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
Lead poisoning; low levels cause increased susceptibility. Lead can cause severe damage to the brain and kidneys and, ultimately, death. By mimicking calcium, lead can cross the blood–brain barrier. It degrades the myelin sheaths of neurons, reduces their numbers, interferes with neurotransmission routes, and decreases neuronal growth. In the human body, lead inhibits porphobilinogen synthase and ferrochelatase, preventing both porphobilinogen formation and the incorporation of iron into protoporphyrin IX, the final step in heme synthesis. This causes ineffective heme synthesis and microcytic anemia. Symptoms of lead poisoning include nephropathy, colic-like abdominal pains, and possibly weakness in the fingers, wrists, or ankles.