Z Gastroenterol 2018; 56(01): E2-E89
DOI: 10.1055/s-0037-1612788
Poster Visit Session IV Tumors, Liver Surgery and Transplantation – Saturday, January 27, 2018, 8:30am – 9:15am, Foyer area West Wing
Georg Thieme Verlag KG Stuttgart · New York

Donor but not recipient CRS predicts fibrosis progression after liver transplantation in a large cohort of HCV-positive and negative patients

A Zimmermann
1   University Medical Center Mainz, 1. Med. Clinic and Polyclinic, Mainz
,
F Darstein
1   University Medical Center Mainz, 1. Med. Clinic and Polyclinic, Mainz
,
F Abel
1   University Medical Center Mainz, 1. Med. Clinic and Polyclinic, Mainz
,
M Hoppe-Lotichius
2   University Medical Center, Department of General-, Visceral- and Transplantation- Surgery, Mainz
,
A Lautem
2   University Medical Center, Department of General-, Visceral- and Transplantation- Surgery, Mainz
,
A Schad
3   University Medical Center, Institute of Pathology, Mainz
,
J Mittler
2   University Medical Center, Department of General-, Visceral- and Transplantation- Surgery, Mainz
,
J Vollmer
1   University Medical Center Mainz, 1. Med. Clinic and Polyclinic, Mainz
,
H Lang
2   University Medical Center, Department of General-, Visceral- and Transplantation- Surgery, Mainz
,
P Galle
1   University Medical Center Mainz, 1. Med. Clinic and Polyclinic, Mainz
,
T Zimmermann
1   University Medical Center Mainz, 1. Med. Clinic and Polyclinic, Mainz
,
D Schuppan
4   University Medical Center, Institute of Translational Immunology, Liver Fibrosis Center, Mainz
› Author Affiliations
Further Information

Publication History

Publication Date:
03 January 2018 (online)

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Questions:

Fibrosis progression (FP) after liver transplantation (LT) is an important cause of post-transplant morbidity and mortality. Genetic and serum biomarkers are needed for early prediction of FP after LT. A seven gene cirrhosis risk score (CRS) of the recipient has been associated with higher risk of FP in hepatitis C virus (HCV) infected patients before and after transplantation. A broader validation of CRS, including non-HCV patients and the donor liver is lacking. We therefore analyzed the impact of donor- and recipient-specific CRS on FP after LT in a large cohort of HCV-positive and-negative patients.

Methods:

Genotyping from liver biopsies (219 donors) and peripheral blood (449 recipients) was performed. CRS was correlated with FP in protocol biopsies from 449 LT patients [median age 54.6 years (range 16.1 – 73.6)].

Results:

Fp ≥F2 was documented in 32.3% of the R-CRS group (defined by recipients' genotype) and in 26.0% of the D-CRS group (defined by the donor's genotype). HCV-infection strongly and independently predicted FP. Shorter fibrosis-free intervals (FFIs) were observed in patients with donor CRS> 0.7 (p = 0.041), and in HCV-negative patients with donor CRS> 0.7 (p = 0.02). The predictive value of donor CRS for FP was independent of known clinical risk factors, especially in HCV-negative patients (p = 0.03). Donor CRS> 0.7 was associated with a high risk of F≥2 in 1-year protocol biopsies (p = 0.001 for the whole D-CRS group and the HCV-negative subgroup). The donors' AZIN1, STXBP5L and TRPM5 genotypes carried higher risks for fibrosis ≥F2 in certain HCV-positive and -negative subgroups.

Conclusion:

Donor CRS > 0.7 predicted faster onset and more rapid FP after LT, especially in HCV negative patients.