Increased liver enzymes were used as surrogates of liver steatosis and alanine aminotransferase concentration was the outcome variable for the multivariate analysis.
Univariate analysis demonstrated that the presence of severe fibrosis was independently associated with older age, female sex, overweight, aspartate/alanine aminotransferase ratio, serum ferritin level, fasting glucose and insulin levels, decreased insulin sensitivity, and with histologic features (degree of necroinflammation and steatosis).
Median serum alanine aminotransferase (ALT) and ferritin levels were higher (P < .001), and median transferrin saturation (P = .01) and hepatic iron concentration (HIC) were lower (P = .003) in subjects with steatosis compared with subjects without steatosis.
Variables associated with the steatosis group were: higher serum levels of AST (P<0.04), alanine aminotransferase (P<0.02), gamma-GT (P<0.004), genotype 3a (P<0.03) and severity of histology (staging P<0.05) but at multiple linear regression analysis only genotype 3a and staging were significantly associated with LS.
NQO1 mRNA levels were also positively correlated with aspartate aminotransferase (P = 0.0028) and alanine aminotransferase (P = 0.0219), markers known to be associated with severity of hepatic steatosis.
A detailed comparison between the hypertriglyceridemic FCHL subjects with (n = 25) and without (n = 13) fatty liver revealed that, despite very similar plasma triglyceride levels (3.5 vs 3.2 mmol/L in subjects with and without fatty liver, respectively), the fatty liver subgroup presented with significantly higher body mass index, visceral adipose tissue (ultrasound), insulin, and alanine aminotransferase levels.
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.
Steatosis was found to correlate with the BMI values and alanine aminotransferase (ALT) levels, and ALT levels were associated with hepatitis B virus (HBV)-DNA levels and histology activity index (HAI) scores, stages of fibrosis were associated with the HAI score and HBV-DNA, as determined by the multivariate analysis.
Laboratorially, a multivariate analysis revealed that aspartate aminotransferase (AST) > or =2 x upper limit of normal (ULN), alpha fetoprotein > or =15 microg/L, and presence of grade 2 and 3 steatosis were independently associated with stage 3 and 4 fibrosis, after adjusting for alanine aminotransferase > or =2 x upper limit of normal, AST/alanine aminotransferase ratio > or =1, HCV genotyping, transferrin saturation, and a histology activity index score > or =7.
The slower progression of chronic hepatitis in patients with persistently normal ALT levels could be related, in part, to a lower frequency of steatosis.
Body mass index, alanine aminotransferase, gamma-glutamyl transferase, and triglyceride levels and substitutions of amino acid 70/Q (glutamine) were significantly associated with the presence of steatosis on univariate analysis.
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).
Frequencies of allele PNPLA3 rs738409(G) in individuals with steatosis and normal alanine aminotransferase (ALT) and AST levels were lower than in alcoholics without steatosis and normal ALT/AST (P(combined) = 0.03).
Also, our study revealed a direct correlation, but less intense, with the necro-inflammatory activity (rs=0.39, p=0.03), the steatosis degree (rs=0.428, p=0.01) and the value of alanine aminotransferase (rs=0.4, p=0.03).
By multivariate analysis, ARFI was not associated with alanine aminotransferase (ALT), body mass index, Metavir grade, and liver steatosis, while TE was significantly correlated with the ALT value (P=0.027).
Univariate analyses revealed SVRs to be associated with age, high alanine aminotransferase (ALT) and low γ-glutamyltransferase (γ-GT) serum activities, a low pretreatment γ-GT/ALT ratio, rapid virological response (RVR), and absence of steatosis.
We used data from the National Health and Nutrition Examination Survey III to validate the association between rs738409 (PNPLA3), rs780094 (GCKR), and rs4240624 (PPP1R3B) with HS, with or without increased levels of ALT, among 3 different ancestries.
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.
This allele combination carrier had higher plasma alanine aminotransferase levels (Diff = 15.08 [7.60-22.57] p = 0.001) and an increased frequency of severe steatosis compared to the reference allele combination (OR = 3.88; 95% CI 1.582-9.531; p<0.001).