Medical Diagnosis Exams

Ceruloplasmin contains 8 copper atoms per molecule and is an acute phase protein and transport protein. Incorporation of copper into the structure occurs during the synthesis of ceruloplasmin in the hepatocytes. Decreased concentrations occur during recessive autosomal hepatolenticular degeneration (Wilson’s disease).

This results in pathological deposits of copper in the liver (with accompanying development of cirrhosis), brain (with neurological symptoms), cornea (Kayser‑Fleischer ring), and kidneys (hematuria, proteinuria, aminoaciduria).

The rare Menke’s syndrome involves a genetically caused copper absorption disorder with concomitant lowering of the ceruloplasmin level. Protein loss syndromes and liver cell failures are the most important causes of acquired ceruloplasmin depressions. As ceruloplasmin is a sensitive reactant to the acute phase, increases occur during acute and chronic inflammatory processes.