Iron deficiency anemia is a syndrome caused by iron deficiency and leading to a violation of hemoglobinopoiesis and tissue hypoxia. Clinical manifestations are represented by general weakness, drowsiness, decreased mental performance and physical endurance, tinnitus, dizziness, fainting, shortness of breath during exercise, palpitation, pallor. Hypochromic anemia is confirmed by laboratory data: a study of clinical blood analysis, serum iron, TIBC and ferritin. Therapy includes a therapeutic diet, iron supplementation, and in some cases, transfusion of erythrocyte mass.
ICD 10
D50 Iron deficiency anemia
Meaning
Iron deficiency (microcytic, hypochromic) anemia is anemia caused by a lack of iron necessary for the normal synthesis of hemoglobin. Its prevalence in the population depends on gender, age and climatogeographic factors. According to generalized data, hypochromic anemia affects about 50% of young children, 15% of women of reproductive age and about 2% of men. Latent tissue iron deficiency is detected in almost every third inhabitant of the planet. Microcytic anemia accounts for 80-90% of all anemia in hematology. Since iron deficiency can develop in a variety of pathological conditions, this problem is relevant for many clinical disciplines: pediatrics, gynecology, gastroenterology, etc.
Causes
About 1 mg of iron is lost daily with sweat, feces, urine, and skin cells, and about the same amount (2-2.5 mg) enters the body with food. An imbalance between the body’s needs for iron and its intake from the outside or losses contributes to the development of iron deficiency anemia. Iron deficiency can occur both under physiological conditions and as a result of a number of pathological conditions and be caused by both endogenous mechanisms and external influences:
Blood loss
Anemia is most often caused by chronic blood loss: copious menstruation, dysfunctional uterine bleeding; gastrointestinal bleeding from erosions of the gastric and intestinal mucosa, gastroduodenal ulcers, hemorrhoids, anal fissures, etc. Hidden, but regular blood loss is noted in helminthiasis, hemosiderosis of the lungs, exudative diathesis in children, etc.
A special group consists of persons with blood diseases – hemorrhagic diathesis (hemophilia, Willebrand’s disease), hemoglobinuria. It is possible to develop posthemorrhagic anemia caused by simultaneous, but massive bleeding during injuries and operations. Hypochromic anemia can occur due to iatrogenic causes – in donors who often donate blood; patients with CRF who are on hemodialysis.
Violation of the intake, absorption and transport of iron
Factors of the alimentary order include anorexia, vegetarianism and following diets with a restriction of meat products, poor nutrition; in children – artificial feeding, late introduction of complementary foods. A decrease in iron absorption is characteristic of intestinal infections, hypoacid gastritis, chronic enteritis, malabsorption syndrome, conditions after resection of the stomach or small intestine, gastrectomy. Much less often, iron deficiency anemia develops due to impaired transport of iron from the depot with insufficient protein-synthetic liver function – hypotransferrinemia and hypoproteinemia (hepatitis, cirrhosis of the liver).
Increased iron consumption
The daily need for a trace element depends on gender and age. The need for iron is highest in premature infants, young children and adolescents (due to high rates of development and growth), women of the reproductive period (due to monthly menstrual losses), pregnant women (due to the formation and growth of the fetus), nursing mothers (due to the consumption of milk). It is these categories that are most vulnerable to the development of iron deficiency anemia. In addition, an increase in the need and consumption of iron in the body is observed in infectious and tumor diseases.
Pathogenesis
By its role in ensuring the normal functioning of all biological systems, iron is the most important element. Oxygen supply to cells, the course of redox processes, antioxidant protection, the functioning of the immune and nervous systems, etc. depend on the level of iron. On average, the iron content in the body is at the level of 3-4 g. More than 60% of iron (> 2 g) is part of hemoglobin, 9% is part of myoglobin, 1% is part of enzymes (heme and non-heme). The rest of the iron in the form of ferritin and hemosiderin is in the tissue depot – mainly in the liver, muscles, bone marrow, spleen, kidneys, lungs, heart. Approximately 30 mg of iron continuously circulates in plasma, being partially bound by the main iron–binding plasma protein – transferrin.
