
[New Latin, from Greek anaimiā : an-, without; see a-1 + haima, blood.]
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Key Terms: Cytokines, Cytomegalovirus, Erythropoiesis, Erythropoietin, Hematocrit.
Description
Anemia is characterized by an abnormally low number of red blood cells in the circulating blood. It frequently affects patients with cancer. In fact, in many cancer diagnoses such as multiple myeloma and acute leukemia, the presence of anemia may be what initially prompts a doctor to suspect an underlying tumor (neoplasm). Whether or not anemia develops depends on the type of cancer found, the treatment used, and the presence or absence of other underlying medical disorders.
Symptoms of malignancy-associated anemia may range from weakness, paleness, and fatigue to shortness of breath and increased heart rate. Symptoms of anemia can compromise a patient's ability to tolerate treatment, and may severely interfere with activities of daily living. Anemia may be particularly problematic in older individuals with cancer. The incidence and severity of anemia tends to increase as the cancer progresses.
Blood is comprised of three major cell types: white blood cells, which help the body fight infection; platelets, which help the blood to clot when necessary; and red blood cells, which transport oxygen from the lungs to the tissues in the body, and then transport carbon dioxide from those tissues back to the lungs. This exchange is enabled by the most important component of red blood cells—the protein called hemoglobin that binds easily to oxygen and carbon dioxide.
Red blood cells are produced in the bone marrow through a process called erythropoiesis. When the bone marrow functions normally, it continuously replaces red blood cells to maintain a normal level that allows for adequate oxygenation of the tissues. The hormone erythropoietin stimulates red blood cell production and sends a message to the bone marrow to increase production when oxygen levels in the body are low. This mechanism is often impaired in patients with cancer.
Causes
The causes of anemia are multiple, and often the factors act in conjunction with one another. Generally, anemia may result from a direct effect of a cancerous tumor, or from an indirect effect of the tumor. The cancer process may directly cause anemia through two main mechanisms: blood loss or bone marrow replacement. However, most cases of anemia in cancer patients result from the indirect effects of the cancer.
Direct Effects of the Tumor
Anemia is a frequent complication of cancers due to bleeding. Cancers of the head and neck, the gastrointestinal and genitourinary system, and the cervix are frequently associated with endogenous bleeding, or bleeding that occurs within the body. Bleeding occasionally develops within the tumor itself, particularly in sarcomas, melanomas, and ovarian and liver carcinomas.
A second direct cause of anemia in cancer is bone marrow replacement, which inhibits the body's ability to appropriately produce red blood cells. Certain cancers, such as acute leukemia, lymphoma and myeloma, directly suppress bone marrow function, thereby causing anemia. Other types of cancer, such as prostate or breast cancer, often spread to the bone marrow, inhibiting red blood cell production by actually replacing the bone marrow itself.
Indirect Effects of the Tumor
Anemia of chronic disease, also called anemia of malignancy, is the most common type of anemia seen in individuals with cancer. It is a diagnosis made only after other possible causes are ruled out and if very specific conditions are met. The presence of low levels of iron coupled with normal levels of storage iron helps distinguish anemia of chronic disease from iron deficiency anemia. Factors that cause anemia of chronic disease are not entirely clear. However, it is believed that cytokines (non-antibody proteins) produced by the tumor reduce production of and impair responsiveness to erythropoietin. Typically, this type of anemia develops slowly. Rapid development of anemia may indicate an other cause.
Treatments used to manage cancer have been implicated in the development of anemia in cancer patients. Radiation therapy to large areas of bone marrow, as in the hip area, may suppress bone marrow function and lead to anemia. Chemotherapy can also cause bone marrow suppression, and some drugs specifically target red blood cell production. Studies have shown that 10% to 40% of patients taking cisplatin develop significant anemia. Cisplatin, a chemotherapy drug with potentially toxic effects to the kidneys, is believed to reduce the production of the hormone erythropoietin in the kidneys. Although most treatment-induced bone marrow suppression is short term, there is some evidence to support the possibility of long-term problems with blood cell production.
Treatment can increase the risk of anemia in other ways. Chemotherapy, for example, causes bone marrow suppression that may reduce the immune system's ability to fight off opportunistic infection. The resulting infections can impact the bone marrow's functioning, possibly leading to the development of anemia.
Hemolytic anemia is a type of anemia in which the red blood cell has a shortened life span (normal life span is 90-120 days). Because the bone marrow is not able to compensate by producing more red blood cells, anemia results. Abnormalities in the red blood cells may originate in the body (intrinsic) or may be caused by environmental factors such as auto-antibodies to red blood cells or damage from chemotherapy.
Although one factor may have a greater influence, it is important to realize that several factors may be causing anemia. For example, approximately 70% of patients with multiple myeloma are anemic at the time of diagnosis. Anemia in these cases is caused by a combination of mechanisms including bone marrow replacement with cancer cells, bone marrow suppression from chemotherapy, and impaired production of erythropoietin.
Treatments
Treatment of the anemia is directed at the underlying cause. In many cases, treating or removing the cancer corrects the red blood cell deficit. Management of autoimmune hemolytic anemia, which can be associated with chronic lymphocytic leukemia, may range from the administration of corticosteroids to the surgical removal of the spleen. More commonly, cancer-related anemias are treated with blood transfusions and/or a drug called epoetin alfa.
Blood Transfusions
Blood transfusions have been the principle treatment for anemia for many years. Until the 1960s, only whole blood was given. Then, methods of separating whole blood were devised, allowing only particular components, such as platelets, red blood cells, or plasma, to be transfused.
Blood transfusions are not without risk, and must be used carefully. Many patients react to the white blood cell antigens by developing a fever. This is so common that patients are routinely premedicated to prevent fever from developing. Individuals with long-term transfusion needs, such as patients with leukemia, may be given blood products with a reduced number of white blood cells to reduce the risk of sensitization to transfused blood.
Cytomegalovirus (CMV) is a virus that may be present in blood products. Although it has no effect on individuals with normally functioning immune systems, cancer patients often have a diminished ability to fight infection. These patients may be at risk for CMV if they are CMV negative and receive CMV-positive blood.
Transfusion-associated graft-versus-host disease (TA-GvHD) is another risk factor associated with blood transfusions in cancer patients. Although it is very rare, it is often fatal. With TA-GvHD, the patient's immune system does not recognize the white blood cells in the donor blood as "nonself." The donor white blood cells, however, recognize the patient as "nonself," and an immune-mediated reaction ensues. To prevent this reaction in at-risk patients, blood may be irradiated prior to transfusion.
Epoetin Alfa
As mentioned previously, erythropoietin is a protein produced in the kidneys that stimulates red blood cell production. Using DNA technology, this hormone has been replicated to create the drug epoetin alfa for the treatment of anemia in select cancer patients. (The drug is also called erythropoietin.) The use of this drug in the cancer setting has shown great promise, both in the treatment of cancer-related anemia, and in the reduction in the need for blood transfusion.
