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GGT is also elevated in 30% of the hepatitis C patients. GGT can increase by 10 times in alcoholism. GGT can increase by 2 to 3 times in 50% of the patients with non-alcoholic liver disease. When GGT levels is elevated, the triglyceride level is elevated also. With insulin treatment, the GGT level can reduce.
Muscle sources of the enzymes, such as intense exercise, are unrelated to liver function and can markedly increase AST and ALT. [5] Cirrhosis of the liver or fulminant liver failure secondary to hepatitis commonly reach values for both ALT and AST in the >1000 U/L range; however, many people with liver disease have normal transaminases.
The proportion of AST to ALT in hepatocytes is about 2.5:1, but because AST is removed from serum by the liver sinusoidal cells twice as quickly (serum half-life t 1/2 = 18 hr) compared to ALT (t 1/2 = 36 hr), so the resulting serum levels of AST and ALT are about equal in healthy individuals, resulting in a normal AST/ALT ratio around 1.
Patients with liver cirrhosis develop liver cancer at a rate of 1.5% per year. [11] In total, 70% of those with alcoholic hepatitis will go on to develop alcoholic liver cirrhosis in their lifetimes. [10] Infection risk is elevated in patients with alcoholic hepatitis (12–26%).
Alanine transaminase (ALT), also known as alanine aminotransferase (ALT or ALAT), formerly serum glutamate-pyruvate transaminase (GPT) or serum glutamic-pyruvic transaminase (SGPT), is a transaminase enzyme (EC 2.6.1.2) that was first characterized in the mid-1950s by Arthur Karmen and colleagues. [1]
Elevated levels of CDT suggest recent heavy alcohol consumption, especially if other liver-associated enzymes (such as GGT) are elevated. Although recent heavy alcohol use is most commonly associated with elevated CDT, certain rare liver disorders can also increase levels of CDT.
According to NICE guidelines, statins can continue unless liver enzyme levels double within three months of starting statins. [66] Treatment with pentoxifylline is not recommended. [14] Omega-3 fatty acids may reduce liver fat and improve blood lipid profile but do not seem to improve liver histology (fibrosis, cirrhosis, cancer). [14]
Despite cessation of alcohol use, only 10% will have normalization of histology and serum liver enzyme levels. [26] As previously noted, the MDF has been used to predict short-term mortality (i.e., MDF ≥ 32 associated with spontaneous survival of 50–65% without corticosteroid therapy, and MDF < 32 associated with spontaneous survival of 90%).