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Ceruloplasmin (or caeruloplasmin) is a ferroxidase enzyme that in humans is encoded by the CP gene. [ 5 ] [ 6 ] [ 7 ] Ceruloplasmin is the major copper -carrying protein in the blood, and in addition plays a role in iron metabolism .
Ceruloplasmin. Levels of ceruloplasmin are abnormally low (<0.2 g/L) in 80–95% of cases. [5] It can be present at normal levels, though, in people with ongoing inflammation, as it is an acute phase protein. Low ceruloplasmin is also found in Menkes disease and aceruloplasminemia, which are related to, but much rarer than Wilson's disease.
Ceruloplasmin is an acute phase protein synthesized in the liver. It is the carrier of the copper ion. It is the carrier of the copper ion. Its level is increased in infections, rheumatoid arthritis , pregnancy, non-Wilson liver disease and obstructive jaundice.
Aceruloplasminemia has an autosomal recessive pattern of inheritance.. Aceruloplasminemia is caused by a mutation (a five-base pair insertion in exon 7 [3]) in the CP gene, which provides instructions for making a protein called ceruloplasmin, a protein involved in iron transport and processing.
Normal total protein levels are not sufficient to rule out multiple myeloma or other malignant paraproteinemias, but they may also be the cause of moderate-to-marked hyperproteinemia. To determine the reason behind the elevated serum total protein, a serum protein electrophoresis should be carried out.
Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is an acute condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue and regenerative nodules as a result of chronic liver disease.
Iron overload (also known as haemochromatosis or hemochromatosis) is the abnormal and increased accumulation of total iron in the body, leading to organ damage. [1] The primary mechanism of organ damage is oxidative stress, as elevated intracellular iron levels increase free radical formation via the Fenton reaction.
When hemoglobinemia is internally caused, it is a result of recessive genetic defects that cause the red blood cells to lyse, letting the hemoglobin spill out of the cell into the blood plasma. In intravascular hemolysis, hemoglobin is released and binds with haptoglobin. This causes haptoglobin levels to decrease.