COPPER

TRACE ELEMENTS FACT SHEET

Introduction

Atomic mass 63.5. Found in nature as the metal and as sulphide ores. Copper is an essential micronutrient for most plants and animals. Inherited defects of copper metabolism have been described. Menkes’ Disease is characterised by impaired intestinal absorption of copper and likely abnormalities in intracellular copper transport. Wilson’s Disease is marked by a reduction in the rate of caeruloplasmin synthesis and failure of biliary excretion leading to copper accumulation in liver and toxicity. Copper deposition may occur in other tissues (for example Kayser-Fleischer rings in the cornea) and may be associated with neuropathy and nephropathy.

Exposure

Daily requirements for copper are of the order of 2mg. Exposure to copper that leads to a significant level of circulating free copper can produce a haemolytic anaemia and renal damage. Ingestion of caustic copper containing solutions or water can cause nausea, vomiting, diarrhoea, maelena, haematemasis and shock. Longer-term exposure to copper can result in liver damage. PaLMS Trace Elements Service has found no reports of risk of copper exposure in industry.

Absorption

Copper is absorbed actively from the small bowel in a competitive process with other trace metals, but especially with zinc. Once absorbed copper is transported to the liver bound to albumin and amino acids.

Distribution

Copper is incorporated into proteins, especially caeruloplasmin, in the liver. Copper is present in many enzyme systems as an essential co-factor or as a part of a functional enzyme group. Plasma copper is low at birth and increases to adult levels by about six months.

Excretion

Copper is normally primarily excreted to the bile. When the copper burden is high there is significant renal excretion.

Pathology

Copper deficiency is associated with osteoporosis, impaired iron insertion into haemoglobin resulting in a hypochromic, normocytic anaemia, abnormal ECG and GTT, elevated cholesterol and urate and the development of a hypercoagulatable state.

Monitoring

Consistently depressed serum copper is a reliable indicator of deficiency. Serum copper is difficult to interpret in cases of exposure because of the possible influence of an acute phase response. Urine copper is a good indicator of acute and chronic copper accumulation. Liver copper content is the definitive test for the diagnosis of Wilson’s Disease.

    Free copper can be estimated by determining caeruloplasmin and serum copper. Caeruloplasmin (g/L) x 50.4 = Bound Copper (umol/L)

    Free copper = total copper – bound copper.

    Normal free copper concentrations are expected to be in the range 3-5 umol/L.

Treatment

Copper supplementation should resolve the clinical signs of deficiency within weeks to months. Penicillamine chelation is recommended for treatment of Wilson’s Disease. Determining urine copper content monitors efficacy of the chelation. The chelation removes zinc as well as copper so the patients zinc status should be monitored.

Analysis

Copper in the various sample matrices is determined by inductively coupled plasma – mass spectrometry.

For further information please contact Graham Hams, PaLMS Trace Elements on (02) 9926 7682.
Last updated: Nov 98