Decreased concentrations of caeruloplasmin occur due to both primary (genetic) and secondary deficiencies. Primary deficiency due to a deletion of the caeruloplasmin gene has been reported. Secondary deficiencies where there is insufficient incorporation of copper into the caeruloplasmin molecule are significantly more common. These include the recessive autosomal hepatolenticular degeneration associated with Wilsons disease. As caeruloplasmin is a sensitive reactant to the acute phase, increases occur during acute and chronic inflammatory processes (peaking 4-20 days post acute insult).
Intralipid causes artificially high caeruloplasmin results
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