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Anemia is a blood disorder characterized by hemoglobin values ​​below 12 g / dL in women and 13 g / dL in men. The causes that can generate anemia are multiple. Vitamin B12 deficiency, defective use of vitamin B12 and folate deficiency are the most common causes of megaloblastic anemia, i.e. the condition in which the average corpuscular volume of red blood cells is pathologically higher than normal.

The most common cause of vitamin B12 deficiency is an impaired secretion of the intrinsic factor by the stomach, usually as a consequence of the production of auto-antibodies. Other possible causes are malabsorption due to chronic gastritis, gastric bypass, food deficiency of vitamin B12 or tapeworm infection. Common causes of folate deficiency include celiac disease and alcoholism. Other causes of vitamin B12 and folate deficiency, and therefore of megaloblastic anemia, include the intake of certain drugs that interfere with the intestinal absorption of vitamins and some metabolic disorders.

Megaloblastic anemia occurs due to a defective DNA synthesis, while the synthesis of RNA continues, resulting in the formation of a large cell with a large nucleus. The red blood cells undergo a maturation defect, in which the cytoplasmic maturation is greater than the maturation of the nucleus. The maturation defect causes cell death in the bone marrow, making the formation of red blood cells ineffective and generating the state of anemia. A limited number of large red blood cells enter the circulation. White blood cells and platelets are also negatively affected by the deficiency of vitamin B12 and folate, which causes megaloblastic anemia.

Megaloblastic anemia develops insidiously and may not cause symptoms until is already in severe state. It is often accompanied by the manifestation of gastrointestinal disorders, including diarrhea, glossitis and anorexia. The deficiency of vitamin B12 that causes megaloblastic anemia also leads to neurological manifestations that can be permanent, including peripheral neuropathy, instability of gait and dementia.

The diagnostic strategy is based on an accurate investigation of the plasma level of the vitamins potentially implicated in megaloblastic anemia: a vitamin B12 level lower than 200 pg / mL or a folate level lower than 2 ng / mL generally confirm a state of deficiency of these two vitamins. The levels of vitamin B12 can be deceiving, so the investigation is often expanded by measuring the levels of methylmalonic acid and homocysteine ​​in the blood. If the levels of methylmalonic acid and homocysteine ​​in the blood are both high it can be concluded that there is a deficiency of vitamin B12, while if the level of homocysteine ​​in the blood is high it can be concluded that there is a deficiency of folate.

The therapeutic strategy is based on the administration of the adequate vitamin and on the reduction or elimination of the factors that determined the deficiency of vitamin B12, folate or both (for example the elimination, from the therapies administered to the patient, of the drugs that inhibit the absorption of vitamin B12). Before the administration of folate it is necessary to exclude the deficiency of vitamin B12, otherwise the risk of the administration of folate masks a concomitant deficiency of vitamin B12, leading to the progression of neurological complications. The method that is usually adopted to avoid the problems just mentioned is to administer both vitamin B12 and folate to patients simultaneously.

Iron deficiency anemia refers to anemia caused by iron deficiency. Iron is present in the body divided into a metabolically active circulating portion and a portion that is deposited. The total amount of iron in the body amounts to approximately 3.5 g in healthy males and 2.5 g in healthy females.

In a normal diet, of the approximately 15 mg of edible iron introduced every day, adults absorb only 1 mg, which is about the amount lost daily due to the cellular desquamation of the skin and the replacement of the cells of the intestinal mucosa. If iron in the body is deficient, intestinal absorption of iron increases thanks to compensatory mechanisms. Children naturally have a greater need for iron and are therefore able to absorb more of it to meet this need.

Since iron absorption is so limited, the body implements mechanisms for recycling and storing iron. These mechanisms provide about 97% of the required daily amount of iron, or about 25 mg of iron.

Iron deficiency develops in various stages. In the first phase, the demand for iron exceeds the quota introduced with the diet, causing the progressive depletion of iron reserves. Due to the reduction of reserves, intestinal absorption of edible iron increases by compensation. During the subsequent stages, the deficiency compromises the synthesis of hemoglobin and the formation of red blood cells causing anemia. Prolonged iron deficiency also compromises the synthesis of other substances necessary for the functioning of the body, such as cellular enzymes that contain iron, which are necessary, for example, to allow cells to produce energy.

Since iron is hardly absorbed in the intestine, food iron can barely cover the daily needs of most people. For this reason, even small blood losses, an increase in iron needs or a reduced intake quickly cause an iron deficit. Blood loss is almost always the main cause of iron deficiency. In elderly men and women, the most frequent cause is chronic occult bleeding, usually from the gastrointestinal tract, often caused by gastroduodenal ulcer, neoplasms or hemorrhoids. In non-menopausal women one of the most frequent causes is blood loss due to menstruation.

An increased demand for iron can help generate a deficiency. From birth to the age of 2 years and during adolescence, when growth is faster, the need for iron increases and the share of edible iron is often insufficient. During pregnancy, the need for iron by the developing fetus increases the maternal need for iron. Breastfeeding also increases the need for iron.

