Paracentesis-induced circulatory dysfunction (PICD) is a serious complication of large-volume (>5 L) paracentesis in cirrhosis and is reduced with albumin infusion.
The two laboratory indices APRI and FIB-4 index could predict advanced (F3-4) liver fibrosis and cirrhosis (F4), with the area under the receiver operating characteristic curve (AUROC) > 0.8 and accuracy >70%.
Mean arterial pressure (MAP), platelet count, and serum albumin were significantly lower and total leucocyte count (TLC), blood urea nitrogen, serum creatinine (SCr), total bilirubin, aspartate aminotransferase, international normalized ratio, Child-Turcotte-Pugh (CTP) score, and model for end-stage liver disease (MELD) score higher in cirrhosis patients with AKI than without AKI (p < 0.05 each).
Unbiased genome-wide association study identified variants in/near PNPLA3 and HFE, and candidate variant analysis identified variants in/near TM6SF2, MBOAT7, SERPINA1, HSD17B13, STAT4, and IFNL4 that reproducibly affected cirrhosis.
PSMP expression was studied in patients with fibrosis/cirrhosis and in 3 murine models of liver fibrosis, including mice treated with carbon tetrachloride (CCl<sub>4</sub>), bile-duct ligation, or a 5-diethoxycarbonyl-1,4-dihydrocollidine diet.
In the present study, tissue samples from normal liver, cirrhosis and HCC were subjected to differentially gene expression analysis, weighted gene correlation network analysis to identify the twenty hub genes (TOP2A, CDC20, PTTG1, CDCA5, CCNB2, PRC1, KIF20A, SF3B4, HSP90AB1, FOXD2, PLOD3, CCT3, SETDB1, VPS45, SPDL1, RACGAP1, MED24, KIAA0101, ZNF282, and USP21) in the pathological progression from cirrhosis to HCC.
In the present study, tissue samples from normal liver, cirrhosis and HCC were subjected to differentially gene expression analysis, weighted gene correlation network analysis to identify the twenty hub genes (TOP2A, CDC20, PTTG1, CDCA5, CCNB2, PRC1, KIF20A, SF3B4, HSP90AB1, FOXD2, PLOD3, CCT3, SETDB1, VPS45, SPDL1, RACGAP1, MED24, KIAA0101, ZNF282, and USP21) in the pathological progression from cirrhosis to HCC.
Significant predictors for HCC were identified using multiple Cox regression analysis in study cohort: treatment age ≥60 years (hazard ratio [HR]: 2.04, 95% confidence interval [CI] = 1.3-3.7), pretreatment bilirubin ≥1.1 mg/dL (HR: 1.99, 95% CI = 1.08-3.67), α-fetoprotein ≥7.9 ng/mL (HR: 2.44, 95% CI = 1.16-5.32), no sustained virological response (SVR; HR: 1.91, 95% CI = 1.05-3.45), and baseline cirrhosis (HR: 4.45, 95% CI = 2.07-9.73).
The AUROCs of TE using M and XL probes, SWE, APRI, and FIB-4 were 0.771, 0.761, 0.700, 0.698, and 0.697 respectively, for significant fibrosis; 0.974, 0.973, 0.929, 0.738, and 0.859, respectively, for advanced fibrosis; and 0.954, 0.949, 0.962, 0.765, and 0.962, respectively, for cirrhosis.
In multiple regression analysis, <i>RASSF1A</i> and <i>E-Cadherin</i> were predictors of HCC within cirrhosis cases, but only <i>E-Cadherin</i> was an independent risk factor for prediction of HCC in cases with low AFP (<i>P</i> = 0.01).<b>Conclusions</b>: The presence of hypermethylated serum <i>RASSF1A, E-Cadherin</i> and <i>RUNX3</i> is linked to HCC in patients with HCV-related cirrhosis.
In multiple regression analysis, <i>RASSF1A</i> and <i>E-Cadherin</i> were predictors of HCC within cirrhosis cases, but only <i>E-Cadherin</i> was an independent risk factor for prediction of HCC in cases with low AFP (<i>P</i> = 0.01).<b>Conclusions</b>: The presence of hypermethylated serum <i>RASSF1A, E-Cadherin</i> and <i>RUNX3</i> is linked to HCC in patients with HCV-related cirrhosis.
The levels of CD34/KDR-positive endothelial progenitor cells, CD133/KDR-positive endothelial progenitor cells, and vascular endothelial growth factor were higher in patients with cirrhosis ± hepatocellular carcinoma than in healthy controls (P = 0.017, P < 0.001 and P < 0.001, respectively).
Immunohistochemical staining of human liver disease tissue arrays showed that HMGCS2 is abundantly expressed in normal liver tissues but is downregulated in cirrhosis and HCC tissues.
Micro-ribonucleic acids (miRNAs) have been identified to play a regulatory role in EMT. miR-215 is important in repressingmigration/invasion of cancer cells.In this study, we aimed to evaluate the crosstalk between miR-215 and EMT specific markers (E- and N-cadherin) with a spotlight on its role in the EMT process in HCVinfected patients.One hundred and forty-five patients were studied, 75 had HCV-induced cirrhosis classified into Child A, B and C and 25 had HCC.
Also a significant difference was found in miR-499 genotypes frequency when compared between HCC and cirrhosis groups as the GG genotype was significantly lower in HCC cases than cirrhosis group (P = 0.006) while the combined miR-499 (AA+AG) genotypes were significantly higher in HCC cases than in cirrhosis group (P = 0.003) [OR (95% CI) = 0.131 (0.028-0.601)].
The pairwise meta-analysis showed that non-HCV (OR = 0.60, 95% CI [0.47-0.78]) had a lower risk of T2DM compared with CHC, while cirrhosis had a significant higher risk (OR = 1.90, 95% CI [1.60-2.26]).
The pairwise meta-analysis showed that non-HCV (OR = 0.60, 95% CI [0.47-0.78]) had a lower risk of T2DM compared with CHC, while cirrhosis had a significant higher risk (OR = 1.90, 95% CI [1.60-2.26]).