However, epoetin alfa therapy is not advisable for everyone. This drug is not recommended for use in cancer-related anemia caused by bleeding, hemolysis, or iron deficiencies. Nor is it recommended for patients with hypertension or albumin sensitivity. Because no human studies are available to determine its effect on a fetus, women taking epoetin alfa should take measures to prevent pregnancy.
Cancer patients with anemia who are undergoing chemotherapy may benefit from this drug. Studies have shown an increased hematocrit (the volume percentage of red blood cells in whole blood) level and a decreased need for blood transfusions after the first month of therapy in this population. Epoetin alfa may be injected up to three times a week, and throughout therapy, blood cell counts are monitored closely. In 2004, it was reported that a form of the drug could be injected only once every two weeks in some cancer patients with the same effect, making its use more convenient.
Resources
Books
Abeloff, M., et al., editors. "Hematopoietic Dysfunction by Hematologic Lineage." In Clinical Oncology. 2nd ed. New York: Churchill Livingstone Publishers, 2000.
Lee, G., and C. Bennett, editors. "Nonmetastatic Effects of Cancer: Other Systems." In Cecil Textbook of Medicine. 21st ed. Philadelphia, PA: W. B. Saunders Co., 2000.
Lee, G., et al., editors. Wintrobe's Clinical Hematology. Baltimore, MD: Williams & Wilkins Publishing, 1999.
Periodicals
"Studies: Aranesp Dosed Semiweekly Is Comparable to Epoetin Alfa Once a Week." Obesity, Fitness & Wellness Week July 10, 2004:59.
—Tamara Brown, R.N.; Teresa G. Odle
A reduction in the total quantity of hemoglobin or of red blood cells (erythrocytes) in the circulation. Because it generally is impractical to measure the total quantity, measures of concentration are used instead. Hemoglobin is contained in red blood cells, which are suspended in plasma, the liquid component of blood. Therefore, concentration is affected not only by quantities of hemoglobin and red blood cells but also by plasma volume. Thus, the apparent anemia found in many women in the third trimester of pregnancy is not really anemia at all: the red cell mass is actually increased, but the plasma volume is expanded even more. In other words, hemodilution is present. Conversely, in dehydration and other circumstances of hemoconcentration, the plasma volume is reduced, thereby tending to mask anemia. See also Blood; Hemoglobin.
The three measures of concentration most often employed are the hemoglobin, the red blood cell count, and the volume of packed red cells. In a group of healthy individuals, the values for hemoglobin, red cell count, and hematocrit approximate a “normal” distribution. Values that are less than 2.5 standard deviations below the mean are indicative of anemia if other clinical factors do not indicate a condition of hemodilution. The mean values are greater for adult males than for adult females, and greater for adults than children. (Lower atmospheric oxygen tension at higher altitudes results in higher mean values for hemoglobin, red cells, and hematocrit in healthy individuals living under these conditions; hence, anemia would be defined at a higher value). In the state of health, the rate of production of new red blood cells (erythropoiesis) equals the rate of removal of senescent red blood cells. Anemia occurs if the rate of erythropoiesis is reduced below normal. It also occurs if hemorrhage or destruction (hemolysis) of red blood cells within the body increases the rate of loss of erythrocytes and the rate of erythropoiesis does not increase enough to compensate.
Mechanisms
Red blood cell production may be affected by several different mechanisms. Erythropoietin, a growth factor produced by healthy kidneys, stimulates the bone marrow to produce more erythroblasts and accelerates their maturation. The proliferative response of the bone marrow to anemia may be defective or absent if the production of erythropoietin is diminished or absent, as occurs in chronic renal disease and some endocrine disorders. Ineffective erythropoiesis also results when, in the intact, stimulated bone marrow, red blood cell precursors either fail to mature, or die in the bone marrow prior to their delivery to the circulation as erythrocytes.
Aplastic anemia occurs when the bone marrow stem cells that give rise to precursors of erythroblasts are markedly diminished in number or respond inadequately to erythropoietin. This condition occurs when the bone marrow is adversely affected by certain chemicals or autoantibodies; is injured by irradiation; atrophies, or is replaced by fat; is replaced by fibrous (scar) tissue; or is infiltrated by cancer cells.
Defective synthesis of deoxyribonucleic acid (DNA) and abnormal nuclear maturation result from malabsorption of vitamin B12 (as in pernicious anemia) or dietary deficiency of folic acid or its malabsorption (sprue). These anemias are generally characterized by large red blood cells (macrocytes) and a specific morphological abnormality of the nuclear chromatin of erythroblasts which characterizes them as megaloblasts, and the condition as megaloblastic anemia.
Defective synthesis of hemoglobin impairs cytoplasmic maturation. The majority of cases are due to deficiency of body stores of iron and to abnormal release of iron from reticuloendothelial stores. The former occurs in iron-deficiency anemia, and the latter in the anemia of chronic inflammatory diseases.
Acute blood loss reduces the total blood volume and produces symptoms of weakness, dizziness, thirst, faintness, and shock, in that order, according to increasing magnitude of blood loss. The anemia which results is not detectable by measures of concentration until hemodilution occurs over subsequent days, or more rapidly if replacement fluids are given intravenously. The proliferative response of the healthy marrow will correct the anemia in 2–6 weeks, depending upon the size of the deficit and provided there are sufficient body stores of iron, folic acid, and vitamin B12, required for hemoglobin synthesis. Chronic blood loss results in iron-deficiency anemia.
Hemolysis, the accelerated destruction of red blood cells, also induces a proliferative response from the marrow. However, it differs from hemorrhage because red blood cells are lost without plasma, and it thus diminishes the measures of concentration at the outset.
Diagnosis and treatment
Pallor, weakness, and fatigue are common to all anemias. They may not be noticed until anemia is advanced, if it is of gradual onset and there has been time for cardiovascular and biochemical adaptation. Faint jaundice in the sclerae is a feature of hemolytic anemia, whereas in anemia due to lack of vitamin B12, glossitis and neuropathy may be noted.
Macrocytic anemias are often found to be megaloblastic and due to deficiency of vitamin B12 or folic acid. Administration of one of those vitamins will only cure individuals in whom its specific deficiency is established. Microcytic-hypochromic anemias are most often due to iron deficiency. The administration of iron will resolve iron-deficiency anemia. Prednisone and other adrenal corticosteroids are helpful in hemolytic anemias associated with autoantibodies.
