Insufficiency and increase of ceruloplasmin
Last reviewed: 23.04.2024
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Insufficiency of ceruloplasmin due to a violation of its synthesis in the liver causes Wilson-Konovalov's disease (hepatocerebral degeneration). With a lack of ceruloplasmin, copper ions go into the extravascular space (the copper content in the blood also decreases). They pass through the renal basement membranes into the glomerular filtrate and are excreted in the urine or accumulate in the connective tissue (for example, in the cornea). The accumulation of copper in the central nervous system is of particular importance. Insufficiency of copper ions in the blood (due to a deficiency of ceruloplasmin) leads to an increase in their resorption in the intestine, which further contributes to its accumulation in the body with subsequent exposure to a number of vital processes. Reduction of the concentration of ceruloplasmin in the blood reveals in 97% of patients with Wilson-Konovalov's disease. Reduction of the content of ceruloplasmin in the blood serum is also noted in nephrotic syndrome, gastrointestinal diseases, severe liver damage (in 23% of cases) due to its losses and disruption of synthesis.
Ceruloplasmin belongs to the acute phase protein (half-life of 6 days), so the increase in its concentration in the blood is observed in patients with acute and chronic infectious diseases, cirrhosis, hepatitis, myocardial infarction, systemic diseases, and lymphogranulomatosis. The increase in the level of ceruloplasmin was noted in patients with schizophrenia.
The content of ceruloplasmin in the blood serum for malignant neoplasms of various localizations (lung, breast, cervical, gastrointestinal) increases (on average 1.5-2 times), especially during the spread of the process. Successful chemo- and radiotherapy reduces the content of ceruloplasmin in the blood, up to normalization. With ineffective therapy, as well as with the progression of the disease, the content of ceruloplasmin remains high.
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