The reduced intestinal absorption of iron can result from surgical removal of the stomach or from malabsorption syndromes such as celiac disease, atrophic gastritis and the reduced production of hydrochloric acid in the stomach.

Iron deficiency anemia determines the onset of some characteristic symptoms such as fatigue, loss of resistance, shortness of breath, weakness, dizziness and pallor. Another frequent manifestation is restless legs syndrome, represented by a continuous need to move the legs during periods of inactivity.

The therapeutic strategy for the treatment of iron deficiency anemia involves a careful investigation to identify the cause of iron deficiency and therefore the oral administration of iron-based drugs or food supplements. Vitamin C is often co-administered since promotes the absorption of iron by the intestine and some B complex vitamins, which are involved in the formation of red blood cells and in the synthesis of hemoglobin.

Iron deficiency or iron deficiency anemia is the most common form of anemia. Anemia is referred to when hemoglobin levels in the blood are less than 13 g / dl in the case of men and 12 g / dl in the case of women. Anemia is often also characterized by a reduced concentration of red blood cells in the blood. The low hemoglobin levels result in a reduced ability to transport oxygen to the various tissues of the body and, consequently, a deterioration in the performance of all organs. The anemic subject manifests pallor and perceives an easy physical and mental fatigue; to suffer for the reduction of the availability of oxygen are also those organs that do not send easily perceivable signals. Anemia therefore exposes to an increased risk of compromised health and therefore must be corrected.

Gastrointestinal disorders are a frequent cause of iron deficiency anemia, especially gastric or intestinal bleeding and malabsorption. These phenomena occur at all ages but worsen significantly with aging.

Intestinal diseases that cause malabsorption, such as celiac disease or chronic inflammatory bowel disease, can cause deficiency of iron and other micronutrients, including vitamins necessary for the correct metabolism of iron. The stomach performs a fundamental function for the correct absorption of iron and some vitamins necessary for the formation of red blood cells and for the synthesis of hemoglobin. Therefore, various forms of gastritis, such as Helicobacter pylori gastritis or atrophic gastritis, can cause anemia.

Blood loss attributable to various pathological conditions can occur throughout the gastrointestinal tract, such as gastric ulcers, duodenal ulcers, hiatal hernias, colorectal polyps and tumors affecting the intestine. In addition, bleeding from the gastrointestinal tract can be caused, or aggravated, by the concomitant intake of certain drugs, especially platelet aggregation inhibitors and anticoagulants.

The correct diagnostic approach requires that the causes of iron deficiency anemia are identified in the patient suffering from gastroenterological disorders. Only after having identified, through appropriate diagnostic tests, the cause of the anemia is a specific therapy undertaken to correct the bleeding or malabsorption and, at the same time, is the correction of the anemic state promoted by the administration of supplements or drugs to iron base and the main vitamins involved in the formation of red blood cells and in the synthesis of hemoglobin, such as vitamin B12 and folate.

Under normal conditions, during pregnancy intense proliferative activity occurs at the level of the bone marrow and the overall mass of red blood cells in the blood increases. However, the overall plasma volume also increases, as the same blood must circulate both in the mother and in the developing fetus. The appropriate term to define this condition is hemodilution. The hematocrit is defined as the relationship between the volume of plasma and the volume of red blood cells in the blood; a low hematocrit indicates a high volume of blood plasma in relation to a low number of circulating red blood cells. Well, due to the hemodilution, the hematocrit, which is between 38 and 45% in healthy non-pregnant women, decreases up to about 34% during the late phase of a single pregnancy and about 30% in the late stage of a multiple pregnancy. Despite hemodilution, the oxygen transport capacity remains normal during pregnancy and the hematocrit usually increases until it returns to normal immediately after birth. So the hemodilution in itself, despite altering the parameters detected with blood tests, does not cause anemia in the pregnant woman.

Given that hemodilution is an expected condition in pregnant women, the parameters for defining anemia during pregnancy are different from those that identify anemia in non-pregnant women. In fact, the World Health Organization defines anemia in pregnancy as follows: in the first trimester the hemoglobin must be less than 11 g / dL, in the second trimester it must be less than 10.5 g / dL and in the third trimester a 11 g / dL. About a third of women, during the third trimester of pregnancy, have anemia and the most frequent causes are iron deficiency and folate deficiency. Iron deficiency, a consequence of insufficient food intake, is corrected by oral intake of iron-based drugs or food supplements. If this therapeutic strategy proves ineffective, folate deficiency is suspected. Folate is a B group vitamin and, together with vitamin B12, it is necessary for the formation of normal red blood cells, for the synthesis of hemoglobin and for the synthesis of DNA. Folate is also necessary for the normal development of the nervous system of the fetus. Up to 1.5% of pregnant women manifest folate deficiency, which is corrected by oral administration of this vitamin.