Hereditary disorders are generally not amenable to therapy, except for those hemolytic diseases which may benefit after splenectomy. In all other cases, the treatment of the anemia is achieved by treating the underlying disease, such as hypothyroidism, rheumatoid arthritis, or leukemia. Blood transfusions are reserved for acute blood loss when symptoms of hypovolemia and shock are present, or in chronic anemia if there are signs of inadequate cardiovascular or pulmonary compensation and an underlying cause cannot be found or treated. See also Clinical pathology; Hematologic disorders.
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Definition
Anemia is a blood disorder characterized by abnormally low levels of healthy red blood cells (RBCs) or reduced hemoglobin (Hgb), the iron-bearing protein in red blood cells that delivers oxygen to tissues throughout the body. Reduced blood cell volume (hematocrit) is also considered anemia. The reduction of any or all of the three blood parameters reduces the oxygen-carrying capability of the blood, causing reduced oxygenation of body tissues, a condition called hypoxia.
Description
All tissues in the human body need a regular supply of oxygen to stay healthy and perform their functions. RBCs contain Hgb, a protein pigment that allows the cells to carry oxygen (oxygenate) tissues throughout the body. RBCs live about 120 days and are normally replaced in an orderly way by the bone marrow, spleen, and liver. As RBCs break down, they release Hgb into the blood stream, which is normally filtered out by the kidneys and excreted. The iron released from the RBCs is returned to the bone marrow to help create new cells. Anemia develops when either blood loss, a slow-down in the production of new RBCs (erythropoiesis), or an increase in red cell destruction (hemolysis) causes significant reductions in RBCs, Hgb, iron levels, and the essential delivery of oxygen to body tissues.
Anemia can be mild, moderate, or severe enough to lead to life-threatening complications. More than 400 different types of anemia have been identified. Many of them are rare. Most are caused by ongoing or sudden blood loss. Other causes include vitamin and mineral deficiencies, inherited conditions, and certain diseases that affect red cell production or destruction.
Anemia in newborn infants is noted when hemoglobin levels are lower than expected for the birth weight and postnatal age. Premature or low birth-weight infants may have lower hemoglobin levels. The normal newborn Hgb is 16.8 dL, which may be 1 to 2 dL lower if birth weight is abnormally low. Anemia may be the first sign of certain disorders in the newborn, such as blood loss that has occurred from transplacental hemorrhage, a condition in which the infant's blood bleeds back into the mother's circulation; bleeding from ruptures in the liver, spleen, adrenals, or kidneys; or hemorrhage within the brain (intracranial hemorrhage). Anemia can also be caused by the destruction of red blood cells or reduced red blood cell production. Newborns may also have low red blood cell volume (hematocrit or Hct) if they were born by cesarean section. It must be noted, however, that hemoglobin decreases naturally (physiologic decrease) in infants by eight to 12 weeks of age, leveling at a normal value of 11 g/dL or better.
Iron-Deficiency Anemia
Iron deficiency anemia is the most common form of anemia worldwide. In the United States, it affects thousands of toddlers between one and two years of age and more than 3 million women of childbearing age. This condition is less common in older children and in adults over 50 and rarely occurs in teenage boys and young men.
The onset of iron deficiency anemia is gradual and may not have early symptoms. The deficiency begins when the body loses more iron than it derives from food and other sources. Because depleted iron stores cannot meet the red blood cell's needs, fewer red blood cells develop. In this early stage of anemia, the red blood cells look normal, but they are reduced in number. Then the body tries to compensate for the iron deficiency by producing more red blood cells, which are characteristically small in size (spherocytosis). Symptoms of anemia, especially weakness and fatigue, develop at this stage. Individuals may be given iron preparations by injection or advised to take oral iron supplements. It sometimes helps to take vitamin C along with oral iron supplementation to encourage better absorption of the iron. Taking iron supplements can result in diarrhea, cramps, or vomiting.
Folic Acid Deficiency Anemia
Folic acid deficiency anemia is the most common type of megaloblastic anemia, arising from a problem with the synthesis of deoxyribonucleic acid (DNA) within the cells of the body. It is characterized by RBCs that are larger than normal and is caused by a deficiency of folic acid, a vitamin that the body needs to produce normal cells and normal DNA.
Folic acid anemia is especially common in infants and teenagers. This condition usually results from a dietary deficiency but may also be due to an inability to absorb (malabsorption) folic acid. Folic acid is available in many foods, such as cheese, eggs, fish, green vegetables, meat, milk, mushrooms, and yeast. Smoking raises the risk of developing this condition by interfering with the absorption of vitamin C, which the body needs to absorb folic acid. Folic acid anemia can be a complication of pregnancy, when a woman's body needs eight times more folic acid than it does otherwise. Folic acid deficiency in pregnant women may lead to birth defects in their children. Supplementation of folic acid is recommended during pregnancy.
Vitamin B12 Deficiency Anemia
Less common in the United States than folic acid anemia, vitamin B12 deficiency anemia is another type of megaloblastic anemia that develops when the body does not absorb enough of this nutrient. Necessary for the creation of healthy RBCs, B12 is found in meat, eggs, whole grains, and most vegetables. Large amounts of B12 are stored in the body, so this condition may not become apparent until up to four years after B12 absorption stops or slows down. The resulting drop in RBC production can cause loss of muscle control; loss of sensation in the legs, hands, and feet; soreness, slickness, or burning of the tongue; weight loss; or yellow-blue color blindness. Confusion, depression, and memory loss may also be associated with the deficiency.
Pernicious anemia is the most common form of B12 deficiency. Since most people who eat meat or eggs get enough B12 in their diets, a deficiency of this vitamin usually means that the body is not absorbing it properly. This condition can be found in those who do not produce adequate amounts of a chemical secreted by the stomach lining that combines with B12 to help its absorption in the small intestine. Pernicious anemia is diagnosed more often in adults between ages 50 and 60 than in children or young people, although there is the possibility of inheriting the condition, with symptoms not appearing until later in life.
Vitamin C Deficiency Anemia
Anemia due to vitamin C deficiency is a rare disorder that causes the bone marrow to manufacture abnormally small red blood cells. Vitamin C deficiency anemia results from a severe, long-standing dietary deficiency or malabsorption of this essential vitamin. It is usually easily corrected with supplementation.
Hemolytic Anemia
Hemolytic anemia can be present at birth (congenital hemolytic anemia or spherocytosis) or acquired later in life. It is the result of either infection or the presence of antibodies that destroy RBCs more rapidly than bone marrow can replace them. Hemolytic anemia can enlarge the spleen, an organ that also produces red blood cells when necessary. Production of cells by the spleen will increase to meet the demands of accelerated RBC destruction (hemolysis). Complications of hemolytic anemia in older children or adults include pain, gallstones, and other serious health problems.
