Table 3.
Risk factors studied for association with more severe hepatitis C virus recurrence
Factor | Evidence |
Donor | |
Age > 40 yr | ↑↑↑ |
Living donor | ↔ |
Split liver | ↔ |
DCD | ↔ |
HCV+ | ↔ |
Macrovesicular steatosis > 30% | ↑↓ |
IRI | ↑↓ |
IL28B “CC” genotype | ↑↓ |
Virus | |
HCV genotype 1 | ↑ |
High pre-transplant HCV RNA | ↑ |
HCV RNA 4 mo post LT ≥ 1 × 109 mEq/mL | ↑↑ |
CMV viremia | ↑↑↑ |
HIV coinfection | ↑↑ |
Recipient | |
Female sex | ↑↑ |
African American D/R mismatch | ↑↑ |
African American D/R match | ↔ |
Metabolic syndrome1 | ↑ |
IL28B non-“CC” genotype | ↑ |
Immunosuppression | |
Pulsed corticosteroids for American College of Rheumatology | ↑↑↑ |
Tacrolimus (vs CsA) | ↑↓ |
Sirolimus | ↑ |
Thymoglobulin | ↔ |
Basiliximab | ↔ |
OKT3 | ↑ |
Metabolic syndrome defined by ATP-III criteria 1 yr post liver transplantation (LT)[37], homeostasis model assessment-estimated insulin resistance > 2.5 4 mo post LT[46], or hepatic steatosis ≥ 5% on an index liver allograft biopsy 1 yr post-LT[47]. ↑: Evidence of increased risk; ↔: Evidence of no increased risk; ↑↓: Indeterminate risk; DCD: Donation after cardiac death; HCV: Hepatitis C virus; CMV: Cytomegalovirus; HIV: Human immunodeficiency virus; CsA: Cyclosporin A; OKT3: Muromonab-CD3; IRI: Ischemia reperfusion injury.