Furthermore, a comparison of clinical parameters among three groups (normal vs no fatty liver by US but increased CAP vs fatty liver based on US) revealed that metabolic parameters, including blood pressure, BMI, waist circumference, aspartate aminotransferase (AST), ALT, triglycerides, fasting glucose, uric acid, insulin, homeostasis model assessment-estimated insulin resistance and liver stiffness measurements, gradually increased across the three groups (all P < .001).
Transgenic expression of MIR122 in hepatocytes of mice with ethanol-induced liver disease and advanced fibrosis significantly reduced serum levels of alanine aminotransferase (ALT) and liver steatosis and fibrosis, compared with mice given injections of the control vector.
Univariate analysis showed that age, sex, HBV genotypes, and viral load were not significantly associated with ultrasonographic fatty liver, whereas ALT abnormality was significantly related to ultrasonographic fatty liver (OR = 4.54, 95% CI: 2.11-9.75, P < 0.001).
There was no significant difference between two groups regarding serum levels of alanine aminotransferase (ALT), high sensitive C-reactive protein (hs-CRP), Tumor necrosis factor-α (TNF-α), grade of fatty liver in ultrasonography, lipid profiles, and other outcomes.
Except for nonfasting levels of ALT, which were slightly higher in the offspring of long-lived siblings compared to controls, no differences were found between groups in the extent of liver steatosis, as assessed with liver biochemical tests and CT.
HBeAg seropositivity and hepatic steatosis contribute to persistent increases in ALT level in patients with CHB receiving suppressive antiviral treatment.
We measured a number of markers associated with early- and later-stage liver disruption, including liver steatosis, measures of liver cytochrome P4502E1 (CYP2E1) and alcohol dehydrogenase (ADH), alcohol metabolism, expression of cytokine mRNA, accumulation of 4-hydroxynonenal (4-HNE) as an indicator of oxidative stress, and alanine transaminase/aspartate transaminase as a measure of hepatocyte injury.
A multivariate analysis showed that the occurrence of ALT abnormalities at the EOT was significantly associated with pegylated interferon (PEG-IFN) alfa-2a (odds ratio [OR], 2.24; 95% confidence interval [CI], 1.45-3.45; P<0.001), baseline fatty liver (OR, 1.76; 95% CI, 1.16-2.76; P = 0.007), and baseline liver cirrhosis (OR, 2.35; 95% CI, 1.35-4.09; P = 0.002).
Patients with LS had significant higher levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), ALT/AST ratio and ferritin than those without, but LIC values were comparable.
Furthermore, these six SNPs showed significant associations with the severity of fatty liver (all p＜2.0×10<sup>-10</sup> in the discovery set and p＜2.0×10<sup>-6</sup> in the validation set) and NAFLD, with elevated levels of alanine aminotransferase (all p＜2.0×10<sup>-10</sup> in the discovery set and p＜2.0×10<sup>-6</sup> in the validation set).
Saroglitazar also improved alanine aminotransferase levels and fatty liver (evaluated by FibroScan™) in non-alcoholic fatty liver disease patients with diabetic dyslipidemia.
Nine to 16 years postpartum, a clinical examination was performed, with measurement of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyl transferase, from which fatty liver scoring indices were calculated to assess liver fat score, fatty liver index, hepatic steatosis index, and liver fat percentage.
Female sex (p = 0.006), serum triglycerides (TG, p = 0.016), serum alanine aminotransferase (ALT, p = 0.007), and liver steatosis (p = 0.001) associated with the small intestinal length (BPL + AL + CC) at baseline.
We sought to identify common genetic variants contributing to NAFLD, using CT measured fatty liver (FL), and alanine aminotransferase levels (ALT), as a biochemical marker of hepatic inflammation.
We evaluated changes in aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase (γ-GTP), alkaline phosphatase (ALP), and fatty liver index (FLI) at 3 months of treatment; the proportion of patients with abnormal liver function whose liver function normalized after 3 months of treatment; and correlations between changes in ALT levels and efficacy variables/laboratory values.
The multivariate analysis demonstrated statistical significance only in the association of body mass index (odds ratio [OR] = 1.22; 95% CI 1.05-1.41; P = 0.01); fatty liver (OR = 2.32; 95% CI 1.58-9.19; P = 0.02); alanine transaminase (OR = 1.04; 95% CI 1.02-1.09; P = 0.04) and cumulative MTX dosage (OR = 1.03; 95% CI 1.01-1.04; P = 0.001).
In vivo, changes observed in p66+/+ mice after 6-week exposure to ethanol in the drinking water, including elevated serum alanine aminotransferase (ALT), liver swelling and evident liver steatosis, were significantly attenuated in p66-/- mutant mice.