Iron Metabolism Disorders

Iron deficiency (sideropenia)[edit | edit source]

Iron deficiency in the body is usually caused by its insufficient absorption from the intestine or chronic blood loss. It can result in sideropenic anemia (hypochromic microcytic anemia), which is one of the most common hematological diseases. However, anemia is usually a late symptom of gradually developing sideropenia. In the blood count, it manifests itself only after the almost complete disappearance of iron. Therefore, it is necessary to detect iron deficiency at an early stage, which is not yet accompanied by anemia.

Based on the determination of the basic parameters of iron metabolism, we distinguish three degrees of deficiency:

Prelate iron deficiency is a designation for a condition in which there is a gradual decrease in reserves, but the supply of iron to the bone marrow erythroblasts is not yet affected. In about half of patients, serum ferritin levels are reduced below 12 μg/l.
With a latent iron deficiency, its reserves are basically depleted. Ferritin is lowered below the lower limit of the norm and is already accompanied at this stage by a decrease in serum iron levels and reduced delivery to bone marrow erythroblasts. The binding capacity for iron increases. A sensitive indicator of latent iron deficiency is a decrease in transferin saturation below 15%. However, anemia is not yet developing.
- With manifest iron deficiency, anemia develops with a decrease in hemoglobin values below the lower limit of the norm. Iron deficiency anemia is characterized by the finding of low serum iron and ferritin, there is an increased concentration of transferrin (binding capacity for iron). In hemolytic anemia or excess iron, on the contrary, serum iron is increased, at the same time the total binding capacity for iron is reduced.

Laboratory findings in iron deficiency
Prelatent iron deficiency	Latent iron deficiency	Manifest iron deficieny
decrease in stored iron – decrease in ferritin	iron deficiency – decrease in ferritin	iron deficiency – decrease in ferritin
	reduction of serum iron	reduction of serum iron
	decrease in transferrin saturation below 15%	transferin decrease below 10%
	increase in total binding capacity for iron	increase in total binding capacity for iron
	increase in sTfR	increase in sTfR
		decrease in hemoglobin concentration – anemia

Excess iron[edit | edit source]

The organism is not equipped with an excretory pathway for iron, and therefore, under certain circumstances, excess iron can accumulate in the tissues. Timely diagnosis can prevent tissue damage from excess iron. Iron overload usually develops very slowly. We distinguish 3 stages:

At the stage of prelate, an excess of iron increases its content in the organs, but without exceeding their storage capacity.
In the period of latent iron overload, the storage capacity of cells is exceeded, but the function of the organs is not yet impaired, the level of ferritin and the level of iron in the serum increases, and the saturation of transferrin rises above 55%.
At the stage of manifest excess iron, some organs are already damaged.

Laboratory findings in excess iron
Prelate excess iron	Latent excess of iron	Manifest excess of iron
increasing iron stores – increasing ferritin	increase in iron reserves – increase in ferritin above 300 μg/l	increase in iron reserves – increase in ferritin (in severe disability above 2000 μg/l)
	increase in serum iron	significant increase in serum iron
	increase in transferrin saturation above 55%	increase in transferrin saturation (in severe disability may exceed 90%)

Hemochromatosis

The accumulation of iron in the tissues is related to a disease that we refer to as hemochromatosis.

Primary hemochromatosis is a hereditary disease caused by increased resorption of iron from the intestine. Excess iron is stored in parenchymatous organs such as the liver, heart, pancreas, adrenal glands. In the affected organs, it acts toxically and disrupts their function by catalyzing chronic reactions leading to the formation of free radicals. The main clinical manifestations are hyperpigmentation of the skin, hepatosplenomegaly and diabetes mellitus.
Secondary haemochromatosis may develop as a result of, for example, repeated transfusions, excessive intake of iron-containing products or haemolytic anaemia. In the biochemical picture we find increasing levels of ferritin and iron in the serum, the saturation of transferrin increases with its simultaneous decrease.

Iron poisoning[edit | edit source]

Accidental ingestion of a larger amount of products is at risk of children (lentil-like tablets). The lethal dose for a child is 600 mg. For an adult, iron intake of 40 mg/kg is toxicologically severe, an intake of 60 mg/kg is fatal

Symptoms include nausea, vomiting (even vomiting with blood), abdominal pain, diarrhea (sometimes bloody). Large fluid losses are the cause of shock, kidney failure and death. If the sick person survives this stage of poisoning, he may fall into unconsciousness, convulsions and liver failure after 12 hours. If it survives this second stage, poisoning can leave permanent consequences (damage to the intestine).

Treatment of acute poisoning

Gastric lavage.
Through a nasogastral probe, administer the chelating agent deferoxamine (5–10 g to 50–100 ml of water).
Consider intravenous administration of desferoxanin to bind absorbed iron. In the urine, a pink-red complex of deferoxamine with iron appears. Treatment should be repeated until the color of urine returns to normal.