anemia

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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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A condition that arises when the amount of haemoglobin, the oxygen-carrying pigment of the red blood cells, is reduced. Those affected are pale, constantly feel tired, become breathless on exertion, and have poor resistance to infection. There are many causes. Iron-deficiency anaemia (see iron) may be due to loss of blood or lack of dietary iron. Haemolytic anaemias result from the increased destruction of red blood cells; this occurs, for example, in haemolytic disease of the newborn, in which the red cells of the fetus are destroyed by antibodies in the mother's blood (see anti-D (Rh₀) immunoglobulin). Anaemia can also occur when the production of red cells is impaired. This may be due to a deficiency of the factors necessary for red cell production, such as vitamin B₁₂ or intrinsic factor (causing pernicious anaemia; see vitamin B complex), folic acid, or erythropoietin, or by suppression of red cell production in the bone marrow, which occurs in leukaemia (see cancer). Such anaemias are characterized by the presence of abnormal red blood cells; for example megaloblasts are present in the bone marrow in folic acid or vitamin B₁₂ deficiency (megaloblastic anaemias). In aplastic anaemia the numbers of red blood cells are very much reduced due to failure of the bone marrow to produce them.

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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:

• recent severe illness
• long-term exposure to industrial chemicals
• chemotherapy, use of anticancer drugs, and certain other medications

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:

• cancer
• gastrointestinal tumors
• diverticulosis
• polyposis
• heavy or frequent menstrual flow
• hemorrhoids
• nosebleeds
• stomach ulcers
• long-standing alcohol abuse

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:

• unusual cravings for ice (chewing on ice cubes), paint, or earth (actually eating dirt)
• headache
• inability to concentrate, memory loss
• inflammation of the mouth (stomatitis) or tongue (glossitis)
• insomnia
• irregular heartbeat
• loss of appetite
• dry, brittle, or ridged nails
• rapid breathing
• sores in the mouth, throat, or rectum
• perspiration, especially around the head and neck
• swelling of hands and feet
• constant thirst
• ringing in the ears (tinnitus)
• unexplained bleeding or bruising
• angina pectoris, i.e., chest pain accompanied by a choking sensation that may provoke anxiety

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 (accessed October 10, 2004).

"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.

Anemia affects more than 30 percent of the world's population, and it is one of the most important worldwide health problems. It has a significant prevalence in both developing and industrialized nations. Causes of anemia include nutritional deficiencies, particularly of iron, vitamin B, and folate (folic acid); excess blood loss from menstruation or chronic illness and infection; ingestion of toxic substances, such as lead, ethanol, and other compounds; and genetic abnormalities such as thalassemia and sideroblastosis.

Anemia is caused by a deficiency in the intake and absorption elements required to make red blood cells. The condition is defined as one in which the blood is deficient in red blood cells, in hemoglobin, or in total volume. This results in blood that is incapable of meeting the oxygen needs of the body's tissues. Anemia is characterized by changes in the size and color of red blood cells. Red blood cells, or erythrocytes, are primarily responsible for oxygen transport from the lungs to the body's many cells. Hemoglobin is an oxygen-carrying protein in the red blood cell that incorporates iron into its structure. Therefore, iron is an essential building block of blood erythrocytes. When red blood cells are larger than normal, the anemia is termed macrocytic, and when they are smaller than normal, it is called microcytic. Normal red cell color is termed normochromic, and if the red cells appear pale, the anemia is called hypochromic. When extensive lab testing is not available for diagnosis, the use of a portable colorimeter can be used to detect anemia.

Iron-Deficiency Anemia
Anemia in the developing world is most commonly caused by an iron deficiency, which affects up to 50 percent of the population in some countries. Iron deficiency not only impairs the production of red cells in the blood, but also affects general cell growth and proliferation in tissues like the nervous system and the gastrointestinal tract. Red cells in a patient with iron-deficiency anemia are both microcytic and hypochromic.