Hemolytic disease of the newborn is a specific variation of hemolytic anemia in which an incompatibility exists between antigens on the cells of the mother and baby, causing antibodies to develop in the mother's circulation. The antibodies are produced as an immune response to what the body views as foreign antigens on the surface of the infant's RBCs. Several specific antigens are responsible for the incompatibilities: Rh type incompatibility, ABO blood group incompatibility, and other incompatibilities involving antigens known as Kell, Duffy, M, N, and P, among many others. Hemolytic disease of the newborn and the anemia that results is detectable within the first few days after birth. Depending on the strength of the antibody, the anemia may clear up on its own or exchange transfusions may be necessary to replace the newborn's blood.
Thalassemia
An inherited form of hemolytic anemia, thalassemia comes from the production of abnormal hemoglobin. It is characterized by low hemoglobin and unusually small and fragile RBCs (microcytosis), although the RBC count may be normal. Thalassemia has several types that involve imbalances in the four chains of amino acids that comprise hemoglobin (alpha- and beta-globins). In thalassemia minor or thalassemia trait (heterozygous thalassemia), also called alpha-thalassemia, there is an imbalance in the production of the alpha chain of amino acids. In thalassemia minor, fetal hemoglobin (HbF), the hemoglobin form that circulates in the fetus, does not decrease normally after birth and may remain high in later life. A child may inherit thalassemia trait when only one parent has the genes responsible for it. It is usually not treated and does not have serious consequences. Thalassemia major (homozygous thalassemia or Cooley's anemia) occurs in children in whom both parents pass on the genes responsible. It is known as beta-thalassemia, because of an imbalance in the beta chain amino acids of hemoglobin. It also involves the persistence of HbF with larger than normal amounts appearing in the child's circulation. Alpha-thalassemias occur most commonly in African Americans; beta-thalassemias most commonly affect people of Mediterranean or middle-Eastern ancestry and Southeast Asians. Hemoglobin H disease is another form of thalassemia in which three of the four beta-globin genes are missing.
Sickle Cell Anemia
Sickle cell anemia is an inherited, chronic, incurable blood disorder that causes the body to produce defective hemoglobin, the abnormal HgbS, which occurs primarily in African Americans. The condition is characterized by abnormal, crescent-shaped RBCs. Unlike normal oval cells, fragile sickle cells cannot hold enough hemoglobin to nourish body tissues. The deformed shape makes it hard for sickle cells to pass through narrow blood vessels. When capillaries become obstructed, a life-threatening condition called sickle cell crisis is likely to occur. A child who inherits the sickle cell gene from each parent will have the disease. A child who inherits the sickle cell gene from only one parent carries the sickle cell trait but does not have the disease.
Aplastic Anemia
Sometimes curable by bone marrow transplant, but potentially fatal, aplastic anemia is characterized by decreased production of red and white blood cells and platelets (disc-shaped cells that are a key component of blood coagulation). This disorder may be inherited or acquired as a result of the following:
Anemia of Chronic Disease
Cancer, chronic infection or inflammation, and kidney and liver disease often cause mild or moderate anemia. Chronic liver failure generally produces the most severe symptoms because the production of RBCs is directly affected.
Causes and Symptoms
Anemias do not all stem from the same causes. Anemia can be the result of injuries, chronic or acute illnesses, complications of surgery or childbirth, metabolic disturbances or deficiencies, and adverse response to drug therapy administered for other conditions. Causes may include sudden or ongoing loss of blood, nutritional deficiencies, decreased red blood cell production, or increased red blood cell destruction. Malnutrition or malabsorption of nutrients can contribute to vitamin deficiency anemia and iron deficiency anemias. Although red cell destruction and replacement is an ongoing process in the body, hereditary disorders and certain diseases can accelerate blood cell destruction, resulting in anemia. However, excessive bleeding is the most common cause of severe anemia, and the speed with which blood loss occurs has a significant effect on the severity of symptoms. Chronic blood loss may be a consequence of the following:
Acute blood loss may occur as a result of injury, a ruptured blood vessel, or a complication of surgery or childbirth. When a lot of blood is lost within a short time, blood pressure and the amount of oxygen in the body drop suddenly, sometimes leading to heart failure or death. Loss of even one third of the body's blood volume in the space of several hours can be fatal. Gradual blood loss is less threatening, because the body has time to replace RBCs and blood volume.
Symptoms
Weakness, fatigue, and a run-down feeling may be the first signs of anemia. Pasty or sallow skin color, or the absence of color in the gums, nail beds, creases of the palm, or lining of the eyelids are other signs of anemia. Individuals who appear to be weak, easily tired, often out of breath, and who may feel faint or dizzy on movement may be severely anemic.
Other symptoms of anemia may include the following:
Demographics
Acquired anemias affect about 4 million individuals in the United States, and over 50 percent of these are under age 45, although less than 10 percent of cases occur in children and adolescents. In the United States, iron deficiency anemia is the most prevalent type of anemia, affecting about 240,000 toddlers between one and two years of age and 3.3 million women of childbearing age. Anemia due to gradual blood loss is more common in women than in men, particularly pregnant women or women of menstruating age. Pernicious anemia is more common in women and in African Americans and is less common in other racial groups. Folate deficiency is not common in young people who eat an adequate diet and is usually associated with malnutrition, pregnancy, and alcoholism. Sickle cell anemia is more frequently diagnosed than thalassemias and occurs most often among African Americans. Thalassemia occurs in four out of 100,000 individuals in the United States, particularly among those of Mediterranean, Asian, or middle Eastern descent.
When to Call the Doctor
When a child exhibits weakness, dizziness, listlessness, or fatigue, it may be the first sign of anemia. The pediatrician should be consulted if the child is also extremely pale or has little or no color in the gums, nail beds, creases of the palm, or lining of the eyelids. Any prolonged bleeding or sudden blood loss requires examination by a physician and testing for anemia.
Diagnosis
The child's medical history will be taken, including the child's age, symptoms, illnesses, and general state of health, and a family history of ancestry and known inherited anemias will be noted. Symptoms noticed in children by their parents may include fatigue, weight loss, inability to concentrate, loss of appetite, and light-headedness when standing up. The physical examination may reveal paleness, lack of color in the creases of the palm, gums, and the linings of the eyelids. The child's breathing rate may be increased and, in advanced cases, the spleen or liver may be enlarged when palpated. If anemia is due to chronic disease, there may be evidence of infection or inflammation. Urine output may be reduced in severe anemia.
