Hepatitis In hemochromatosis, excess amounts of iron accumulate in multiple body sites, including the liver, which can lead to cirrhosis. In Wilson's disease, excess amounts of copper accumulate in the liver and brain, causing cirrhosis and dementia. When the liver is involved, alpha-1-antitrypsin deficiency and Wilson's disease tend to present as hepatitis in the neonatal period or in childhood. Hemochromatosis typically presents in adulthood, with the onset of clinical disease usually after age 50. Ischemic hepatitis (also known as shock liver) results from reduced blood flow to the liver as in shock, heart failure, or vascular insufficiency. The condition is most
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.