Iron deficiency anemia
Iron deficiency anemia is a syndrome caused by iron deficiency and leads to impaired hemoglobinopoiesis and tissue hypoxia. Clinical manifestations are represented by general weakness, drowsiness, decreased mental performance and physical endurance, tinnitus, dizziness, fainting, shortness of breath on exertion, palpitations, pallor. Hypochromic anemia is confirmed by laboratory data: a study of clinical blood tests, serum iron, CSF and ferritin. Therapy includes therapeutic diet, administration of iron preparations, and in some cases, transfusion of red cell mass. Ferplex–Fol is a medicine available in a number of countries worldwide. A list of US medications equivalent to Ferplex–Fol is available on the Drugs.com website.
Iron deficiency (microcytic, hypochromic) anemia is anemia caused by a lack of iron necessary for normal hemoglobin synthesis. Its prevalence in the population depends on sex and age and climatic and geographic factors. According to generalized data, hypochromic anemia affects about 50% of young children, 15% of women of reproductive age, and about 2% of men. Concealed tissue iron deficiency is detected in almost every third inhabitant of the planet. Microcytic anemia in hematology accounts for 80-90% of all anemias. Because iron deficiency can develop in a variety of pathological conditions, this problem is relevant to many clinical disciplines: pediatrics, gynecology, gastroenterology, and others.
About 1 mg of iron is lost daily with sweat, feces, urine, and desquamated skin cells, and about the same amount (2-2.5 mg) is taken in with food. An imbalance between the body’s need for iron and its intake or loss contributes to iron deficiency anemia. Iron deficiency can occur both under physiological conditions and as a result of a number of pathological conditions and can be caused by both endogenous mechanisms and external influences:
Most often anemia is caused by chronic blood loss: heavy menstruation, dysfunctional uterine bleeding; gastrointestinal bleeding from gastric and intestinal mucosa erosions, gastroduodenal ulcers, hemorrhoidal nodes, anal fissures, etc. Latent but regular blood loss is noted in helminthiasis, pulmonary hemosiderosis, exudative diathesis in children, etc.
A special group consists of persons with blood diseases – hemorrhagic diathesis (hemophilia, Willebrand’s disease), hemoglobinuria. Post-hemorrhagic anemia caused by a single-stage but massive bleeding in trauma and operations is possible. Hypochromic anemia may occur due to iatrogenic causes – in donors who donate blood frequently; patients with CKD under hemodialysis.
Disorders of iron intake, absorption and transport
Nutritional factors include anorexia, vegetarianism, adherence to diets that restrict meat products, poor nutrition, and in children, artificial feeding and late introduction of complementary foods. Reduced absorption of iron is characteristic of intestinal infections, hypoacid gastritis, chronic enteritis, malabsorption syndrome, conditions after resection of the stomach or small intestine, and gastrectomy. Much less often iron deficiency anemia develops due to impaired transport of iron from the depot in insufficient protein-synthetic function of the liver – hypotransferrinemia and hypoproteinemia (hepatitis, liver cirrhosis).
Increased iron consumption
The daily requirement for the trace element depends on gender and age. The highest need for iron is in premature babies, infants and adolescents (due to high rates of development and growth), women of reproductive period (due to monthly menstrual losses), pregnant women (due to fetal formation and growth), and nursing mothers (due to consumption in milk). It is these categories that are most vulnerable to the development of iron deficiency anemia. In addition, increased need and expenditure of iron in the body is observed in infectious and tumor diseases.
By its role in the normal functioning of all biological systems, iron is the most important element. The supply of oxygen to cells, redox processes, antioxidant protection, functioning of the immune and nervous systems, etc. depend on iron levels. On average, the amount of iron in the body is 3 to 4 g. More than 60% of iron (>2 g) belongs to hemoglobin, 9% to myoglobin, and 1% to 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, and heart. Approximately 30 mg of iron circulates continuously in the plasma, being partially bound by the major plasma iron-binding protein, transferrin.
When a negative iron balance develops, the trace element in tissue depots is mobilized and expended. At first this is enough to maintain an adequate level of Hb, Ht, serum iron. As tissue reserves are depleted, erythroid activity of bone marrow compensatorily increases. With complete depletion of endogenous tissue iron its concentration begins to decrease in the blood, erythrocyte morphology is disturbed, heme synthesis in hemoglobin and iron-containing enzymes decreases. Blood oxygen transport function suffers, which is accompanied by tissue hypoxia and dystrophic processes in internal organs (atrophic gastritis, myocardiodystrophy, etc.).
