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Insufficiency and increase in ceruloplasmin
Last reviewed: 06.07.2025
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Deficiency of ceruloplasmin due to impaired synthesis in the liver causes Wilson-Konovalov disease (hepatocerebral degeneration). With ceruloplasmin deficiency, copper ions enter the extravascular space (the copper content in the blood also decreases). They pass through the basal membranes of the kidneys into the glomerular filtrate and are excreted in the urine or accumulate in the connective tissue (for example, in the cornea). Of particular importance is the accumulation of copper in the central nervous system. Deficiency of copper ions in the blood (due to ceruloplasmin deficiency) leads to increased resorption in the intestine, which further contributes to its accumulation in the body with subsequent impact on a number of vital processes. A decrease in the concentration of ceruloplasmin in the blood is detected in 97% of patients with Wilson-Konovalov disease. A decrease in 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 loss and impaired synthesis.
Ceruloplasmin is an acute phase protein (half-life 6 days), so its blood concentration increases in patients with acute and chronic infectious diseases, liver cirrhosis, hepatitis, myocardial infarction, systemic diseases, and lymphogranulomatosis. Increased ceruloplasmin levels have been noted in patients with schizophrenia.
The content of ceruloplasmin in the blood serum in malignant neoplasms of various localizations (lung cancer, breast cancer, cervical cancer, gastrointestinal tract cancer) increases (on average by 1.5-2 times), especially when the process spreads. Successful chemo- and radiation therapy help to reduce the content of ceruloplasmin in the blood, up to normalization. If therapy is ineffective, as well as with disease progression, the content of ceruloplasmin remains high.
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