Table 1.
Clinical and Demographic Characteristics of Patients.
Figure 1.
Random forest analysis of the thirty most important metabolites distinguishing patients with severe acute AAH from stable, alcoholic cirrhotic controls.
Figure 2.
Principal component analysis (PCA) of metabolomics data reveals clustering of data into separate cohorts.
Control: alcoholic cirrhosis; hepatitis: severe AAH.
Figure 3.
Global network analysis of relative measured metabolites in patients with alcoholic cirrhosis and severe AAH.
Red nodes depict metabolites that are increased in severe AAH when compared to alcoholic cirrhosis; yellow nodes depict metabolites that are decreased in severe AAH when compared to alcoholic cirrhosis.
Figure 4.
Schematic representations of altered triglyceride hydrolysis and mitochondrial fatty acid beta-oxidation in severe AAH.
(A) Triglyceride hydrolysis. (B). Mitochondrial fatty acid beta-oxidation.
Figure 5.
Schematic representations of altered fatty acid omega-oxidation and lysolipid and phospholipid turnover in severe AAH.
(A) Fatty acid omega-oxidation. (B) Lysolipid and phospholipid turnover.
Figure 6.
Alterations in serum bile acid levels in patients with severe acute alcoholic hepatitis (hepatitis) and stable alcoholic cirrhosis (control).
(A) Secondary bile acids. (B) Sulfated bile acids. (C) Products of gut microbial bile acid metabolism. (D) Schematic representation of altered bile acid turnover in severe AAH. * p<0.05, ** p<0.01, *** p<0.001.
Figure 7.
Alterations in serum levels of metabolites derived from intestinal microbial benzoate metabolism in patients with severe acute alcoholic hepatitis (hepatitis) and stable alcoholic cirrhosis (control).
* p<0.05, ** p<0.01, *** p<0.001.
Figure 8.
Schematic representations of altered serum metabolites involved in glucose utilization and TCA cycle activity in severe AAH.
(A) Glucose utilization pathways. (B) TCA cycle.
Table 2.
Serum levels of protein degradation products.
Figure 9.
Alterations in inflammation-associated metabolites in AAH.
(A) Serum levels of tryptophan metabolites in patients with severe acute alcoholic hepatitis (hepatitis) and stable alcoholic cirrhosis (control). (B) Schematic representation of altered indoleamine 2,3-dioxygenase activity in severe AAH. (C) Serum levels of lipid-derived inflammatory mediators in patients with severe acute alcoholic hepatitis (hepatitis) and stable alcoholic cirrhosis (control). * p<0.05, ** p<0.01, *** p<0.001. IDO, indoleamine 2,3-dioxygenase; TNF-α, tumor necrosis factor α; IFN-γ, interferon-γ.
Table 3.
Serum levels of significantly altered metabolites between AAH survivors and nonsurvivors.
Table 4.
Metabolic predictors of 180-day survival in severe AAH by logistic regression analysis.