The integration with iron and folate is proposed routinely to pregnant women to prevent the onset of anemia, in order to preserve the health of the pregnant woman and to facilitate the normal development of the fetus.

In the case of the woman, anemia is generally referred to when the hemoglobin levels in the blood are below 12 g/dl. Anemia can also be characterized by a reduced concentration of red blood cells in the blood. The low hemoglobin levels result in a reduced ability to transport oxygen to the various tissues of the body and, consequently, a deterioration in the performance of all organs. The anemic subject manifests pallor and perceives an easy physical and mental fatigue; in reality, the organs that do not send easily perceptible signals also suffer from the reduction of oxygen availability. Anemia therefore exposes to an increased risk of compromised health and therefore must be corrected.

One of the most frequent causes of anemia is excessive blood loss, which can be acute or chronic. Particularly abundant menstruation causes excessive blood loss. As a consequence of a series of physiological mechanisms, anemia appears only several hours after acute blood loss. In fact, blood loss causes anemia when it exceeds the body’s ability to compensate: following the loss of blood, the erythropoiesis process, by which new red blood cells are produced and new hemoglobin is synthesized, accelerates and causes the depletion of the iron reserves of the body causing the state of anemia. The process is aggravated both in dependence on the intensity of blood losses and in dependence on the reduced iron intake in the diet. For these reasons, women with particularly heavy menstruation often have to resort to iron supplementation by means of appropriate food supplements or medications. The reintegration of iron reserves facilitates erythropoiesis and resolves the state of anemia with very favorable consequences for the state of well-being and the prevention of other diseases.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease and represents a serious health problem worldwide. According to the World Health Organization, 65 million people worldwide have moderate to severe COPD. COPD is therefore a widespread pathology with high morbidity and mortality, characterized by progressive obstruction of the bronchi with limitation of the air flow and is rarely reversible.

Exposure to tobacco smoke and biomass combustion smoke, together with genetic predisposition, are the main risk factors for the development of COPD. Diseases that occur in association with COPD are important events in the development and course of the disease and have a negative effect on the quality of life and mortality of patients with COPD. Diabetes, hypertension, cardiovascular disease, lung cancer, osteoporosis and depression are common comorbidities observed in patients with COPD.

Anemia is believed to be present as comorbidity in various states of chronic disease and therefore it is important to understand its pathogenesis. In recent years, anemia has emerged as a common comorbidity in COPD patients and has been associated with impaired functional capacity, worsening dyspnea, limitation of exercise tolerance, worsening quality of life, increased likelihood of hospitalization and early mortality.

The anemia that occurs in conjunction with chronic diseases is an immune-driven anomaly associated with chronically very low levels of circulating hemoglobin, which has been observed in many inflammatory diseases. Systemic inflammation, which occurs throughout the body, is recognized as a characteristic of COPD and is most likely one of the causes of anemia.

Hemoglobin is the main oxygen transport molecule. According to the World Health Organization, men with hemoglobin levels <13 g/dl and women with hemoglobin levels <12 g/dl are defined as anemic. Any reduction in hemoglobin levels causes a corresponding decrease in the ability to carry oxygen in the blood. The deterioration of this mechanism has a negative impact on the patient's clinical status. Clinical trial results show that many of the COPD patients who exhibit anemia suffer from iron deficiency. For this reason, the first solution to tackle the problem of anemia in these patients is represented by the administration of drugs and food supplements containing iron and vitamins involved in the formation of red blood cells and in the synthesis of hemoglobin, such as vitamin B12, vitamin B2 and the folate. In the same scientific studies, it is shown that the correction of the status of iron and anemia in patients with COPD can improve lung function, in particular this is highlighted thanks to the significant improvement in dyspnea.

Generally, we speak of anemia when the hemoglobin levels in the blood are lower than 13 g/dl in the case of men and 12 g/dl in the case of women. Anemia can also be characterized by a reduced concentration of red blood cells in the blood. The low hemoglobin levels result in a reduced ability to transport oxygen to the various tissues of the body and, consequently, a deterioration in the performance of all organs. The anemic subject manifests pallor and perceives an easy physical and mental fatigue; to suffer for the reduction of the availability of oxygen are also those organs that do not send easily perceivable signals. Anemia therefore exposes to an increased risk of compromised health and therefore must be corrected.

In people with chronic kidney disease, anemia occurs with high frequency, both due to iron deficiency, and blood loss, and due to the maldistribution of iron already present in the body. To correct the anemia conditions of people with chronic kidney disease, the specialist doctor may resort to the administration of iron orally or injected. Iron can be associated with certain vitamins that are involved in the synthesis of hemoglobin and in the formation of new red blood cells, such as vitamin B12 and folate. In some cases, the doctor must resort to the administration of drugs called erythropoiesis stimulating agents, which require the simultaneous administration of iron to perform its function in the best possible way. The specialist doctor determines which therapeutic measure to use based on the clinical picture presented by the patient and based on the subjective response to the therapies undertaken from time to time.