Iron deficiency affects young children, adolescents, and women of reproductive age—three periods of rapid growth during which the body's iron needs are higher than normal. In children, iron requirements are highest between the ages of six and eighteen months, and can be ten times the requirement of a normal adult. Iron is commonly absorbed from both human milk and cow's milk, and, if consumed in good quantities, these sources can meet the body's iron needs. A deficiency can result from inadequate intake, or it can occur if milk remains the sole source of a child's nutrition after the age of four months, when iron needs exceed that provided by milk alone. Research in Chile has shown that 40 percent of children whose main source of nutrition was breast milk developed iron-deficiency anemia. Such children can appear tired and inattentive, and they can suffer from delayed motor development. Some children can even develop mild to moderate mental retardation as a result of iron-deficiency anemia. Recent research has shown that iron-deficiency anemia can also contribute to emotional development problems, with malnourished children acting more irritable and fussy.

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)

Pregnant women can have up to double the requirement of iron for a normal adult, with the majority of the mother's iron being transferred to her growing fetus. Adult diets in most of the developing world tend to be iron-poor, and a low dietary intake can result in iron deficiency. Deficiency can also occur as a result of poor iron absorption due to gastrointestinal pathology, blood loss due to normal menstruation, blood loss from parasitic infections such as hookworm and malaria, and blood loss from chronic diarrhea—all of which are common in developing countries.

Other Causes
The two other primary causes of nutritional anemia are deficiencies in vitamin B and folic acid, both of which are necessary for the production of DNA, RNA, and protein. Without these necessary factors, red blood cells can develop abnormally, or even die prematurely in the bone marrow where they are made. This leads to what is known as megaloblastic anemia.

Folate deficiency is most often caused by poor intestinal absorption or low intake of folate-rich foods, such as human milk, cow's milk, fruits, green vegetables, and certain meats. It is also caused by congenital defects in intestinal absorption. Just as with iron, folic acid requirements are highest during periods of rapid growth, particularly infancy and pregnancy. Folate-deficient children present with common symptoms of anemia, as well as chronic diarrhea. Folate deficiency can also occur with kwashiorkor or marasmus. If it occurs during pregnancy, folate deficiency can lead to neural tube defects, spontaneous abortions, and prematurity.

Vitamin B, derived from a substance called cobalamin, is mainly found in meats and other animal products—humans cannot synthesize this vitamin on their own. A good amount of its absorption depends on the presence of a substance called intrinsic factor (see sidebar). It does not normally occur with kwashiorkor or marasmus. Both folate and vitamin B deficiencies have also been linked to cardiovascular disease, mood disorders, and increased frequency of chromosomal breaks (which may contribute to the development of cancer).

Treatment
Each of the important causes of nutritional anemia can be eradicated through prevention and treatment. Many countries have begun this process by instituting food supplementation programs in which grains and cereals are fortified with iron, folate, or vitamin B. Given adequate resources, these deficiencies can also be ameliorated with direct oral supplements of absorbable iron, vitamin B, and folic acid. Injectable forms of iron are also available. It has been found that the supplementation of vitamin A to at-risk populations improves anemia more efficiently than iron supplementation alone.

Treatment plans must also focus on the causes of anemia and therefore must include sanitation, treatment of infections such as malaria and HIV, and, most important, treatment of intestinal parasites. Much work is needed to address general malnutrition—not only concerning these deficiencies, but also other commonly occurring ones (e.g., vitamin A, zinc, copper, calcium). Programs dedicated to decreasing the rates of infection and illness in developing countries—through health education, immunization, sanitation, and appropriate treatment—will also contribute to a lower incidence and prevalence of worldwide anemia.

See also Kwashiorkor; Malnutrition; Marasmus; Nutritional deficiency; Vitamins, water soluble.

Bibliography
Behrman, Robert E.; Kliegman, Robert M.; and Jenson, Hal B., eds. (2000). Nelson Textbook of Pediatrics, 16th edition. Philadelphia, PA: W. B. Saunders.
Hoffbrand, A. V., and Herbert, V. (1999). "Nutritional Anemias." Seminars in Hematology 36(4).
Isselbacher, Kurt J. (1994). Harrison's Textbook of Internal Medicine, 13th edition. New York: McGraw-Hill.
Pollitt, E. (2000). "Developmental Sequela from Early Nutritional Deficiencies: Conclusive and Probability Judgments." Journal of Nutrition 130.
Ramakrishnan, U., ed. (2001). Nutritional Anemias. Boca Raton, FL: CRC Press.
Rhoades, R. A., and Tanner, G. A. (1995). Medical Physiology. Boston: Little Brown.
Yip, R., and Ramakrishnan, U. (2002). "Experiences and Challenges in Developing Countries." Journal of Nutrition 132.