With the development of a negative iron balance, the reserves of the trace element contained in tissue depots are mobilized and consumed. At first, this is enough to maintain an adequate level of Hb, Ht, and serum iron. As the tissue reserves are depleted, the erythroid activity of the bone marrow compensatorily increases. With complete depletion of endogenous tissue iron, its concentration begins to decrease in the blood, the morphology of erythrocytes is disturbed, the synthesis of heme in hemoglobin and iron-containing enzymes decreases. The oxygen transport function of the blood suffers, which is accompanied by tissue hypoxia and dystrophic processes in internal organs (atrophic gastritis, myocardiodystrophy, etc.).
Classification
Iron deficiency anemia does not occur immediately. At first, prelatent iron deficiency develops, characterized by depletion of only deposited iron reserves while preserving the transport and hemoglobin pool. At the stage of latent deficiency, there is a decrease in the transport iron contained in the blood plasma. Hypochromic anemia itself develops with a decrease in all levels of metabolic iron reserves – deposited, transport and erythrocyte. In accordance with the etiology, anemia is distinguished: posthemorrhagic, alimentary, associated with increased consumption, initial deficiency, insufficient resorption and impaired iron transport. According to the severity of iron deficiency anemia are divided into:
- Mild (Hb 120-90 g / l). They occur without clinical manifestations or with their minimal severity.
- Medium-heavy (Hb 90-70 g/l). They are accompanied by circulatory hypoxic, sideropenic, hematological syndromes of moderate severity.
- Heavy (Hb <70 g/l). All manifestations are of extreme severity.
Symptoms
Circulatory hypoxic syndrome is caused by a violation of hemoglobin synthesis, oxygen transport and the development of hypoxia in tissues. This is expressed in a feeling of constant weakness, increased fatigue, drowsiness. Patients are haunted by tinnitus, flashing “flies” in front of their eyes, dizziness, turning into fainting. Typical complaints are palpitations, shortness of breath that occurs during physical exertion, increased sensitivity to low temperatures. Circulatory-hypoxic disorders can aggravate the course of concomitant coronary heart disease, chronic heart failure.
The development of sideropenic syndrome is associated with the insufficiency of tissue iron-containing enzymes (catalase, peroxidase, cytochromes, etc.). This explains the occurrence of trophic changes in the skin and mucous membranes. Most often they are manifested by dry skin; striated, brittle and deformed nails; increased hair loss. On the part of the mucous membranes, atrophic changes are typical, which is accompanied by the phenomena of glossitis, angular stomatitis, dysphagia, atrophic gastritis. Addiction to pungent odors (gasoline, acetone), taste distortion (desire to eat clay, chalk, tooth powder, etc.) may occur. Signs of sideropenia also include paresthesia, muscle weakness, dyspeptic and dysuric disorders. Asthenovegetative disorders are manifested by irritability, emotional instability, decreased mental performance and memory.
Complications
Since IgA loses its activity in conditions of iron deficiency, patients become susceptible to frequent incidence of acute respiratory viral infections, intestinal infections. Patients are haunted by chronic fatigue, loss of strength, decreased memory and concentration. A prolonged course of iron deficiency anemia can lead to the development of myocardiodystrophy, recognized by the inversion of the T teeth on the ECG. With extremely severe iron deficiency, anemic precoma develops (drowsiness, shortness of breath, sharp pallor of the skin with a cyanotic tinge, tachycardia, hallucinations), and then coma with loss of consciousness and lack of reflexes. With massive rapid blood loss, hypovolemic shock occurs.
Diagnostics
The presence of iron deficiency anemia may indicate the appearance of the patient: pale, alabaster-tinged skin, pasty face, shins and feet, edematous “bags” under the eyes. During auscultation of the heart, tachycardia, deafness of tones, low systolic noise, and sometimes arrhythmia are detected. In order to confirm anemia and determine its causes, a laboratory examination is carried out.
