425 NE Evergreen Pkwy, Hillsboro, OR, 97124, USA.

Netanya Utay (N)

Department of Internal Medicine, University of Texas Health Science Center at Houston, 7000 Fannin St # 1200, Houston, TX, 77030, USA.

Heather L Stevenson (HL)

Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX, 77555-0144, USA. hlsteven@utmb.edu.
Department of Pathology, The University of Texas Medical Branch, 712 Texas Avenue, Clinical Services Wing-Room 5.506Q, Galveston, TX, 77555-0416, USA. hlsteven@utmb.edu.

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