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(uh-nee-mee-uh)

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.

Because people suffering from anemia often appear weak and pale, the term is frequently used to describe general apathy or weakness: “The team's performance has been pretty anemic these past few weeks.”

IN BRIEF: A condition in which there are too few red blood cells.

Did Paul know that he had anemia?

LearnThatWord.com is a free vocabulary and spelling program where you only pay for results!

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.

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a variant spelling (esp. Brit.) of anemia.

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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.

• aplastic a. — a form of anemia generally unresponsive to specific antianemia therapy. It is often chronic, accompanied by granulocytopenia and thrombocytopenia, in which the bone marrow is usually acellular or hypoplastic. It may, however, be rapidly fatal. The term is actually all-inclusive and most probably encompasses several clinical syndromes. See pure red cell aplasia.
• autoimmune hemolytic a. — immune-mediated hemolytic anemia, which occurs in many species, particularly dogs, in which autoantibodies directed against red blood cells are produced. Different classes of immunoglobulins may be involved giving rise to differing clinical syndromes. Signs include pallor, lethargy, splenomegaly, and sometimes icterus, bilirubinuria and hemoglobinuria. There may also be an accompanying thrombocytopenia with bleeding tendencies. Diagnosis is based on a positive Coombs test.
• avian infectious a. — see chicken anemia.
• blood loss a. — see hemorrhagic anemia (below).
• a. of chronic disease — see anemia of inflammatory disease (below).
• cold antibody a. — an immune-mediated hemolytic anemia in which the antibody is maximally active at temperatures below 98.6°F (37°C). See also cold agglutinin disease.
• cold (or cold water) a. — a disease of cattle, especially calves, housed in warm barns and given near freezing water to drink. Dyspnea and the passage of red urine occur several hours after a large drink.
• Coombs-positive a. — immunoglobulin-mediated anemia that gives a positive reaction to Coombs tests, indicating the presence of immunoglobulins on the red cell surface. See also autoimmune hemolytic anemia (above), alloimmune hemolytic anemia of the newborn.
• deficiency a. — nutritional anemia.
• drug-induced hemolytic a. — some drugs such as quinine, quinidine, para-aminosalicylic acid, phenacetin, penicillin, insecticides, chlorpromazine, sulfonamides and dipyrone may be directly injurious to red cells or act to initiate an immune response in which red cells are destroyed.
• familial nonspherocytic a. of Basenji dogs — an inherited pyruvate kinase deficiency causes a hemolytic anemia with shortened red cell life span. In early stages, the disease is characterized by very active erythropoiesis but eventually, usually by the second or third year of life, a terminal myelofibrosis and osteosclerosis develops. The disease is inherited as an autosomal recessive trait.
• feline infectious a. — see feline infectious anemia.
• fragmentation a. — see microangiopathic anemia (below).
• Heinz body a. — hemolytic anemia resulting from oxidation of globin and formation of Heinz bodies, which are seen in blood smears as dark refractile intracytoplasmic bodies and stain with new methylene blue. Some common causes are ingestion of onions and plants in the Brassicaeae family, phenazopyridine, methylene blue and acetaminophen (paracetamol). Cats are particularly susceptible to Heinz body formation.
• hemolytic a. — see hemolytic anemia.
• hemorrhagic a. — is caused by loss of whole blood. If this is very rapid hypovolemic shock develops. At a slower rate there is anemic anoxia and the animal is suffering from anemia. Called also blood loss anemia.
• hypochromic a. — anemia in which the decrease in hemoglobin is proportionately much greater than the decrease in number of erythrocytes.
• hypoplastic a. — anemia due to incapacity of blood-forming organs, i.e. inactivity of the bone marrow. See also aplastic anemia (above).
• idiopathic immune a. — see autoimmune hemolytic anemia (above).
