IRON, whole blood
fB-Fe KL 3748
Iron stands as a crucial micronutrient for humans, serving primarily to ensure a steady supply of oxygen within the body. The majority of iron’s functions within the body are associated with various components like red blood cell hemoglobin, liver hemosiderin, muscle myoglobin, and enzymes containing iron. In the bloodstream, iron moves in conjunction with its carrier protein called transferrin. In the liver, iron is stored within ferritin, which acts as the body’s primary iron reservoir. The iron found in food is absorbed from the small intestine in its ferrous form (Fe2+). To bind with the transport protein, the ferrous form must undergo oxidation to become the ferric form (Fe3+), a process facilitated by a copper enzyme and the copper transport protein ceruloplasmin. Iron linked to transferrin is transported to target cells through an endocytosis process mediated by the transferrin receptor.
Control over the body’s iron balance is governed by hepcidin, a key peptide hormone synthesized in the liver. This hormone plays a pivotal role in regulating iron homeostasis. Another player in the regulation of iron balance is lactoferrin, a protein that has a special affinity for iron and significantly influences the immune defenses of the intestines.
The majority of iron (around 70-90 %) is directed towards the bone marrow, where it is utilized for the synthesis of hemoglobin within red blood cells. Hemoglobin, as well as muscle myoglobin, have crucial roles in transporting oxygen throughout the body. Hemoglobin carries oxygen from the lungs to the body’s tissues, while myoglobin is essential in the storage, transport, and release of oxygen during muscle contractions. Additionally, iron is engaged in the transportation of electrons and contributes to the creation of energy-rich ATP within mitochondria, thanks to its involvement in cytochrome enzymes. Acting as a component of peroxidase enzymes, iron serves as a protective agent against the oxidative impact of hydrogen peroxide, functioning as an antioxidant as well.
Determining the body’s iron concentrations.
5 mL of lithium or sodium heparin blood. 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.
Fast and do not take any trace element supplements 12 hours before sampling.
Storage and delivery
Ship at room temperature on sampling day (shipping Mon-Thu). Store frozen over the weekend, ship at room temperature.
Reference ranges, calculated
6.2 – 10.4 mmol/L
The same sample can be used to measure Cu, K, Mg, Mn, Se, P and Zn.
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
The human body contains approximately 4-5 grams of iron in males and 2-3 grams in females. The recommended daily intake of iron varies, with men requiring around 7 milligrams, women of childbearing age needing 10 milligrams, and postmenopausal women requiring 6 milligrams.
Iron deficiency anemia ranks as the most widespread micronutrient deficiency globally. When iron levels drop mildly, the body attempts to sustain oxygen delivery to tissues by increasing heart rate. Anemia develops gradually and symptoms become evident only when hemoglobin levels fall below 80 g/L. Signs of anemia encompass paleness, fatigue, breathlessness, and an elevated heart rate. Immune defenses weaken, and reduced thyroid hormone production can compromise body temperature regulation. Iron is integral to the enzyme that oversees thyroid hormone synthesis, and iron deficiency hinders the binding of the active thyroid hormone, T3, to its cell surface receptor, limiting its effects. Furthermore, iron deficiency can enhance the absorption of other divalent metal ions, potentially leading to toxicity.
Iron deficiency may arise due to inadequate dietary iron intake, impaired iron absorption, increased iron needs (e.g., due to aging or medication effects like acid blockers), intestinal inflammation, latent celiac disease, or excessive iron loss. Excessive loss might be triggered by heavy menstrual periods, intestinal ailments, parasite-induced intestinal bleeding, or certain medications like anti-inflammatories. During early pregnancy, iron deficiency anemia has been associated with preterm birth, low birth weight, and fetal mortality.
When the body’s iron regulation mechanism malfunctions, excessive iron can accumulate, even from an excessive intake of iron-rich foods. Prolonged overuse of iron supplements, genetic mutations, and chronic liver disease can lead to iron buildup. In chronic excessive consumption, iron becomes stored in macrophages, bound to hemosiderin. This condition is known as hemosiderosis, unless tissue damage occurs. Hereditary hemochromatosis, a genetic disorder, results in excessive iron accumulation, damaging the liver and potentially progressing to cirrhosis and liver cancer if untreated. Iron buildup in the pancreas disrupts insulin production, leading to diabetes. Additionally, excessive iron accumulation can contribute to cardiomyopathy, kidney impairment, joint issues, and skin discoloration.
Last update 10.8.2023