- Laboratory test. In favor of the iron-deficiency nature of anemia, a decrease in hemoglobin, hypochromia, micro- and poikilocytosis in the blood test indicates. When assessing biochemical parameters, there is a decrease in serum iron levels and ferritin concentrations (<30 mcg /l) against the background of an increase in the total iron binding capacity of serum (TIBC >60 mmol /L), a decrease in transferrin saturation with iron (<25%). To identify the source of hidden bleeding, feces for hidden blood and helminth eggs are examined
- Instrumental techniques. To determine the cause of chronic blood loss, an endoscopic examination of the gastrointestinal tract (EGDS, colonoscopy,), X-ray diagnostics (irrigoscopy, stomach radiography) should be performed. Examination of the organs of the reproductive system in women includes ultrasound of the pelvis, examination on a chair, according to indications – hysteroscopy with RVV.
Examination of bone marrow punctate. Smear microscopy (myelogram) shows a significant decrease in the number of sideroblasts, characteristic of hypochromic anemia. Differential diagnosis is aimed at excluding other types of iron deficiency conditions – sideroblastic anemia, thalassemia.
Treatment
The basic principles of iron deficiency anemia therapy include elimination of etiological factors, correction of the diet, replenishment of iron deficiency in the body. Etiotropic treatment is prescribed and carried out by specialists gastroenterologists, gynecologists, proctologists, etc.; pathogenetic – hematologists. In iron-deficient conditions, a full-fledged diet is indicated with the mandatory inclusion in the diet of products containing heme iron (veal, beef, lamb, rabbit meat, liver, tongue). It should be remembered that ascorbic, citric, succinic acid contribute to the strengthening of ferrosorption in the gastrointestinal tract. Oxalates and polyphenols (coffee, tea, soy protein, milk, chocolate), calcium, dietary fiber and other substances inhibit the absorption of iron.
At the same time, even a balanced diet is not able to eliminate the already developed iron deficiency, therefore, patients with hypochromic anemia are shown replacement therapy with ferropreparations. Iron preparations are prescribed for a course of at least 1.5-2 months, and after normalization of the Hb level, maintenance therapy is carried out for 4-6 weeks with a half dose of the drug. For the pharmacological correction of anemia, preparations of divalent and trivalent iron are used. In the presence of vital indications, hemotransfusion therapy is resorted to.
Prognosis and prevention
In most cases, hypochromic anemia is successfully corrected. However, with an unresolved cause, iron deficiency can recur and progress. Iron deficiency anemia in young and young children can cause a delay in psychomotor and intellectual development. In order to prevent iron deficiency, it is necessary to monitor the parameters of the clinical blood test annually, complete nutrition with sufficient iron content, timely elimination of sources of blood loss in the body. It should be borne in mind that the iron contained in meat and liver in the form of heme is best absorbed; non–heme iron from plant foods is practically not absorbed – in this case, it must first be restored to heme with the participation of ascorbic acid. Persons at risk may be shown preventive intake of iron-containing drugs as prescribed by a specialist.
Literature
- Detivaud L., Nemeth E., Boudjema K. et al. Hepcidin levels in humans are correlated with hepatic iron stores, hemoglobin levels and hepatic function. Blood. 2005; 106 (2): 746—8.
- Papanikolaou G., Tzilianos M., Christakis J.I. Hepcidin in iron overload disorders. Blood. 2005; 10: 4103—5. link
- Park C.H., Valore E.V., Waring A.J. et al. Hepcidin: a urinary antibacterial peptide synthesized in the liver. J. Biol. Chem. 2001; 276: 7806—10. link
- Levina A.A., Cybulskaya M.M., Shcherbinina S.P., Romanova E.A., Mamukova Y.I. Diagnostic value of a comprehensive study of metabolism of iron in clinical practice. Gematologiya i transfuziologiya. 2005; 5: 23—8.
- Hunt J.R., Roughead Z.K. Adaptation of iron absorption in men consuming diets with high or low iron biovavailability. Amer. J. Clin. Nutr. 2000; 71: 94—102. link
- Nemeth E., Valore E.V., Territo M. et al. Hepcidin a putative mediator of anemia of inflammation is a type II acutephase protein. Blood. 2003;101: 2461—3. link
- Nemeth E., Rivera S., Gabajan V. et al. IL6 mediates hypoferremia inducing the synthesis of the iron regulatory hormone hepcidin. J. Clin. Inv. 2004; 113 (9): 1271—6.
