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Alpha-fetoprotein (AFP, α-fetoprotein; also sometimes called alpha-1-fetoprotein, alpha-fetoglobulin, or alpha fetal protein) is a protein [5] [6] that in humans is encoded by the AFP gene. [ 7 ] [ 8 ] The AFP gene is located on the q arm of chromosome 4 (4q13.3). [ 9 ]
Acute fatty liver of pregnancy is a rare life-threatening complication of pregnancy that occurs in the third trimester or the immediate period after delivery. [1] It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the fetus, caused by long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. [2]
Liver function tests (LFTs or LFs), also referred to as a hepatic panel or liver panel, are groups of blood tests that provide information about the state of a patient's liver. [1] These tests include prothrombin time (PT/INR), activated partial thromboplastin time (aPTT), albumin , bilirubin (direct and indirect), and others.
Alpha-fetoprotein (AFP), the predominant serum protein of the fetus which gives way to albumin in the adult. AFP is categorized as an oncofetal protein because it is also found in tumors. [1] Fetal hemoglobin, the fetal version of hemoglobin. [2] Fetal Troponin T and Troponin I isoforms. Structure of Fetal Hemoglobin
In oncology, AFP-L3 is an isoform of alpha-fetoprotein (AFP), a substance typically used in the triple test during pregnancy and for screening chronic liver disease patients for hepatocellular carcinoma (HCC).
Most enzymes of glycolysis also participate in gluconeogenesis, as it is mostly the reverse metabolic pathway of glycolysis; a deficiency of these liver enzymes will therefore impact both glycolysis and gluconeogenesis. (Note: gluconeogenesis is taking place only in the liver and not in other cells like e.g. muscle cells.)
The most common method of testing for hepatoblastoma is a blood test checking the alpha-fetoprotein level. Alpha-fetoprotein (AFP) is used as a biomarker to help determine the presence of liver cancer in children. At birth, infants have relatively high levels of AFP, which fall to normal adult levels by the second year of life.
Genetic causes of hepatitis include alpha-1-antitrypsin deficiency, hemochromatosis, and Wilson's disease. [33] In alpha-1-antitrypsin deficiency, a co-dominant mutation in the gene for alpha-1-antitrypsin results in the abnormal accumulation of the mutant AAT protein within liver cells, leading to liver disease. [52]