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In medicine, the presence of elevated transaminases, commonly the transaminases alanine transaminase (ALT) and aspartate transaminase (AST), may be an indicator of liver dysfunction. [ 1 ] [ 2 ] Other terms include transaminasemia , [ 3 ] and elevated liver enzymes (though they are not the only enzymes in the liver).
Gallstones are more common in pregnant women due to elevated hormones and cholesterol levels, which block the bile duct and obstruct bilirubin excretion. [11] Besides, preeclampsia and eclampsia, denoted by high blood pressure, are linked to hyperbilirubinemia through damaging highly perfused organs, particularly liver and kidneys. [12]
Jaundice, also known as icterus, is a yellowish or greenish pigmentation of the skin and sclera due to high bilirubin levels. [3] [6] Jaundice in adults is typically a sign indicating the presence of underlying diseases involving abnormal heme metabolism, liver dysfunction, or biliary-tract obstruction. [7]
But scientific studies found no clear pattern of adverse symptoms related to the elevated levels of unconjugated bilirubin in adults. However, other substances glucuronidized by the affected enzymes in those with Gilbert's syndrome could theoretically, at their toxic levels, cause these symptoms.
Treatment of the condition is specific to the cause of hemolysis, but intense phototherapy and exchange transfusion can be used to help the patient excrete accumulated bilirubin. [11] Complications related to hemolytic jaundice include hyperbilirubinemia and chronic bilirubin encephalopathy, which may be deadly without proper treatment. [12] [13]
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When GGT levels is elevated, the triglyceride level is elevated also. With insulin treatment, the GGT level can reduce. With insulin treatment, the GGT level can reduce. Other causes of elevated GGT are: diabetes mellitus, acute pancreatitis , myocardial infarction, anorexia nervosa , Guillain–Barré syndrome , hyperthyroidism, obesity and ...
Aspartate transaminase (AST) or aspartate aminotransferase, also known as AspAT/ASAT/AAT or (serum) glutamic oxaloacetic transaminase (GOT, SGOT), is a pyridoxal phosphate (PLP)-dependent transaminase enzyme (EC 2.6.1.1) that was first described by Arthur Karmen and colleagues in 1954.