Clinical use
Raised Urinary Copper can be indicative of Wilson’s disease in adults.
Background
Copper is now well established as an essential trace element. The major circulating form, caeruloplasmin, synthesised in the liver. It is an acute phase reactant and can increase greatly in response to infection, injury, chronic inflammatory conditions or steroid hormones (pregnancy, certain contraceptive pills and oestrogen therapy).Excess copper is excreted in the bile, only small amounts being found in urine, unless renal damage is present, or substances which bind copper are excreted. Copper deficiency presents as a microcytic hypochromic anaemia with marked neutropenia, which is resistant to iron therapy. Wilson’s disease is an autosomal recessive disorder, the frequency being of the order of 1 in 100,000 live births. Copper cannot be excreted via the bile, or incorporated into caeruloplasmin, and consequently accumulates within the liver.
Reference ranges
0 – 0.9 umol/ 24h
Patient preparation
For information and instructions on to collect the sample, please refer to the instructions resource page.
Be advised
You should only use information or follow instructions contained in this patient leaflet if advised to do so directly by staff involved in your care.
Specimen requirements
24hr urine collection bottle with container for collecting sample.
Turnaround time
1 week
Additional Information
For patients on chelation therapy (penicillamine or trientine) treatment should be omitted for 48 h prior to (and throughout) 24h collection. In well de-coppered patients target urine Cu is less than or = 0.6 umol/day but may be > 0.6 in patients with proteinuria.
Location
Department of Clinical Chemistry, Northern General Hospital, S5 7AU