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The liver transaminases aspartate transaminase (AST or SGOT) and alanine transaminase (ALT or SGPT) are useful biomarkers of liver injury in a patient with some degree of intact liver function. [2] [3] [4] Most liver diseases cause only mild symptoms initially, but these diseases must be detected early. Hepatic (liver) involvement in some ...
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 ]
Alpha globulins are round transport proteins that have a wide variety of functions. Human AFP is produced in the liver, yolk sac, and GI tract of a fetus and dispersed into plasma. The mother of the fetus also obtains AFP directly from the fetus. [8] AFP was first found in human fetal serum in 1965 and determined to be the fetal version of albumin.
Second-trimester maternal serum screening (AFP screening, triple screen, quad screen, or penta screen) can check levels of alpha fetoprotein, β-hCG, inhibin-A, estriol, and h-hCG (hyperglycosolated hCG) in the woman's serum. The triple test measures serum levels of AFP, estriol, and beta-hCG, with a 70% sensitivity and 5% false-positive rate.
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.)
Inborn errors of metabolism form a large class of genetic diseases involving congenital disorders of enzyme activities. [1] The majority are due to defects of single genes that code for enzymes that facilitate conversion of various substances into others . In most of the disorders, problems arise due to accumulation of substances which are ...
Liver complications have been serious in some patients. Adenomas of the liver can develop in the second decade or later, with a small chance of later malignant transformation to hepatoma or hepatic carcinomas (detectable by alpha-fetoprotein screening). Several children with advanced hepatic complications have improved after liver transplantation.
Unless another specific enzyme is mentioned, CAH in most contexts refers to 21-hydroxylase deficiency, and different mutations related to enzyme impairment have been mapped on protein structures of the enzyme. [5] It is one of the most common autosomal recessive genetic diseases in humans. [6] [7] [8]