• infectious equine a. — see equine infectious anemia.
• a. of inflammatory disease — a nonregenerative, usually mild, anemia that occurs in association with malignancy or chronic infection. Although other causes of anemia such as hemolysis and blood loss may also occur with these conditions, there is altered iron metabolism with decreased serum iron and iron-binding capacity but with increased iron storage that results in decreased erythropoiesis.
• iron-deficiency a. — a form characterized by low or absent iron stores, low serum iron concentration, low transferrin saturation, elevated transferrin (iron-binding capacity), low hemoglobin concentration or hematocrit, and hypochromic, microcytic red blood corpuscles, and thrombocytosis. See also iron.
• isoimmune hemolytic a. — see alloimmune hemolytic anemia of the newborn.
• lizard viral a. — produces inclusion bodies in erythrocytes, commonly mistaken for protozoan parasites.
• macrocytic a. — anemia in which the erythrocytes are much larger than normal. The MCV (mean corpuscular volume) and MCH (mean corpuscular hemoglobin) are increased and the MCHC (mean corpuscular hemoglobin concentration) is normal.
• megaloblastic a. — anemia characterized by the presence of megaloblasts in the bone marrow and macrocytic erythrocytes. It occurs in vitamin B₁₂, cobalt and folic acid deficiencies and in some myeloproliferative disorders in cats.
• microangiopathic a. — anemia due to fragmentation of erythrocytes in blood vessels whose endothelium has been badly damaged, usually by an infectious disease such as septicemias, disseminated intravascular coagulation and salmonellosis. Called also fragmentation anemia.
• microcytic a. — anemia characterized by decrease in size of the erythrocytes.
• myelopathic a., myelophthisic a. — anemia due to destruction or crowding out of hematopoietic tissues by space-occupying lesions, neoplasms and fibrosis.
• nonregenerative a. — one occurring without an appropriate erythropoietic response by the bone marrow.
• normochromic a. — that in which the hemoglobin content of the red cells as measured by the MCHC and MCH is within the normal range.
• normocytic a. — the anemia in which the red blood cells are normal in size.
• nutritional a. — anemia due to a deficiency of an essential substance in the diet, which may be caused by poor dietary intake or by malabsorption; called also deficiency anemia. See also pyridoxine, vitamin b12, folic acid, copper, iron.
• parasitic a. — hemorrhagic anemia due to blood loss caused by blood-sucking parasites such as fleas, hookworms and Haemonchus contortus.
• pernicious a. — see pernicious anemia.
• physiological a. — the anemia which occurs as part of a natural event, e.g. in neonates.
• piglet a. — see iron nutritional deficiency.
• primary immune a. — see autoimmune hemolytic anemia (above).
• regenerative a., responsive a. — associated with active erythropoiesis with increased numbers of reticulocytes, nucleated red blood cells, anisocytosis and polychromasia in the peripheral blood.
• spur-cell a. — anemia in which the red cells have a bizarre spiculated shape and are destroyed prematurely, primarily in the spleen; it is an acquired form occurring in severe liver disease, and represents an abnormality in the cholesterol content of the red cell membrane.
• unresponsive a. — see nonregenerative anemia (above).

(ənē′mē-ə)
n

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.

For a list of words related to anemia, see:

• Afflictions and Conditions - anemia: reduced hemoglobin in blood, causing fatigue, breathlessness, and pallor

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See words rhyming with "anaemia."

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

Français (French)
n. - anémie

Deutsch (German)
n. - Blutarmut, Anämie

Ελληνική (Greek)
n. - (παθολ.) αναιμία

Italiano (Italian)
anemia

Português (Portuguese)
n. - anemia (f) (Med.)

Русский (Russian)
анемия

Español (Spanish)
n. - anemia

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

한국어 (Korean)
n. - 빈혈, 결핍

日本語 (Japanese)
n. - 貧血, 生気のなさ

idioms:

• sickle-cell anaemia/anemia    鎌状赤血球貧血

العربيه (Arabic)
‏(الاسم) انيميا : فقر الدم‏

עברית (Hebrew)
n. - ‮חוסר-דם, מיעוט-דם, אנמיה‬

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