The main conclusions and recommendations are as follows: (i) Albumin measurement forms a limited, but useful part of the investigation of liver disease; a normal serum albumin concentration makes the diagnosis of cirrhosis unlikely, while a low level in viral hepatitis suggests either severe hepatocellular damage or other complications.
Albumin mRNA was not found in peripheral blood from normal humans (0 of 6), from patients with liver cirrhosis (0 of 10), from other tumors metastatic to liver (0 of 10), or during liver transplant surgery for cirrhosis (0 of 10).
The following were associated with a significantly higher rate of liver complications: age; birth in Asia, Europe, Mediterranean region, or Egypt; transmission by blood transfusion or sporadic cases; HCV genotypes 1b and 4 (compared with 1/1a); fibrosis stage 3 or 4 (cirrhosis); serum albumin; bilirubin; prothrombin time; and alpha-fetoprotein.
To explore the expression of albumin (ALB), insulin-like growth factor (IGF)-1, and insulin-like growth factor binding protein (IGFBP)-3 in tumor tissues and adjacent non-tumor tissues of hepatocellular carcinoma (HCC) patients with cirrhosis.
Patients who had compensated liver cirrhosis due to hepatitis C virus with baseline serum albumin levels between 3.6 and 4.5 g/dl were assigned to the TK-98 group, which was treated with BCAA granules (TK-98) for 168 weeks, or to a control group (no treatment).
Immunopositive staining for albumin (Alb) and cytokeratin 18 (CK18), and reverse transcription-polymerase chain reaction (RT-PCR) for Alb, alpha fetoprotein (AFP), CK18, cytokeratin 19 (CK19) ascertained that MSC-HGF-CNP treatment could be an effective combination to repopulate liver parenchymal cells in the liver cirrhosis.
This study aimed to assess IMA and IMAR as a liver function test and to investigate whether albumin infusion changes IMAR in patients with liver cirrhosis.
When comparing the 124 late-onset HCC cases with 199 age-matched HBV controls, gender (odds ratio (OR)=4.4; P<0.05) and cirrhosis (OR=9.6; P<0.05) or surrogate labs (i.e., platelets, international normalized ratio, total bilirubin, albumin) were found to be associated with HCC development.
Multivariate analysis showed that, in addition to gender, age, ALT, albumin and HBV DNA, PD1 +8669 genotype AA was associated with cirrhosis compared with patients without cirrhosis (OR, 2.410; P=0.001).
Among cirrhotic patients, males with the TIMP-1 372 T allele developed cirrhosis at a younger age, and patients who were homozygous for the higher-transcription TIMP-2 -418 G allele had significantly lower serum albumin concentrations.
1078 patients with bridging fibrosis (n=552) or cirrhosis (n=526) diagnosed by either liver biopsy or non-invasive markers, with compensated bone marrow (neutrophils >1500/mm(3), Hb >12/13 g/dl) and liver function (Albumin >3.3g/dl, Platelets >90,000/ml) received TVR PR for 12 weeks, followed by a PR tail according to label.
King's score, Göteborg university cirrhosis index, APRI (the AST/platelet count ratio index), and Fibrosis-4 (FIB-4) had the highest predictive accuracy for cirrhosis, with the APRI (cutoff, 2) and FIB-4 (cutoff, 3.25) showing the highest diagnostic accuracy.We derived the study score 8.5 - 0.2(albumin, g/dL) +0.01(AST, IU/L) -0.02(platelet count, 10(9)/L), which at a cutoff of >4.7 had a predictive accuracy of 0.868 (95% confidence interval, 0.833-0.904) for cirrhosis.
We performed a comprehensive search of large databases and abstract books of conference proceedings up to March 15th 2016 for randomized controlled trials, testing the infusion of human albumin against alternatives (vs no treatment, vs plasma expanders; vs vasoconstrictors) in HCC-free patients suffering from cirrhosis.
Univariate and multivariate logistic regression analysis revealed significant association of low albumin (<3.5), cirrhosis and Fib-4 score (>3.25) with treatment failure.
Our study aimed to investigate the applicability of albumin-bilirubin (ALBI), Child-Pugh and model for end-stage liver disease (MELD) scores to the long-term prognosis prediction of HBV-related cirrhosis.
Cirrhosis (P = 0.001), albumin level ≤40 g/L (P = 0.011) and platelet count ≤153 × 10<sup>9</sup> (P < 0.001) had a superimposition effect on anti-gp210 antibody as a risk factor.
Significant variables (P < 0.05) on univariate analysis included serum total bilirubin (TB) and albumin at 3 months post-HPE, bridging fibrosis or cirrhosis on initial liver biopsy, ascites of <3 months post-HPE, type 3 BA anatomy, age at HPE of >45 days, change in length z scores within 3 months of HPE, and center.
We retrospectively reviewed the patients' medical records and assessed their history, etiology of liver cirrhosis, disease conditions, treatment options for GFV bleeding, medications administered before and after onset of GFV bleeding, blood test results (hemoglobin, albumin, and bilirubin concentrations), and imaging results (including computed tomography and abdominal ultrasonography).
The aORs (95% CIs) for high versus undetectable serum AFB<sub>1</sub> -albumin adduct levels were 2.45 (1.51-3.98) for cirrhosis (p = 0.0003), 5.47 (2.20-13.63) for cirrhotic HCC (p = 0.0003), and 5.39 (1.11-26.18) for non-cirrhotic (p = 0.0368) HCC, respectively.