Anemia, Hypochromic
Iron
alpha-Globins
Anemia, Refractory
Hemoglobins
Anemia, Sideroblastic
alpha-Thalassemia
Erythropoietin
Anemia, Iron-Deficiency
Erythrocyte Indices
Anemia, Aplastic
Ferritins
beta-Thalassemia
Erythropoiesis
Anemia, Hemolytic
Protoporphyrins
Transferrin
Reticulocytes
Erythrocytes, Abnormal
Fanconi Anemia
Thalassemia
Hemoglobin H
Erythrocytes
Anemia, Hemolytic, Autoimmune
Hepcidins
Receptors, Transferrin
Anemia, Macrocytic
Anemia, Pernicious
Renal Dialysis
Anemia, Sickle Cell
Anemia, Megaloblastic
Infectious Anemia Virus, Equine
Equine Infectious Anemia
Chicken anemia virus
Anemia, Dyserythropoietic, Congenital
Anemia, Diamond-Blackfan
Fanconi Anemia Complementation Group Proteins
Pregnancy Complications, Hematologic
Anemia, Neonatal
Hematinics
Anemia, Refractory, with Excess of Blasts
Fanconi Anemia Complementation Group C Protein
Fanconi Anemia Complementation Group D2 Protein
Hematocrit
Fanconi Anemia Complementation Group A Protein
The effect of chelating agents on iron mobilization in Chang cell cultures. (1/490)
The investigation of chelating agents with potential therapeutic value in patients with transfusional iron overload has been facilitated by the use of Chang cell cultures. These cells have been incubated with [59Fe]transferrin for 22 hr, following which most of the intracellular radioiron is found in the cytosol, distributed between a ferritin and a nonferritin form. Iron release from the cells depends on transferrin saturation in the medium, but when transferrin is 100% saturated, which normally does not allow iron release, desferrioxamine, 2,3-dihydroxybenzoic acid, rhodotorulic acid, cholythydroxamic acid, and tropolone all promote the mobilization of ferritin iron and its release from cells. They are effective to an approximately equal degree. The incubation of [59Fe]transferrin with tropolone in vitro at a molar ratio of 1:500 results in the transfer of most of the labeled iron to the chelator, reflecting the exceptionally high binding constant of this compound. How far these phenomena relate to therapeutic potentially remains to be seen. (+info)Evidence for and consequences of chronic heme deficiency in Belgrade rat reticulocytes. (2/490)
The Belgrade rat has a microcytic, hypochromic anemia inherited as an autosomal recessive trait (gene symbol b). Transferrin-dependent iron uptake is defective because of a mutation in Nramp2 (now DMT1, also called DCT1), the protein responsible for endosomal iron efflux. Hence, Belgrade reticulocytes are iron deficient. We show that a chromatographic method is able to measure the amount of 'free' heme in reticulocytes. Most of the 'free' heme is the result of biosynthesis. Succinylacetone, an inhibitor of heme synthesis, decreases the level of 'free' heme and cycloheximide, an inhibitor of globin synthesis, increases the 'free' heme level. In a pulse-chase experiment with 59Fe-transferrin, the 'free' heme pool behaves as an intermediate, with a half-life of just over 2 h. Belgrade reticulocytes contain about 40% as much 'free' heme as do heterozygous or homozygous reticulocytes. This deficiency of 'free' heme slows initiation of translation in Belgrade reticulocytes by increasing the level of an inhibitor of initiation. Thus the Belgrade rat makes a whole animal model available with chronic heme deficiency. (+info)Hypochromic red cells and reticulocyte haemglobin content as markers of iron-deficient erythropoiesis in patients undergoing chronic haemodialysis. (3/490)
BACKGROUND: In patients on chronic haemodialysis, because of a non-specific increase in serum ferritin, iron deficiency may be overlooked leading to failure of erythropoietin treatment. A reticulocyte haemglobin content < 26 pg and a percentage of hypochromic red cells > 2.5 have been proposed as markers of iron-deficient erythropoiesis in such subjects, but it is unclear which parameter is superior. METHODS: We measured haematocrit, reticulocyte haemglobin content, ferritin and the percentage of hypochromic red cells over 10-150 days in 36 chronic haemodialysis patients in a university hospital. Transferrin saturation was also measured in a subset of 25 patients; iron deficiency was defined as a transferrin saturation < 15%. RESULTS: The diagnostic sensitivity