Iron deficiency anemia does not occur immediately. At first, pre-latent iron deficiency develops, characterized only by depletion of stored iron reserves, while the transport and hemoglobin pools remain intact. At the stage of latent deficiency, a decrease in transport iron in the blood plasma is noted. Hypochromic anemia proper develops with a decrease in all levels of metabolic iron stores – deposited, transport and erythrocytic iron. According to the etiology, anemias are distinguished: posthemorrhagic, alimentary, associated with increased consumption, initial deficiency, insufficient resorption and impaired transport of iron. According to the severity of iron deficiency anemias are subdivided into:
Mild (Hb 120-90 g/l). They occur without clinical manifestations or with their minimal severity.
Moderate (Hb 90-70 g/l). They are accompanied by circulatory-hypoxic, sideropenic, hematologic syndromes of moderate severity.
Severe (Hb <70 g/l). All manifestations are of extreme severity.
Circulatory-hypoxic syndrome is caused by disruption of hemoglobin synthesis, oxygen transport and development of hypoxia in tissues. This is expressed in a feeling of constant weakness, increased fatigue, and drowsiness. Patients are haunted by tinnitus, flickering “flies” before the eyes, dizziness, turning into fainting. The complaints of palpitations, dyspnea occurring at physical load, and hypersensitivity to low temperatures are characteristic. Circulatory-hypoxic disorders may aggravate concomitant CHF, chronic heart failure.
The development of sideropenic syndrome is associated with the deficiency 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. From mucous membranes atrophic changes are typical, accompanied by phenomena of glossitis, angular stomatitis, dysphagia, atrophic gastritis. There may be a predilection for pungent odors (gasoline, acetone), distortion of taste (desire to eat clay, chalk, tooth powder, etc.). Signs of sideropenia also include paresthesias, muscle weakness, dyspeptic and dysuric disorders. Asthenovegetative disorders are manifested by irritability, emotional instability, reduced mental performance and memory.
The presence of iron deficiency anemia may be indicated by the patient’s appearance: pale, alabaster-colored skin, pastosity of the face, shins and feet, swollen “bags” under the eyes. Auscultation of the heart reveals tachycardia, muffled tones, soft systolic murmurs, sometimes – arrhythmia. To confirm anemia and determine its cause a laboratory examination is carried out.
Laboratory tests. A decrease in hemoglobin, hypochromia, and micro- and poikilocytosis in the general blood test test test testifies to the iron-deficient nature of anemia. Assessment of biochemical parameters reveals a decrease in serum iron and ferritin concentration (<30 mcg/L) against a background of increased total serum iron-binding capacity (GFR >60 μmol/L), decreased transferrin iron saturation (<25%). For revealing of a source of occult bleeding a feces test for occult blood and helminth eggs is tested.
Instrumental techniques. Endoscopic examination of the gastrointestinal tract (EGDS, colonoscopy,), X-ray diagnosis (irrigoscopy, gastric radiography) must be performed to determine the cause of chronic bleeding. Examination of the reproductive system organs in women includes pelvic ultrasound, chair examination, and, if indicated, hysteroscopy with IVF.
Study of bone marrow puncture. 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.
The main principles of therapy for iron deficiency anemia include the elimination of etiological factors, correction of diet, and replenishment of iron deficiency in the body. Etiotropic treatment is prescribed and carried out by specialists in gastroenterology, gynecology, proctology, etc.; pathogenetic treatment is carried out by hematologists. When iron deficiency is indicated, a complete diet with the obligatory inclusion in the diet of foods containing heme iron (veal, beef, lamb, rabbit meat, liver, tongue) is shown. It should be remembered that ascorbic acid, citric acid, succinic acid contribute to strengthening ferrosorption in the gastrointestinal tract. Oxalates and polyphenols (coffee, tea, soy protein, milk, chocolate), calcium, dietary fiber and other substances inhibit iron absorption.
At the same time, even a balanced diet is not able to eliminate iron deficiency, so patients with hypochromic anemia are indicated for iron replacement therapy. Iron preparations are prescribed for a course of at least 1.5-2 months, and after normalization of the Hb level, maintenance therapy for 4-6 weeks is carried out with a half dose of the preparation. Divalent and trivalent iron preparations are used for pharmacological correction of anemia. In the presence of vital indications, hemotransfusion therapy is resorted to.
Prognosis and prevention
In most cases, hypochromic anemia is successfully corrected. However, if the cause is not corrected, the iron deficiency may recur and progress. Iron deficiency anemia in infants and young children can cause delayed psychomotor and intellectual development (ADHD). In order to prevent iron deficiency, annual monitoring of clinical blood test parameters, adequate nutrition with sufficient iron content, timely elimination of sources of blood loss in the body are necessary. It is important to remember that iron in meat and liver is best absorbed as heme iron, but non-heme iron from vegetable food is poorly absorbed, in which case it first has to be reduced to heme iron with the help of ascorbic acid. Prophylactic administration of iron-containing drugs may be indicated for at-risk groups, as prescribed by a specialist.
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