The liver stiffness value correlated well with the baseline alanine aminotransferase level (r = 0.33; P < .001) and was significantly different among various stages of liver fibrosis (P < .001).
Tanshinol prominently mitigated liver fibrosis and reduced levels of alanine aminotransferase (ALT), aspartate transaminase (AST), hydroxyproline content, and other serum markers of liver fibrosis.
Biochemical assays and histopathological investigations showed that amarogentin delayed the formation of liver fibrosis; decreased alanine aminotransferase, aspartate aminotransferase, malondialdehyde and hydroxyproline levels; and increased albumin, cyclic guanosine monophosphate, glutathione peroxidase, and superoxide dismutase levels.
In addition, concomitant significant liver fibrosis was identified in 60 (5.1%) subjects with NAFLD, and its independent predictors were age [odds ratio (OR) 1.054], ALT level (OR 1.019), BMI (OR 1.217), and diabetes (OR 1.987) (all P < 0.05).
Serum from 38 pregnant/post-partum CHB carriers (median age 32 years, 53% Asian, 8 HBeAg<sup>+</sup> ) was tested for HBV DNA, quantitative HBV surface antigen, ALT and liver fibrosis by transient elastography (TE).
Linear regression analysis revealed that alanine aminotransferase (odds ratio [OR]: 0.03, 95% confidence intervals [CI]: 0.02-0.05, P < 0.001), AST (OR: -0.1, 95% CI: -0.02 to -0.01, P < 0.001), and liver fibrosis (OR: 0.30, 95% CI: 0.01-0.59, P = 0.043) were the independent factors correlated to serum WFA<sup>+</sup>-M2BP level.
This study aimed to evaluate the diagnostic performance of GP model for liver fibrosis and cirrhosis in CHB patients with high HBV DNA and mildly elevated alanine transaminase (ALT) levels.
Severe liver fibrosis was defined, according to guidelines, as a liver stiffness measurement greater than 9.0 kPa in patients with normal level of alanine aminotransferase (ALT) or greater than 12.0 kPa in patients with a level of ALT 1-5-fold the upper limit of normal.
We aimed to evaluate the diagnostic value of serum hepatitis B surface antigen (HBsAg) levels for liver fibrosis in hepatitis B e antigen-positive [HBeAg (+)] chronic hepatitis B (CHB) patients with alanine transaminase (ALT)≤twice upper limit of normal (ULN).
In addition, dapagliflozin decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), hepatic lipid accumulation as determined by H&E and Oil Red O staining, and Coherent Anti-Stokes Raman Scattering (CARS) microscopy, and hepatic fibrosis as determined by picrosirius red (PSR) staining and TPE-SHG microscopy in WD-fed mice.
This may be partially handled by combining LSM with a serum-based formula, which is independent of ALT such as the Forns index and enhanced liver fibrosis test.
Univariate analysis revealed that, compared to patients without advanced liver fibrosis, patients with advanced liver fibrosis (Metavir fibrosis score 3-4) had an older age, a lower platelet count, a higher α-fetoprotein level, a higher alanine aminotransferase level, a higher incidence of diabetes, and a higher frequency of rs8099917 non-TT genotype carriage.Logistic regression analysis revealed that factors significantly associated with advanced liver fibrosis included age (odds ratio [OR]/95% confidence interval [CI]: 1.023/1.009-1.037, P = .001), diabetes (OR/CI: 1.736/1.187-2.539, P = .004), α-fetoprotein (OR/CI: 1.007/1.002-1.012, P = .009), platelet count (OR/CI: 0.991/0.988-0.993, P < .001), and carriage of the rs8099917 non-TT genotype (OR/CI: 0.585/0.400-0.856, P = .006).
Importantly, most of these miRNAs significantly and positively correlated with ALT and aspartate aminotransferase (AST) levels, and liver fibrosis stage (p < 0.05).
In the 12-week arm, significant improvements were observed in biomarkers of liver injury (alanine aminotransferase: -53.7 U/L, P < 0.001; aspartate aminotransferase: -35.9 U/L, P < 0.001) and liver fibrosis (aspartate aminotransferase to platelet ratio index: -0.987, P < 0.001; fibrosis-4 index: -1.165, P < 0.001).
It is suggested that this noninvasive score system can accurately predict hepatic fibrosis and may reduce the need for liver biopsy in HBeAg-positive patients with normal or minimally elevated ALT levels.
We evaluated liver fibrosis in patients with chronic hepatitis B (CHB) and mildly raised alanine transaminase (ALT) activities between 1-2 times the upper limit of normal (ULN) which was near the threshold for initiating treatment.
In vivo, overexpression of Sestrin 2 reduced the ALT and AST levels as well as the α-SMA and Col1A1 protein expression in the CCl4 model of liver fibrosis.
Liver fibrosis was assessed using the fibrosis-4 index (FIB-4) [age (years)× aspartate aminotransferase level (IU/L)/platelet count (10<sup>9</sup>/L)/√alanine aminotransferase (IU/L)].
Interferon-λ3 levels were significantly higher after viral clearance in patients who developed HCC and were associated with a higher potential for hepatocarcinogenesis, such as a higher frequency of non-hypervascular hypointensive nodules (P = 0.046), higher stages of liver fibrosis (P < 0.001), and higher post-treatment levels of Wisteria floribunda agglutinin positive Mac-2 binding protein (P < 0.001) and alanine aminotransferase (P < 0.001).