and specificity of a reticulocyte haemoglobin content < 26 pg in detecting iron deficiency were 100% and 73% respectively, compared with 91% and 54% for a percentage of hypochromic red cells > 2.5. Paradoxical reticulocyte haemglobin concentrations occurred on follow-up in five patients receiving 4000 U erythropoietin per haemodialysis (HD). In three patients, reticulocyte haemglobin content exceeded 26 pg despite a persistent lack of iron. In a fourth, iron gluconate (62.5 mg i.v./HD) increased transferrin saturation to 27% and reduced the percentage of hypochromic red cells from 12 to 4, while reticulocyte haemglobin remained > 30 pg. In the final patient, iron gluconate increased transferrin saturation from 8 to 30% and reduced the percentage of hypochromic red cells from 40 to below 5, but reticulocyte haemglobin content remained < or = 26 pg throughout. CONCLUSIONS: The reticulocyte haemglobin content is superior to the percentage of hypochromic red cells in detecting iron deficiency in haemodialysis patients. (+info)The contribution of alpha+-thalassaemia to anaemia in a Nigerian population exposed to intense malaria transmission. (4/490)
The proportion to which alpha-thalassaemia contributes to anaemia in Africa is not well recognized. In an area of intense malaria transmission in South-West Nigeria, haematological parameters of alpha-thalassaemia were examined in 494 children and 119 adults. The -alpha3.7 type of alpha+-thalassaemia was observed at a gene frequency of 0.27. Nine and 36.5% of individuals were homozygous and heterozygous, respectively. P.falciparum-infection was present in 78% of children and in 39% of adults. The alpha-globin genotypes did not correlate with the prevalence of P. falciparum-infection. alpha+-thalassaemic individuals had significantly lower mean values of haemoglobin, mean corpuscular volume, and mean corpuscular haemoglobin than non-thalassaemic subjects. Anaemia was seen in 54. 7% of children with a normal alpha-globin genotype, in 69.9% of heterozygous (odds ratio: 1.99, 95% confidence interval: 1.32-3.00, P = 0.001), and in 88.4% of homozygous alpha+-thalassaemic children (odds ratio: 7.72, 95% confidence interval: 2.85-20.90, P = 0.0001). The findings show that alpha+-thalassaemia contributes essentially to mild anaemia, microcytosis, and hypochromia in Nigeria. (+info)Fe(III)-EDTA complex as iron fortification. Further studies. (5/490)
The data presented confirm the advantages of Fe(III)-EDTA as a salt for iron fortification. This iron compound exchanges completely with intrinsic wheat iron in the lumen of the gut. The iron absorption data from this salt tested with six different food vehicles compared with the absorption of ferrous sulfate administered with the same vehicles indicate that while the mean absorption from ferrous sulfate varies from 2 to 30% according to the food vehicle mixed with the salt, the absorption from Fe(III)-EDTA remains practically the same. Apparently, the iron absorption from Fe(III)-EDTA complex is slightly or not affected by the presence of vegetable foods or milk. All these data suggest that only a small amount of iron from this salt, about 10 mg/day, would be necessary to prevent iron deficiency anemia even in those populations relying for their subsistence on vegetable food only. (+info)Isoimmune haemolysis in pathogenesis of anaemia after cardiac surgery. (6/490)
A patient who had received multiple transfusions developed antiglobulin-positive haemolytic anaemia due to a delayed haemolytic transfusion reaction. Many cases of haemolytic anaemia after cardiac surgery could be explained on this basis. (+info)Cardiorespiratory, hematological and physical performance responses of anemic subjects to iron treatment. (7/490)
