Etiology	Laboratory tests and results
Alcoholic liver disease	AST:ALT ratio > 2*
	Elevated GGT
α1-Antitrypsin deficiency	Decreased serum α1-antitrypsin
	Genetic screening recommended in equivocal cases
Autoimmune hepatitis (type 1)	Positive ANA and/or ASMA in high titer
Chronic hepatitis B	Positive HBsAg and HBeAg qualitative assays
	Once HBeAg is negative and HBeAb is positive, HBsAg should be monitored periodically to determine viral clearance.
	Hepatitis B virus DNA quantification used to document viral clearance
	Elevated AST and/or ALT*
Chronic hepatitis C	Positive hepatitis C virus antibody qualitative assay
	HCV RNA quantification used to document viral clearance
	HCV viral genotype to determine potential response to antiretroviral therapy
	Elevated AST and/or ALT*
Hepatocellular carcinoma	Elevated alpha fetoprotein, AST, and/or ALT*
	Elevated ALP with obstruction or cholestasis
Hereditary hemochromatosis	Elevated fasting transferrin saturation, unsaturated iron-binding capacity, or ferritin. A transferrin saturation ≥45 percent or an unsaturated iron-binding capacity 155 mcg per dL (27.7 μmol per L) should be followed by analysis for HFE (hemochromatosis) gene mutations.
Nonalcoholic fatty liver disease	Elevated AST and/or ALT*
	Ultrasonography or biopsy necessary to establish diagnosis.
Primary biliary cirrhosis and primary sclerosing cholangitis	Diagnosis made via contrast cholangiography, can be supported clinically by positive antimitochondrial antibody (primary biliary cirrhosis) or antineutrophil cytoplasmic antibody (primary sclerosing cholangitis) in high titers.
	Elevated AST, ALT, and ALP common
Wilson’s disease	Serum ceruloplasmin < 20 mg per dL (200 mg per L) (normal: 20 to 60 mg per dL [200 to 600 mg per L]), or low serum copper level (normal: 80 to 160 mcg per dL [12.6 to 25.1 μmol per L])
	Basal 24-hour urinary copper excretion > 100 mcg (1.57 μmol) (normal: 10 to 80 mcg [0.16 to 1.26 μmol])
	Genetic screening recommended in equivocal cases, but must be able to detect multiple mutations in Wilson’s disease gene.