Everolimus immunosuppression reduces the serum expression of fibrosis markers in liver transplant recipients.

摘要: AIM: To evaluate the expression of serum fibrosis markers in liver transplantation (LT) recipients on everolimus monotherapy compared to patients an anti-calcineurin regimen. METHODS: This cross-sectional case-control study included LT (cases) (E) (n = 30) and matched controls regimen (calcineurin inhibitors, CNI), paired by etiology disease time since 30). Clinical characteristics, blood tests elastography were collected. Serum levels transforming growth factor-β (TGF-β), angiopoietin-1, tumor necrosis factor (TNF), platelet derived factor, amino-terminal propeptide type III procollagen (PIIINP), hyaluronic acid (HA), VCM-1 (ng/mL), interleukin (IL)-10, interferon-inducible protein 10 (IP-10), vascular endothelial hepatocyte (HGF) (pg/mL) determined enzyme-linked immunosorbent assay. Expression these between E CNI was compared. Stratified analysis done according factors that may influence fibrosis. Variables are described with medians (interquartillic range) or percentages. RESULTS: A total 60 [age: 59 (49-64), hepatitis C virus (HCV): n 21 (35%), from LT: 73 mo (16-105)] included. Patients had been for a median 15 mo. No differences inflammatory activity, APRI test found groups. significant observed groups PIIINP, metalloproteinase 1, angiopoietin, HGF, IP-10, TNF-α, IL-10 cell adhesion molecule. lower TGF-β [E: 12.7 (3.7-133.6), CNI: 152.5 (14.4-333.2), P 0.009] HA 702.89 (329.4-838.2), 1513.6 (691.9-1951.4), 0.001] than those CNI. difference maintained stratified when recipient age is more 50 years (TFG-β1: 0.06; HA: 0.005), without active neoplasia (TFG-β1, 0.009; 0.01), (> 5 years, TFG-β1: 0.001; 0.002), related previous history biliary complications (HA: 0.01) HCV recurrence 0.004). Liver transplant less y anti-calcineurins. remains classifying donor LT. Due small sample size, examining prior recurrent HCV, non-significant but trends towards TFG-β1 group. Mammalian target rapamycin (mTOR) plays role transformation quiescent hepatocellular stellate their profibrotic state, experimental models have demonstrated potential activity mTOR inhibition attenuating fibrogenesis. CONCLUSION: supports possible modulation after clinical setting suggests tailoring immunosuppression could avoid progression allograft.