Twenty-nine adult iron-deficient anemis subjects (13 men and 16 women) with hemoglobin levels of 4.0 to 12.0 g/100 ml blood were divided into either an iron treatment or placebo group. Hematological, cardiorespiratory and performance data were collected before, during, and after treatment and compared with data from a control group of subjects (4 men and 6 women) from the same socioeconomic population. Hemoglobin levels for the iron treatment group improved from 7.7 to 12.4 g for the women and from 7.1 to 14.0 g for the men. Values for the control group were 13.9 g and 14.3 g for the women and men, respectively. The placebo group showed virtually no change over the 80-day period (8.1-8.4 g for women and 7.7-7.4 g for men). Peak exercise heart rates (5 min, 40-cm step test) were significantly reduced after treatment from 155 to 113 for the iron treatment men and 152 to 123 for the women compared with the placebo group which showed no changes. Values for the control group were 119 and 142 for the men and women, respectively. In response to the exercise test, no difference in oxygen consumption was found between the iron treatment and placebo group although 15% more O2 was delivered per pulse in the iron treatment group. Blood lactates were significantly highein the placebo than iron treatment group both at rest, 1.18 versus 0.64 mmole/liter, and 1 min after exercise, 5.30 versus 2.68 mmoles/liter. No changes in handgrip or shoulder adductor strength were observed following treatment. These results clearly support the concept that performance requiring high oxygen delivery is significantly affected by hemoglobin levels. (+info)Anemia in the elderly. (8/490)
Anemia should not be accepted as an inevitable consequence of aging. A cause is found in approximately 80 percent of elderly patients. The most common causes of anemia in the elderly are chronic disease and iron deficiency. Vitamin B12 deficiency, folate deficiency, gastrointestinal bleeding and myelodysplastic syndrome are among other causes of anemia in the elderly. Serum ferritin is the most useful test to differentiate iron deficiency anemia from anemia of chronic disease. Not all cases of vitamin B12 deficiency can be identified by low serum levels. The serum methylmalonic acid level may be useful for diagnosis of vitamin B12 deficiency. Vitamin B12 deficiency is effectively treated with oral vitamin B12 supplementation. Folate deficiency is treated with 1 mg of folic acid daily. (+info)Hypochromic anemia is a type of anemia characterized by the presence of red blood cells that have lower than normal levels of hemoglobin and appear paler in color than normal. Hemoglobin is a protein in red blood cells that carries oxygen from the lungs to the rest of the body. In hypochromic anemia, there may be a decrease in the production or increased destruction of red blood cells, leading to a reduced number of red blood cells and insufficient oxygen supply to the tissues.
Hypochromic anemia can result from various underlying medical conditions, including iron deficiency, thalassemia, chronic inflammation, lead poisoning, and certain infections or chronic diseases. Treatment for hypochromic anemia depends on the underlying cause and may include iron supplements, dietary changes, medications, or blood transfusions.
Anemia is a medical condition characterized by a lower than normal number of red blood cells or lower than normal levels of hemoglobin in the blood. Hemoglobin is an important protein in red blood cells that carries oxygen from the lungs to the rest of the body. Anemia can cause fatigue, weakness, shortness of breath, and a pale complexion because the body's tissues are not getting enough oxygen.
Anemia can be caused by various factors, including nutritional deficiencies (such as iron, vitamin B12, or folate deficiency), blood loss, chronic diseases (such as kidney disease or rheumatoid arthritis), inherited genetic disorders (such as sickle cell anemia or thalassemia), and certain medications.
There are different types of anemia, classified based on the underlying cause, size and shape of red blood cells, and the level of hemoglobin in the blood. Treatment for anemia depends on the underlying cause and may include dietary changes, supplements, medication, or blood transfusions.
Erythrocyte count, also known as red blood cell (RBC) count, is a laboratory test that measures the number of red blood cells in a sample of blood. Red blood cells are important because they carry oxygen from the lungs to the rest of the body. A low erythrocyte count may indicate anemia, while a high count may be a sign of certain medical conditions such as polycythemia. The normal range for erythrocyte count varies depending on a person's age, sex, and other factors.
