Copper

Disorders



Copper deficiency

Symptoms of deficiency: altered heart rate, hair loss, weakness.

Copper deficiency in infants affect slow growth, pale skin, anemia, diarrhea, lack of pigment in the hair and skin, bulging varicose veins.
 

  • Menkes disease (MNK, also called Menkes syndrome). The symptoms are stiff and brittle hair. This disorder is linked to the X chromosome, which leads to poor absorption of copper from the small intestine. In patients with this disease absorption and the transport of copper in the cells of the mucous membrane are normal. But the transport through the diaphragm of serous mucous cells, ie. third stage of transport is abnormal. When copper is added intravenously in children with the disease organism normally absorbe it. In this way, many severe symptoms of the disease (mental retardation, unstable body temperature, abnormal bone development and susceptibility to infections) may be prevented if you start treatment early enough.


In adults copper deficiency leads to anemia, water retention in the body, weakening the walls of blood vessels, irritability, brittle bones, hair depigmentation, loss of quality.

People who consume a lot of dietary phytate, which binds copper in the intestine, then people who have impoverished diet, people with diarrhea for a long period of time and the people who bring large amounts of zinc, cadmium, fluoride and molybdenum are the highest risk for symptoms of copper deficiency.

Poor absorption of copper may occur in patients with rheumatoid arthritis.

Copper deficiency leads to reduced resistance to infection, since the activity of white blood cells and cellular immune response are reduced. The ratio of zinc and copper can also affect the efficiency of the immune response. Susceptibility to disease is likely to increase when there is a high intake of copper and low intake of zinc.

Overdose
 

  • Wilson's disease. Autosomal, recessive inborn defect of copper fitting into a new synthesized apoceruloplasmin wat is needed to be created ceruloplasmin. It is not known whether this is a genetic defect in the structural gene for ceruloplasmin or defect in the process of installing Cu2+ in ceruloplasmin. In addition, patients with this disease have a reduced ability of the liver to the biliary excretion of copper. Therefore, the body retains more copper. This particularly occurs in the liver, brain and kidneys. Since the patient's plasma ceruloplasmin doesn't contain Cu2+, the concentration of copper in serum is low. In these patients is therefore significantly increased copper excretion in the urine. These patients have no signs of abnormality in the absorption of iron, although we know that ceruloplasmin without copper can not act as ferroxidase. Giving compounds that bind copper can reduce organ damage.


Copper toxicosis is rare, but can occur if the entries are more than 200 mg of copper per day. It can lead to nausea, vomiting, abdominal pain, diarrhea, muscle pain, abnormal mental status, headache and decreased immune response. The lethal dose of copper is about 3.5 g. Unbalanced ratio of copper and zinc may be an important factor in copper poisoning.

In patients with ulcerative colitis the copper in the tissues can be incereased and excess of it may aggravate the disease. High levels of copper can be causative of many heart diseases.

The symptoms of copper poisoning include blue and green diarrhea, saliva, acute hemolysis and some renal function abnormalities.