Transport of proteases across neonatal intestine and development of liver disease in infants with alpha-1 antitrypsin deficiency.
The transport of macromolecules from the intestinal lumen into the systemic circulation is considerably greater in neonatal than in adult animals. Transport of both immunoglobin and non-immunoglobulin proteins is enhanced. It is postulated that luminal enzymes are also transported into the systemic circulation of the neonate and reach the liver. In the absence of protease inhibitors, such as occurs in alpha 1-antitrypsin (alpha 1-AT) deficiency, these intestinal enzymes may cause inflammation and, eventually, fibrosis of the liver. If this hypothesis is valid, treatment with trypsin inhibitors and elemental diets until the excessive macromolecular transport across the intestine ceases may help to prevent the liver disease associated with (alpha 1-AT) deficiency.
D001692:Biological Transport; D006801:Humans; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000188:drug therapy / Q000517:prevention & control*; D007422:Intestines / Q000201:enzymology*; D008099:Liver / Q000201:enzymology; D008103:Liver Cirrhosis / Q000517:prevention & control*; D046911:Macromolecular Substances / Q000378:metabolism; D008895:Milk, Human / Q000201:enzymology; D008954:Models, Biological; D010447:Peptide Hydrolases / Q000378:metabolism*; D014361:Trypsin Inhibitors / Q000627:therapeutic use*; D019896:alpha 1-Antitrypsin Deficiency
D046911:Macromolecular Substances; D014361:Trypsin Inhibitors; D010447:Peptide Hydrolases