Liver function tests protein synthesized in the liver. It is the carrier of the copper ion. Its levels is increased in infections, rheumatoid arthritis, pregnancy, non Wilson liver disease and obstructive jaundice. In Wilson disease, the ceruloplasmin level is depressed which lead to copper accumulation in body tissues. AFP is significantly expressed in foetal liver. However, the mechanism that led to the suppression of AFP synthesis in adults is not fully known. Exposure of the liver to cancer-causing agents and arrest of liver maturation in childhood can lead to the rise in AFP. AFP can reach until 400–500 μg/L in hepatocellular carcinoma. AFP
Copper in health childhood cirrhosis) are associated with the improper utilization of copper in the body. All of these diseases involve mutations of genes containing the genetic codes for the production of specific proteins involved in the absorption and distribution of copper. When these proteins are dysfunctional, copper either builds up in the liver or the body fails to absorb copper. These diseases are inherited and cannot be acquired. Adjusting copper levels in the diet or drinking water will not cure these conditions (although therapies are available to manage symptoms of genetic copper excess disease). The study of genetic copper metabolism diseases and