Diagnostic testing begins with a complete blood count (CBC) and differential to reveal the RBC count, white blood cell (WBC) count, hemoglobin (Hgb), and hematocrit (Hct); any of these counts can be altered, and in most anemias the RBC and hemoglobin will be reduced. The mean corpuscular volume (MCV) will be measured to compare the size of RBCs with normal RBCs. A reticulocyte (young RBCs) count will help determine if anemia is caused by impaired RBC production or increased RBC destruction. Iron, vitamin C, vitamin B12, and folate levels will be measured to evaluate and identify possible deficiencies. Diagnosing thalassemia and sickle cell anemia, both of which involve disorders of hemoglobin, will require measuring the different types of hemoglobin through a laboratory testing method called hemoglobin electrophoresis. In some anemias, a bone marrow sample will be removed (bone marrow biopsy) for microscopic examination, especially to confirm iron deficiency anemia or the megaloblastic anemias. Kidney function tests, coagulation tests, and stool examinations for occult blood may also be performed.
Treatment
Surgery may be necessary to correct blood losses caused by injury or hemorrhage (nose bleeds, aneurysm, cerebral hemorrhage, bleeding ulcer) or childbirth. Transfusions of packed red blood cells or whole blood may also be used to replace blood volume and to stimulate the body's own production of red blood cells. Medication or surgery may also be necessary to control heavy menstrual flow or to remove polyps (growths or nodules) from the bowels.
Anemia due to nutritional deficiencies can usually be treated with iron replacement therapy, specific vitamin supplements, or self-administered injections of vitamin B12. People with folic acid anemia may be advised to take oral folic acid.
Vitamin B12 deficiency anemia requires a life-long regimen of B12 shots to maintain vitamin levels and control symptoms of pernicious anemia. The patient may be advised to limit physical activity until treatment restores strength and balance.
Anemia resulting from chronic disease is typically corrected by treating the underlying illness. This type of anemia rarely becomes severe. If it does, transfusions or hormone treatments to stimulate red blood cell production may be given.
Thalassemia minor is typically not treated. Thalassemia major may be treated with regular transfusions, surgical resection of the spleen to avoid its removal of RBCs from circulation, and sometimes iron chelation therapy. Symptoms are treated as they occur. Children or young adults with thalassemia major may require periodic hospitalization to receive blood transfusions or, in some cases, bone marrow transplants.
Sickle cell anemia will be monitored by regular eye examinations and diagnostic blood work. Immunizations for pneumonia and infectious diseases are part of treatment along with prompt treatment for sickle cell crises and infections of any kind. Psychotherapy or counseling may help older children deal with the emotional symptoms characteristic of this condition.
Children with aplastic anemia are especially susceptible to infection. Treatment for aplastic anemia may involve blood transfusions and bone marrow transplantation to replace malfunctioning cells with healthy ones.
Hemolytic anemia of the warm-antibody type may be treated with large doses of intravenous and oral corticocosteroids (cortisone). Individuals who do not respond to medical therapy, may undergo surgery to remove the spleen, which controls the anemia in some individuals by helping to add more RBCs to the circulation. Immune-system suppressants are prescribed when surgery is not successful. There is no specific treatment for cold-anti-body hemolytic anemia.
Treatment of newborn anemia depends on the severity of symptoms, the level of Hgb, and the presence of any other diseases that may affect oxygen delivery, such as lung or heart disease or hyaline membrane disease. Transfusions may be given in certain situations or exchange transfusions if hemolytic disease of the newborn is not quickly resolved. The risk of transfusion (such as transfusion reactions, potential toxins, and infections such as HIV or hepatitis) are carefully weighed against the severity of the anemia in the infant.
Alternative Treatment
Vitamin C is noted for helping to absorb iron and folate supplements. Cooking in a cast iron skillet may leach small amounts of absorbable iron into the diet. Folic acid can be readily absorbed from raw salad greens such as lettuce, spinach, arugula, alfalfa sprouts, and others. Blackstrap molasses is a good source of iron and B vitamins. Herbal supplements that will benefit individuals who have anemia include bilberry, dandelion, goldenseal, mullein, nettle, Oregon grape root, red raspberry, and yellow dock. Herbs are available as tinctures and teas or in capsules.
Nutritional Concerns
The diet is a ready source of nutrients that prevent and treat anemia. Children with anemia can include more of these nutrients in their diet by eating a broad variety of whole grains, fruits and vegetables, beans, lean meat, poultry and fish, and supplementing the diet regularly with vitamins, minerals, and iron (as recommended). Pediatricians should be consulted before iron supplements are taken, however, because of the difficulty in absorbing non-food sources of iron. Vitamin C can stimulate iron absorption. Good food sources of iron include: almonds, broccoli, dried beans, raisins, dried apricots, seaweed (as soup stock), whole-grain breads and cereals, brown rice, lean red meat, liver, potatoes, poultry, and shellfish.
Because light and heat destroy folic acid, fruits and vegetables should be eaten raw or cooked as little as possible to help assimilation of folic acid. Folic acid can also be taken as a supplement.
Prognosis
Most anemias can be treated or managed. The prognosis for anemias generally depends upon the severity of the anemia, the type of anemia, and the response to treatment. The hereditary anemias, such as the thalassemias and sickle cell anemia, may require life-long treatment and monitoring whereas other types of anemia, once treated, are apt not to recur. Thalassemia major may cause deformities and may shorten life expectancy. Severe anemia may lead to other serious conditions, particularly if oxygen delivery is compromised for long periods of time or RBC destruction is more rapid than can be controlled by normal RBC replacement or specific treatment. Severe blood loss or prolonged anemia can result in life-threatening complications.
Prevention
Safety is the primary preventive measure for blood loss by injury. A wholesome, balanced diet rich in nutrients can help prevent dietary deficiencies that lead to anemia. Hereditary anemias cannot be prevented; parents can seek genetic testing and counseling if they are concerned about inherited anemias noted in their families or ethnic background.
Nutritional Concerns
Sources of iron such as liver, red meat, whole grains, and poultry may help maintain hemoglobin levels and reduce the likelihood of deficiency-related anemias. Vitamin C is noted for helping to improve assimilation of iron taken as supplements.
Parental Concerns
Parents may be particularly concerned about the possibility of inherited anemias. Genetic testing is available to address their doubts. Nutrition education is readily available from public health sources, books, and the reliable Internet sources for parents who are concerned about providing essential nutrients for children who may be susceptible to deficiency anemias. Regular physical examinations can help evaluate a child's overall health and reveal possible signs or symptoms of anemia.
Resources
Books
"Blood Disorders." The Merck Manual of Medical Information, 2nd Home ed. Edited by Mark H. Beers et al. White House Station, NJ: Merck & Co., 2003.
Hill, Shirley, A. Managing Sickle Cell Disease in Low-Income Families. Philadelphia: Temple University Press, 2003.
Lande, Bruce. Aplastic Anemia and Other Autoimmune Diseases: Help Your Body Heal Itself. Syracuse, NY: Action Enterprises, 2003.
Ross, Allison J. Everything You Need to Know about Anemia. New York: Rosen Publishing Group, 2001.
