COPPER, whole blood and red blood cell
B -Cu ATK 8010
E -Cu ATK 8013
Copper is a vital micronutrient for humans, serving as a necessary co-factor for enzymes that contain copper and are present in the body. The liver and brain have the highest concentrations of copper. These copper-based enzymes play a crucial role in essential biochemical reactions and metabolic processes within the body. An example of such an enzyme is superoxide dismutase (Cu-Zn-SOD), which contains both copper and zinc; it functions to eliminate harmful oxygen radicals produced during the mitochondrial electron transport chain. Moreover, copper contributes to iron metabolism through copper-containing iron oxidases, aiding in the conversion of iron to its ferric state. This transition is necessary for iron to attach to its transporter protein, transferrin.
Copper’s significance extends to the immune system’s proper functioning. Insufficient dietary copper intake leads to a weakened immune response that persists even after prolonged periods of increased copper consumption. Copper also plays a pivotal role in the synthesis of connective tissue proteins like collagen and elastin. This involvement is vital for bone health, blood vessel wall elasticity, and maintaining healthy lung structures. Furthermore, copper’s contribution is crucial in the metabolism of neurotransmitters like noradrenaline, dopamine, and serotonin.
Copper travels through the bloodstream with the assistance of ceruloplasmin, with about 95% of the body’s copper residing in this protein. During acute phases, such as inflammation, serum copper levels and ceruloplasmin concentrations rise, posing challenges to the accuracy of plasma or serum measurements. A more accurate gauge of copper levels in the body is obtained through copper measurement in whole blood or red blood cells. The majority of copper is excreted through feces, with only a small percentage (1-4%) being eliminated through urine.
Assessment of intracellular copper levels in the body.
B -Cu 5 mL of lithium-heparin blood
E -Cu 10 mL of lithium-heparin blood (3 mL of red blood cell mass, see instructions below)
Mix the sample well. The tube must not contain any clots. Take trace element samples last in order to cleanse the sampling needle of possible trace element residues. If this is the only test requisition, first take one extra tube.
No fasting is needed. No trace element supplements 12 hours before sampling. The result is normalised to whole blood hematocrit (Hct) value (B -PVK, engl. Complete Blood Count, B -CBC). The client should determine the hematocrit prior to shipping the sample and write the result on the test requisition.
The Hct is essential for interpretation of results. Without a measured Hct value, standard Hct is used.
E -Cu sample treatment
➢ centrifuge the whole blood tube
➢ after centrifugation, remove the plasma and white blood cells off the top of the red blood cells
➢ add a 0.9% NaCl solution volume equivalent to the plasma into the tube
➢ mix the sample by turning
➢ remove the wash solution (NaCl) off the top of the red blood cells
➢ mix well before shipping
Storage and delivery
Ship at room temperature on sampling day (shipping Mon-Thu). Store frozen over the weekend, ship at room temperature.
ICP-MS, Accredited method (B -Cu).
Reference ranges, calculated
women 11.9 – 18.5 mmol/L (Hct 0.39)
men 11.9 – 18.5 mmol/L (Hct 0.42)
The Hct value affects the reference ranges. The same sample can be used to measure K, Mg, Mn, P, Se and Zn.
Reference ranges, calculated
women 8.6 – 13.1 mmol/L (Hct 0.39)
men 8.9 – 13.2 mmol/L (Hct 0.42)
The reference areas have been calculated from the Mineral Laboratory Milan research database. Outliers that significantly differed from the reference distribution were excluded. A mid-percentile range of 90% has been established based on the refined dataset. The most recent update was in 2017.
Interpretation of results
Dietary sources of copper encompass meat, offal, grain products, seeds, fruits, berries, and cocoa.
Due to the abundant presence of copper in a regular diet, experiencing a copper deficiency is improbable. However, various health issues can disturb the equilibrium of copper in the body. An excess intake of zinc from either food sources or dietary supplements can induce a copper deficiency. This is attributed to the competition between zinc and copper for transport and binding to metallothionein, as well as for absorption from the intestines.
Indications and manifestations of copper deficiency encompass anemia, diminished neutrophil count (neutropenia), osteoporosis, paleness, and loss of hair pigmentation. Among children suffering from copper deficiency due to malnutrition or other ailments, there can be occurrences of blood vessel aneurysms, central nervous system disorders, growth impediments, reduced muscle tone and muscle weakness, as well as lowered body temperature (hypothermia).
Acute copper toxicity symptoms entail abdominal discomfort, vomiting, and diarrhea. In more severe instances, excessive copper levels can lead to heart and kidney failure, liver impairment, cerebral disease or dysfunction, and even mortality.
Wilson’s disease, a rare hereditary disorder characterized by copper accumulation, often presents with low plasma copper levels while whole blood copper levels remain within normal limits. Plasma ceruloplasmin, a copper-binding protein, is deficient, while 24-hour urine copper levels are exceedingly high. Clinically, copper deposits manifest as brown Kayser-Fleischer rings around the cornea. The liver primarily accumulates copper, as its expulsion into the intestines is obstructed. The diagnosis is typically confirmed through a liver biopsy.
The measurement of both zinc and copper bears significant importance in the prevention and treatment of ailments stemming from deficiencies or excesses of these metals. A balanced intake and absorption of zinc and copper are vital contributors to the body’s typical metabolism and overall well-being.
Last update 8.8.2023