Although recurrent hepatitis C virus (HCV) after liver transplantation (LT) is universal, a minority of patients will develop cirrhosis within 5 years of surgery, which places them at risk for allograft failure. This retrospective study investigated whether 2 serum fibrosis markers, serum hyaluronic
Serum chemokine CXC ligand 10 (CXCL10) predicts fibrosis progression after liver transplantation for hepatitis C infection
โ Scribed by Marie-Luise Berres; Christian Trautwein; Maximilian Schmeding; Dennis Eurich; Frank Tacke; Marcus Bahra; Peter Neuhaus; Ulf P. Neumann; Hermann E. Wasmuth
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 311 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
โฆ Synopsis
The recurrence of liver fibrosis after liver transplantation (LT) for hepatitis C virus (HCV) infection is responsible for graft loss and patient mortality. Although the contribution of the immune system to fibrosis recurrence is anticipated, systematic studies evaluating immune parameters as predictive markers of allograft fibrosis are lacking. The infiltration of immune cells into the graft is governed by chemokines. Here we assessed the predictive value of serum levels of chemokines [chemokine (C-X-C motif) ligand 9 (CXCL9), CXCL10, CXCL11, and chemokine (C-C motif) ligand 2 (CCL2)] with respect to fibrosis recurrence after LT in 90 HCV-infected organ recipients. Chemokines were determined within the first and third years after LT and were correlated with histological fibrosis progression in protocol biopsy samples at 1, 3, 5, and 7 years (median follow-up = 3 years). The association of chemokines with fibrosis progression was assessed by univariate and multivariate analyses and by Cox regression analysis. The results for the analyzed chemokines showed that CXCL10 levels in the first year after LT were strongly associated with early fibrosis recurrence (P = 0.005) independently of risk confounders (including the donor age, HCV viral load, HCV genotype, acute rejection, and inflammatory activity). As assessed by Cox regression analysis, a CXCL10 serum level โค 140 pg/mL was significantly predictive of the absence of F2 fibrosis (P = 0.001), whereas a level โค 220 pg/mL early after LT predicted the absence of F3 fibrosis during follow-up (P = 0.035).
Conclusion:
Cxcl10 is an independent biomarker of the recurrence of significant fibrosis after lt for hcv infection. these results might guide patients' care after transplantation and help us to select optimal candidates for antiviral therapy post-lt.
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