Wick, M., et al. Iron Metabolism, Anemias, Clinical Aspects and Laboratory. New York: Springer, 2003.
Organizations
National Heart, Lung, and Blood Institute (NHLBI). 6701 Rockledge Drive, PO Box 30105, Bethesda, MD 20824–0105. Web site:
Web Sites
"Anemia." KidsHealth. Available online at
"Understanding Anemia: Your Life May Depend on It." Anemia Lifeline. Available online at www.anemia.com (accessed October 10, 2004).
[Article by: L. Lee Culvert Maureen Haggerty]
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Pernicious Anemia Pernicious anemia is a common cause of cobalamin/vitamin B deficiency. It is primarily a disease of the elderly and caused by an abnormality in the immune system where the body creates antibodies to intrinsic factor (a substance that facilitates absorption of vitamin B) or to the cells in the stomach that secrete it. The lack of intrinsic factor B leads to vitamin B deficiency. It can also be caused by physiologic or anatomic disturbances of the stomach that might prevent intrinsic factor secretion. In children, an atypical and rare form of pernicious anemia can be inherited. It is an autosomal recessive disorder that results in an inability to secrete intrinsic factor, and it presents with anorexia, weakness, a painful red tongue, and neurologic abnormalities. |
| Type | Lab values | Causes |
| Macrocytic, normochromic | MCV: > 100fl MCHC: 34 | Vitamin B deficiency, folate deficiency, vitamin C deficiency, chemotherapy (megaloblastic marrow); aplastic anemia, hypothyroidism (normoblastic marrow) |
| Microcytic, hypochromic | MCV: < 80 MCHC: < 30 | Iron deficiency, thalassemia, sideroblastic anemia, chronic lead poisoning, anemia of chronic illness |
| Normocytic, normochromic | MCV: 80–99fl MCHC: 34 + / -2 | Iron deficiency (early), chronic disease |
| MCV: mean corpuscular volume MCHS: mean corpuscular hemoglobin concentration fl: femtoliter (one quadrillionth of a liter) | ||
One of the most common anemias, iron-deficiency anemia, is caused by insufficient iron, an element essential for the formation of hemoglobin in the erythrocytes. In most adults (except pregnant women) the cause is chronic blood loss rather than insufficient iron in the diet, and, therefore, the treatment includes locating the source of abnormal bleeding in addition to the administration of iron.
Pernicious anemia causes an increased production of erythrocytes that are structurally abnormal and have attenuated life spans. This condition rarely occurs before age 35 and is inherited, being more prevalent among persons of Scandinavian, Irish, and English extraction. It is caused by the inability of the body to absorb vitamin B12 (which is essential for the maturation of erythrocytes).
There are several conditions that cause the destruction of erythrocytes, thereby producing anemia. Allergic-type reactions to bacterial toxins and various chemical agents, among them sulfonamides and benzene, can cause hemolysis, which requires emergency treatment. In addition, there are unusual situations in which the body produces antibodies against its own erythrocytes; the mechanism triggering such reactions remains obscure.
There are several inherited anemias that are more common among dark-skinned people. Sickle cell disease is inherited as a recessive trait almost exclusively among blacks; the condition is characterized by a chemical abnormality of the hemoglobin molecule that causes the erythrocytes to be misshapen. In 1957 Vernon Ingram determined the amino acid sequence of hemoglobin, and found the beta-globins (which is one of the two polypeptide chain types) that are found in the tetrameric (four-chain) hemoglobin protein. In sickle cell disease a single mutation produces the amino acid valine instead of glutamic acid in one of the protein chain types that make up the hemoglobin molecule.
In thalassemia major (Cooley's anemia), which is the most serious of the hereditary anemias among people of Mediterranean, Middle Eastern, and S Chinese ancestry, the erythrocytes are abnormally shaped. Symptoms include enlarged liver and spleen and jaundice. Thalassemia major usually causes death before adulthood is reached.
Any disease or injury to the bone marrow can cause anemia, since that tissue is the site of erythrocyte synthesis. Bone marrow destruction can also be caused by irradiation, disease, or various chemical agents. In cases of renal dysfunction, the severity of the associated anemia correlates highly with the extent of the dysfunction; it is treated with genetically engineered erythropoietin.
A condition in which the capacity of the blood to carry oxygen is decreased because of too few red blood cells in circulation or because of too little hemoglobin.
Did Paul know that he had anemia?
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Anemia is a disease of the blood that has come, in some quarters, to be associated with vampirism. Anemia is caused by a reduction of either red blood cells or hemoglobin (the oxygen-carrying pigment of the cells) relative to the other ingredients in the blood. The symptoms include a pale complexion, fatigue, and in its more extreme instances, fainting spells. All are symptoms usually associated with a vampire attack. In Bram Stoker's novel, Dracula during the early stages of Lucy Westenra's illness, Dr. John Seward hypothesized that possibly she was suffering from anemia. He later concluded that she was not suffering from the loss of red blood cells, but from the loss of whole blood. Dr. Abraham Van Helsing agreed with his friend, "I have made careful examination, but there is no functional cause. With you I agree that there has been much blood lost; it has been, but is not. But the conditions of her are in no way anaemic." (Chapter 9) Thus, the association of anemia and vampirism was dismissed.
A reduction below normal in the number or volume of erythrocytes or in the quantity of hemoglobin in the blood. Clinically it is manifested by weakness, exercise intolerance, hyperpnea which is only moderate, pallor of mucosae, tachycardia and a large increase in the intensity of the heart sounds. There are often accompanying signs related to the site of blood or hemoglobin loss.
A term indicating that the concentration of hemoglobin or the number of red blood cells is below the accepted normal value with respect to age and sex. In true anemia the total concentration of hemoglobin, or the total number of erythrocytes, is below normal regardless of concentration values. Symptoms, which may not be evident, include weakness, pallor, anorexia, and those related to the cause of the anemia.

| Anemia | |
|---|---|
| Classification and external resources | |
| ICD-10 | D50-D64 |
| ICD-9 | 280-285 |
| DiseasesDB | 663 |
| MedlinePlus | 000560 |
| eMedicine | med/132 emerg/808 emerg/734 |
| MeSH | D000740 |
Anemia (/əˈniːmiə/; also spelled anaemia and anæmia; from Ancient Greek: ἀναιμία anaimia, meaning lack of blood) is a decrease in number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.[1][2] However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency.
Because hemoglobin (found inside RBCs) normally carries oxygen from the lungs to the tissues, anemia leads to hypoxia (lack of oxygen) in organs. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences.
Anemia is the most common disorder of the blood. There are several kinds of anemia, produced by a variety of underlying causes. Anemia can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, and discernible clinical spectra, to mention a few. The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis).
