We reported a case a couple of years ago (Ann Clin Biochem 33:462-464,
1996) of a patient with extensive burns on TPN who had undetectable copper
and caeruloplasmin. The copper and caeruloplasmin both increased with
copper supplementation, although the patient did eventually die.
Caeruloplasmin accounts for about 95% of serum copper (the remainder is
bound to albumin and transcuprein) and will always be low in copper
deficiency. In general in patients on nutritional support the coppper and
caeruloplasmin concentrations will always change in parallel. There is
probably no need to measure both.
The low caeruloplasmin in Wilson's Disease is due to a failure in the
intracellular transport of copper in the hepatocyte, so that in this case
there is tissue accumulation of copper, but systemic copper deficiency.
Barry Sampson
Barry Sampson
Trace Element Laboratory
Clinical Chemistry
Charing Cross Hospital
London W6 8RF
UK
Phone +44-181-846-7080
Fax +44-181-846-7007
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