In the context of medicine, iron is an essential micromineral and key component of various proteins and enzymes. It plays a crucial role in oxygen transport, DNA synthesis, and energy production within the body. Iron exists in two main forms: heme and non-heme. Heme iron is derived from hemoglobin and myoglobin in animal products, while non-heme iron comes from plant sources and supplements.
The recommended daily allowance (RDA) for iron varies depending on age, sex, and life stage:
* For men aged 19-50 years, the RDA is 8 mg/day
* For women aged 19-50 years, the RDA is 18 mg/day
* During pregnancy, the RDA increases to 27 mg/day
* During lactation, the RDA for breastfeeding mothers is 9 mg/day
Iron deficiency can lead to anemia, characterized by fatigue, weakness, and shortness of breath. Excessive iron intake may result in iron overload, causing damage to organs such as the liver and heart. Balanced iron levels are essential for maintaining optimal health.
Alpha-globins are a type of globin protein that combine to form the alpha-globin chains of hemoglobin, the oxygen-carrying protein in red blood cells. Hemoglobin is composed of four globin chains, two alpha-globin chains and two beta-globin chains, that surround a heme group. The alpha-globin genes are located on chromosome 16 and are essential for normal hemoglobin function. Mutations in the alpha-globin genes can lead to various forms of hemoglobin disorders such as alpha-thalassemia.
Refractory anemia is a type of anemia that does not respond to typical treatments, such as iron supplements or hormonal therapy. It is often associated with various bone marrow disorders, including myelodysplastic syndromes (MDS), a group of conditions characterized by abnormal blood cell production in the bone marrow.
In refractory anemia, the bone marrow fails to produce enough healthy red blood cells, leading to symptoms such as fatigue, weakness, shortness of breath, and pale skin. The condition can be difficult to treat, and treatment options may include more aggressive therapies such as immunosuppressive drugs, chemotherapy, or stem cell transplantation.
It is important to note that the term "refractory" in this context refers specifically to the lack of response to initial treatments, rather than a specific severity or type of anemia.
Hemoglobin (Hb or Hgb) is the main oxygen-carrying protein in the red blood cells, which are responsible for delivering oxygen throughout the body. It is a complex molecule made up of four globin proteins and four heme groups. Each heme group contains an iron atom that binds to one molecule of oxygen. Hemoglobin plays a crucial role in the transport of oxygen from the lungs to the body's tissues, and also helps to carry carbon dioxide back to the lungs for exhalation.
There are several types of hemoglobin present in the human body, including:
* Hemoglobin A (HbA): This is the most common type of hemoglobin, making up about 95-98% of total hemoglobin in adults. It consists of two alpha and two beta globin chains.
* Hemoglobin A2 (HbA2): This makes up about 1.5-3.5% of total hemoglobin in adults. It consists of two alpha and two delta globin chains.
* Hemoglobin F (HbF): This is the main type of hemoglobin present in fetal life, but it persists at low levels in adults. It consists of two alpha and two gamma globin chains.
* Hemoglobin S (HbS): This is an abnormal form of hemoglobin that can cause sickle cell disease when it occurs in the homozygous state (i.e., both copies of the gene are affected). It results from a single amino acid substitution in the beta globin chain.
* Hemoglobin C (HbC): This is another abnormal form of hemoglobin that can cause mild to moderate hemolytic anemia when it occurs in the homozygous state. It results from a different single amino acid substitution in the beta globin chain than HbS.
Abnormal forms of hemoglobin, such as HbS and HbC, can lead to various clinical disorders, including sickle cell disease, thalassemia, and other hemoglobinopathies.
Sideroblastic anemia is a type of anemia characterized by the presence of ringed sideroblasts in the bone marrow. Ringed sideroblasts are red blood cell precursors that have an abnormal amount of iron accumulated in their mitochondria, which forms a ring around the nucleus. This results in the production of abnormal hemoglobin and impaired oxygen transport.