There are two major approaches to diagnosis: the "kinetic" approach which involves evaluating production, destruction and loss,[3] and the "morphologic" approach which groups anemia by red blood cell size. The morphologic approach uses a quickly available and low cost lab test as its starting point (the MCV). On the other hand, focusing early on the question of production may allow the clinician to expose cases more rapidly where multiple causes of anemia coexist.
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Anemia goes undetermined in many people, and symptoms can be minor or vague. The signs and symptoms can be related to the anemia itself, or the underlying cause.
Most commonly, people with anemia report non-specific symptoms of a feeling of weakness, or fatigue, general malaise and sometimes poor concentration. They may also report dyspnea (shortness of breath) on exertion. In very severe anemia, the body may compensate for the lack of oxygen-carrying capability of the blood by increasing cardiac output. The patient may have symptoms related to this, such as palpitations, angina (if preexisting heart disease is present), intermittent claudication of the legs, and symptoms of heart failure.
On examination, the signs exhibited may include pallor (pale skin, mucosal linings and nail beds) but this is not a reliable sign. There may be signs of specific causes of anemia, e.g., koilonychia (in iron deficiency), jaundice (when anemia results from abnormal break down of red blood cells — in hemolytic anemia), bone deformities (found in thalassemia major) or leg ulcers (seen in sickle-cell disease).
In severe anemia, there may be signs of a hyperdynamic circulation: tachycardia (a fast heart rate), bounding pulse, flow murmurs, and cardiac ventricular hypertrophy (enlargement). There may be signs of heart failure.
Pica, the consumption of non-food based items such as dirt, paper, wax, grass, ice, and hair, may be a symptom of iron deficiency, although it occurs often in those who have normal levels of hemoglobin.
Chronic anemia may result in behavioral disturbances in children as a direct result of impaired neurological development in infants, and reduced scholastic performance in children of school age.
Restless legs syndrome is more common in those with iron-deficiency anemia.
Less common symptoms may include swelling of the legs or arms, chronic heartburn, vague bruises, vomiting, increased sweating, and blood in stool.
Anemia is typically diagnosed on a complete blood count. Apart from reporting the number of red blood cells and the hemoglobin level, the automatic counters also measure the size of the red blood cells by flow cytometry, which is an important tool in distinguishing between the causes of anemia. Examination of a stained blood smear using a microscope can also be helpful, and is sometimes a necessity in regions of the world where automated analysis is less accessible.
In modern counters, four parameters (RBC count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, MCH and MCHC) to be calculated, and compared to values adjusted for age and sex. Some counters estimate hematocrit from direct measurements.
| Age or gender group | Hb threshold (g/dl) | Hb threshold (mmol/l) |
|---|---|---|
| Children (0.5–5.0 yrs) | 11.0 | 6.8 |
| Children (5–12 yrs) | 11.5 | 7.1 |
| Teens (12–15 yrs) | 12.0 | 7.4 |
| Women, non-pregnant (>15yrs) | 12.0 | 7.4 |
| Women, pregnant | 11.0 | 6.8 |
| Men (>15yrs) | 13.0 | 8.1 |
Reticulocyte counts, and the "kinetic" approach to anemia, have become more common than in the past in the large medical centers of the United States and some other wealthy nations, in part because some automatic counters now have the capacity to include reticulocyte counts. A reticulocyte count is a quantitative measure of the bone marrow's production of new red blood cells. The reticulocyte production index is a calculation of the ratio between the level of anemia and the extent to which the reticulocyte count has risen in response. If the degree of anemia is significant, even a "normal" reticulocyte count actually may reflect an inadequate response.
If an automated count is not available, a reticulocyte count can be done manually following special staining of the blood film. In manual examination, activity of the bone marrow can also be gauged qualitatively by subtle changes in the numbers and the morphology of young RBCs by examination under a microscope. Newly formed RBCs are usually slightly larger than older RBCs and show polychromasia. Even where the source of blood loss is obvious, evaluation of erythropoiesis can help assess whether the bone marrow will be able to compensate for the loss, and at what rate.
When the cause is not obvious, clinicians use other tests: ESR, ferritin, serum iron, transferrin, RBC folate level, serum vitamin B12, hemoglobin electrophoresis, renal function tests (e.g. serum creatinine).
When the diagnosis remains difficult, a bone marrow examination allows direct examination of the precursors to red cells.
In the morphological approach, anemia is classified by the size of red blood cells; this is either done automatically or on microscopic examination of a peripheral blood smear. The size is reflected in the mean corpuscular volume (MCV). If the cells are smaller than normal (under 80 fl), the anemia is said to be microcytic; if they are normal size (80–100 fl), normocytic; and if they are larger than normal (over 100 fl), the anemia is classified as macrocytic. This scheme quickly exposes some of the most common causes of anemia; for instance, a microcytic anemia is often the result of iron deficiency. In clinical workup, the MCV will be one of the first pieces of information available; so even among clinicians who consider the "kinetic" approach more useful philosophically, morphology will remain an important element of classification and diagnosis.
The "kinetic" approach to anemia yields what many argue is the most clinically relevant classification of anemia. This classification depends on evaluation of several hematological parameters, particularly the blood reticulocyte (precursor of mature RBCs) count. This then yields the classification of defects by decreased RBC production versus increased RBC destruction and/or loss. Clinical signs of loss or destruction include abnormal peripheral blood smear with signs of hemolysis; elevated LDH suggesting cell destruction; or clinical signs of bleeding, such as guaiac-positive stool, radiographic findings, or frank bleeding.
The following is a simplified schematic of this approach:
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Anemia |
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Reticulocyte production index shows inadequate production response to anemia. |
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Reticulocyte production index shows appropriate response to anemia = ongoing hemolysis or blood loss without RBC production problem. |
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No clinical findings consistent with hemolysis or blood loss: pure disorder of production. |
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Clinical findings and abnormal MCV: hemolysis or loss and chronic disorder of production*. |
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Clinical findings and normal MCV= acute hemolysis or loss without adequate time for bone marrow production to compensate**. |
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Macrocytic anemia (MCV>100) |
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Normocytic anemia (80<MCV<100) |
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Microcytic anemia (MCV<80) |
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* For instance, sickle cell anemia with superimposed iron deficiency; chronic gastric bleeding with B12 and folate deficiency; and other instances of anemia with more than one cause.
** Confirm by repeating reticulocyte count: ongoing combination of low reticulocyte production index, normal MCV and hemolysis or loss may be seen in bone marrow failure or anemia of chronic disease, with superimposed or related hemolysis or blood loss.
Here is a schematic representation of how to consider anemia with MCV as the starting point:
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Macrocytic anemia (MCV>100) |
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Normocytic anemia (MCV 80–100) |
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High reticulocyte count |
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Other characteristics visible on the peripheral smear may provide valuable clues about a more specific diagnosis; for example, abnormal white blood cells may point to a cause in the bone marrow.
