4.7 Article

Modifications of liver stiffness and CXCL4, TGF-β1 and HGF are similar in HCV- and HIV/HCV-infected patients after DAAs

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SCIENTIFIC REPORTS
卷 11, 期 1, 页码 -

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NATURE RESEARCH
DOI: 10.1038/s41598-021-89370-6

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资金

  1. Secretaria General de Investigacion, Desarrollo e Innovacion en Salud, Junta de Andalucia, Iniciativa Territorial Integrada 2014-2020 para la provincia de Cadiz, Spain [PI-0076-2017]
  2. Consejeria de Salud, Proyectos de Investigacion en Salud, Junta de Andalucia, Convocatoria 2018 [PI 0128/2018]
  3. FEDER (Fondo Europeo de Desarrollo Regional)

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This study aimed to identify predictive factors for fibrosis regression in HCV-monoinfected and HIV/HCV-coinfected patients after treatment with direct antiviral agents. The results showed that both groups experienced a significant reduction in liver stiffness after achieving sustained virological response, but this improvement was not correlated with changes in serum markers.
The objective of this work was to identify predictive factors of fibrosis regression after direct antiviral agents (DAAs) in HCV-monoinfected and HIV/HCV-coinfected patients. This was a prospective study of HCV-monoinfected (n=20), HIV/HCV-co-infected (n=66) patients and healthy controls (n=15). Patients had started DAAs and achieved sustained virological response. Liver stiffness (LS) and serum concentrations of profibrotic transforming growth factor (TGF)-beta 1 and CXC chemokine ligand 4 (CXCL4) and antifibrotic HGF hepatocyte growth factor (HGF) were analyzed at baseline (M0) and 12 months after starting DAAs (M12). A M12 LS achievement of <= 9.5 kPa was considered the cutoff point to discharge from a liver clinic. The LS decrease from M0 to M12 was 34%. No significant differences were observed in LS decline between HCV- and HIV/HCV-infected individuals. Changes of serum CXCL4, TGF-beta 1 and HGF levels did not correlate with LS improvement. 16 out from 56 patients (28%) with a baseline LS>9.5 achieved a M12 LS <= 9.5. HCV-monoinfected and HIV/HCV coinfected patients experienced a significant reduction of LS after sustained virological response. This improvement did not correlate with changes in serum profibrotic or antifibrotic markers. A 29% of those with a baseline LS>9.5 achieved a LS under this cutoff point.

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