Sideroblastic anemia can be classified as congenital or acquired. Congenital sideroblastic anemias are caused by genetic defects that affect heme synthesis or mitochondrial function, while acquired sideroblastic anemias are associated with various conditions such as myelodysplastic syndromes, chronic alcoholism, lead toxicity, and certain medications.
Symptoms of sideroblastic anemia may include fatigue, weakness, shortness of breath, and pallor. Diagnosis is typically made through a bone marrow aspiration and biopsy, which can identify the presence of ringed sideroblasts. Treatment depends on the underlying cause but may include iron chelation therapy, vitamin B6 supplementation, or blood transfusions.
Alpha-thalassemia is a genetic disorder that affects the production of hemoglobin, a protein in red blood cells that carries oxygen throughout the body. It is caused by deletions or mutations in the genes that produce the alpha-globin chains of hemoglobin.
There are several types of alpha-thalassemia, ranging from mild to severe. The most severe form, called hydrops fetalis, occurs when all four alpha-globin genes are deleted or mutated. This can cause stillbirth or death shortly after birth due to heart failure and severe anemia.
Less severe forms of alpha-thalassemia can cause mild to moderate anemia, which may be asymptomatic or associated with symptoms such as fatigue, weakness, and jaundice. These forms of the disorder are more common in people from Mediterranean, Southeast Asian, and African backgrounds.
Treatment for alpha-thalassemia depends on the severity of the condition and may include blood transfusions, iron chelation therapy, or occasionally stem cell transplantation.
Erythropoietin (EPO) is a hormone that is primarily produced by the kidneys and plays a crucial role in the production of red blood cells in the body. It works by stimulating the bone marrow to produce more red blood cells, which are essential for carrying oxygen to various tissues and organs.
EPO is a glycoprotein that is released into the bloodstream in response to low oxygen levels in the body. When the kidneys detect low oxygen levels, they release EPO, which then travels to the bone marrow and binds to specific receptors on immature red blood cells called erythroblasts. This binding triggers a series of events that promote the maturation and proliferation of erythroblasts, leading to an increase in the production of red blood cells.
In addition to its role in regulating red blood cell production, EPO has also been shown to have neuroprotective effects and may play a role in modulating the immune system. Abnormal levels of EPO have been associated with various medical conditions, including anemia, kidney disease, and certain types of cancer.
EPO is also used as a therapeutic agent for the treatment of anemia caused by chronic kidney disease, chemotherapy, or other conditions that affect red blood cell production. Recombinant human EPO (rhEPO) is a synthetic form of the hormone that is produced using genetic engineering techniques and is commonly used in clinical practice to treat anemia. However, misuse of rhEPO for performance enhancement in sports has been a subject of concern due to its potential to enhance oxygen-carrying capacity and improve endurance.
Iron-deficiency anemia is a condition characterized by a decrease in the total amount of hemoglobin or red blood cells in the blood, caused by insufficient iron levels in the body. Hemoglobin is a protein in red blood cells that carries oxygen from the lungs to the rest of the body. When iron levels are low, the body cannot produce enough hemoglobin, leading to the production of smaller and fewer red blood cells, known as microcytic hypochromic anemia.
Iron is essential for the production of hemoglobin, and a deficiency in iron can result from inadequate dietary intake, chronic blood loss, or impaired absorption. In addition to fatigue and weakness, symptoms of iron-deficiency anemia may include shortness of breath, headaches, dizziness, pale skin, and brittle nails. Treatment typically involves iron supplementation and addressing the underlying cause of the iron deficiency.
Erythrocyte indices are a set of calculated values that provide information about the size and hemoglobin content of red blood cells (erythrocytes). These indices are commonly used in the complete blood count (CBC) test to help diagnose various types of anemia and other conditions affecting the red blood cells.
The three main erythrocyte indices are:
1. Mean Corpuscular Volume (MCV): This is the average volume of a single red blood cell, measured in femtoliters (fL). MCV helps to differentiate between microcytic, normocytic, and macrocytic anemia. Microcytic anemia is characterized by low MCV values (100 fL).