Microcytic anemia is primarily a result of hemoglobin synthesis failure/insufficiency, which could be caused by several etiologies:
Iron deficiency anemia is the most common type of anemia overall and it has many causes. RBCs often appear hypochromic (paler than usual) and microcytic (smaller than usual) when viewed with a microscope.
Macrocytic anemia can be further divided into "megaloblastic anemia" or "non-megaloblastic macrocytic anemia". The cause of megaloblastic anemia is primarily a failure of DNA synthesis with preserved RNA synthesis, which result in restricted cell division of the progenitor cells. The megaloblastic anemias often present with neutrophil hypersegmentation (6–10 lobes). The non-megaloblastic macrocytic anemias have different etiologies (i.e. there is unimpaired DNA globin synthesis,) which occur, for example in alcoholism.
In addition to the non-specific symptoms of anemia, specific features of vitamin B12 deficiency include peripheral neuropathy and subacute combined degeneration of the cord with resulting balance difficulties from posterior column spinal cord pathology.[11] Other features may include a smooth, red tongue and glossitis.
The treatment for vitamin B12-deficient anemia was first devised by William Murphy who bled dogs to make them anemic and then fed them various substances to see what (if anything) would make them healthy again. He discovered that ingesting large amounts of liver seemed to cure the disease. George Minot and George Whipple then set about to isolate the curative substance chemically and ultimately were able to isolate the vitamin B12 from the liver. All three shared the 1934 Nobel Prize in Medicine.[12]
Normocytic anemia occurs when the overall hemoglobin levels are decreased, but the red blood cell size (mean corpuscular volume) remains normal. Causes include:
When two or more causes of anemia act simultaneously, e.g., macrocytic hypochromic, due to hookworm infestation leading to deficiency of both iron and vitamin B12 or folic acid [13] or following a blood transfusion more than one abnormality of red cell indices may be seen. Evidence for multiple causes appears with an elevated RBC distribution width (RDW), which suggests a wider-than-normal range of red cell sizes.
Heinz bodies form in the cytoplasm of RBCs and appear like small dark dots under the microscope. There are many causes of Heinz body anemia, and some forms can be drug induced. It is triggered in cats by eating onions[14] or acetaminophen (paracetamol). It can be triggered in dogs by ingesting onions or zinc, and in horses by ingesting dry red maple leaves.
Hyperanemia is a severe form of anemia, in which the hematocrit is below 10%.
Refractory anemia is an anemia which does not respond to treatment.[15] It is often seen secondary to myelodysplastic syndromes.[16]
Iron deficiency anemia may also be refractory as a clinical manifestation of gastrointestinal problems which disrupt iron metabolism. [17]
WHO Grading of anemia:[18][19]
National Cancer Institute Grading of Anemia:[20]
Broadly, causes of anemia may be classified as impaired red blood cell (RBC) production, increased RBC destruction (hemolytic anemias), blood loss and fluid overload (hypervolemia). Several of these may interplay to cause anemia eventually. Indeed, the most common cause of anemia is blood loss, but this usually doesn't cause any lasting symptoms unless a relatively impaired RBC production develops, in turn most commonly by iron deficiency.[21] (See Iron deficiency anemia)
Anemias of increased red blood cell destruction are generally classified as hemolytic anemias. These are generally featuring jaundice and elevated LDH levels.
Fluid overload (hypervolemia) causes decreased hemoglobin concentration and apparent anemia:
Treatments for anemia depend on severity and cause.
Iron deficiency from nutritional causes is rare in men and post-menopausal women. The diagnosis of iron deficiency mandates a search for potential sources of loss such as gastrointestinal bleeding from ulcers or colon cancer. Mild to moderate iron-deficiency anemia is treated by oral iron supplementation with ferrous sulfate, ferrous fumarate, or ferrous gluconate. When taking iron supplements, it is very common to experience stomach upset and/or darkening of the feces. The stomach upset can be alleviated by taking the iron with food; however, this decreases the amount of iron absorbed. Vitamin C aids in the body's ability to absorb iron, so taking oral iron supplements with orange juice is of benefit.
Vitamin supplements given orally (folic acid) or intramuscularly (vitamin B-12) will replace specific deficiencies.
In anemia of chronic disease, anemia associated with chemotherapy, or anemia associated with renal disease, some clinicians prescribe recombinant erythropoietin, epoetin alfa, to stimulate red-cell production.
In severe cases of anemia, or with ongoing blood loss, a blood transfusion may be necessary.
Doctors attempt to avoid blood transfusion in general, since multiple lines of evidence point to increased adverse patient clinical outcomes with more intensive transfusion strategies. The physiological principle that reduction of oxygen delivery associated with anemia leads to adverse clinical outcomes is balanced by the finding that transfusion does not necessarily mitigate these adverse clinical outcomes.
In severe, acute bleeding, transfusions of donated blood are often lifesaving. Improvements in battlefield casualty survival is attributable, at least in part, to the recent improvements in blood banking and transfusion techniques.[citation needed]
Transfusion of the stable but anemic hospitalized patient has been the subject of numerous clinical trials.
Four randomized controlled clinical trials have been conducted to evaluate aggressive versus conservative transfusion strategies in critically ill patients. All four of these studies failed to find a benefit with more aggressive transfusion strategies.[28][29][30][31]
In addition, at least two retrospective studies have shown increases in adverse clinical outcomes in critically ill patients that underwent more aggressive transfusion strategies.[32][33]
Treatment of exceptional blood loss (anemia) is recognized as an indication for hyperbaric oxygen (HBO) by the Undersea and Hyperbaric Medical Society.[34][35] The use of HBO is indicated when oxygen delivery to tissue is not sufficient in patients who cannot be transfused for medical or religious reasons. HBO may be used for medical reasons when threat of blood product incompatibility or concern for transmissible disease are factors.[34] The beliefs of some religions (ex: Jehovah's Witnesses) may require they use the HBO method.[34]
In 2002, Van Meter reviewed the publications surrounding the use of HBO in severe anemia and found that all publications report a positive result.[36]
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This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
Dansk (Danish)
n. - anæmi, blodmangel
Nederlands (Dutch)
bloedarmoede
Deutsch (German)
n. - Blutarmut, Anämie
Ελληνική (Greek)
n. - (παθολ.) αναιμία
Português (Portuguese)
n. - anemia (f) (Med.)
Svenska (Swedish)
n. - blodbrist
中文(简体)(Chinese (Simplified))
贫血, 贫血症
中文(繁體)(Chinese (Traditional))
n. - 貧血, 貧血症
idioms:
العربيه (Arabic)
(الاسم) انيميا : فقر الدم
עברית (Hebrew)
n. - חוסר-דם, מיעוט-דם, אנמיה
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