2. Mean Corpuscular Hemoglobin (MCH): This is the average amount of hemoglobin present in a single red blood cell, measured in picograms (pg). MCH helps to assess the oxygen-carrying capacity of red blood cells. Low MCH values may indicate hypochromic anemia, where the red blood cells have reduced hemoglobin content.
3. Mean Corpuscular Hemoglobin Concentration (MCHC): This is the average concentration of hemoglobin in a single red blood cell, measured as a percentage. MCHC reflects the hemoglobin concentration relative to the size of the red blood cells. Low MCHC values may indicate hypochromic anemia, while high MCHC values could suggest spherocytosis or other conditions affecting red blood cell shape and integrity.
These erythrocyte indices are calculated based on the red blood cell count, hemoglobin concentration, and hematocrit results obtained from a CBC test. They provide valuable information for healthcare professionals to diagnose and manage various hematological conditions.
Aplastic anemia is a medical condition characterized by pancytopenia (a decrease in all three types of blood cells: red blood cells, white blood cells, and platelets) due to the failure of bone marrow to produce new cells. It is called "aplastic" because the bone marrow becomes hypocellular or "aplastic," meaning it contains few or no blood-forming stem cells.
The condition can be acquired or inherited, with acquired aplastic anemia being more common. Acquired aplastic anemia can result from exposure to toxic chemicals, radiation, drugs, viral infections, or autoimmune disorders. Inherited forms of the disease include Fanconi anemia and dyskeratosis congenita.
Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, easy bruising or bleeding, frequent infections, and fever. Treatment options for aplastic anemia depend on the severity of the condition and its underlying cause. They may include blood transfusions, immunosuppressive therapy, and stem cell transplantation.
Ferritin is a protein in iron-metabolizing cells that stores iron in a water-soluble form. It is found inside the cells (intracellular) and is released into the bloodstream when the cells break down or die. Measuring the level of ferritin in the blood can help determine the amount of iron stored in the body. High levels of ferritin may indicate hemochromatosis, inflammation, liver disease, or other conditions. Low levels of ferritin may indicate anemia, iron deficiency, or other conditions.
Beta-thalassemia is a genetic blood disorder that affects the production of hemoglobin, a protein in red blood cells that carries oxygen throughout the body. Specifically, beta-thalassemia is caused by mutations in the beta-globin gene, which leads to reduced or absent production of the beta-globin component of hemoglobin.
There are two main types of beta-thalassemia:
1. Beta-thalassemia major (also known as Cooley's anemia): This is a severe form of the disorder that typically becomes apparent in early childhood. It is characterized by a significant reduction or absence of beta-globin production, leading to anemia, enlarged spleen and liver, jaundice, and growth retardation.
2. Beta-thalassemia intermedia: This is a milder form of the disorder that may not become apparent until later in childhood or even adulthood. It is characterized by a variable reduction in beta-globin production, leading to mild to moderate anemia and other symptoms that can range from nonexistent to severe.
Treatment for beta-thalassemia depends on the severity of the disorder and may include blood transfusions, iron chelation therapy, and/or bone marrow transplantation. In some cases, genetic counseling and prenatal diagnosis may also be recommended for families with a history of the disorder.
Erythropoiesis is the process of forming and developing red blood cells (erythrocytes) in the body. It occurs in the bone marrow and is regulated by the hormone erythropoietin (EPO), which is produced by the kidneys. Erythropoiesis involves the differentiation and maturation of immature red blood cell precursors called erythroblasts into mature red blood cells, which are responsible for carrying oxygen to the body's tissues. Disorders that affect erythropoiesis can lead to anemia or other blood-related conditions.
Hemolytic anemia is a type of anemia that occurs when red blood cells are destroyed (hemolysis) faster than they can be produced. Red blood cells are essential for carrying oxygen throughout the body. When they are destroyed, hemoglobin and other cellular components are released into the bloodstream, which can lead to complications such as kidney damage and gallstones.
Hemolytic anemia can be inherited or acquired. Inherited forms of the condition may result from genetic defects that affect the structure or function of red blood cells. Acquired forms of hemolytic anemia can be caused by various factors, including infections, medications, autoimmune disorders, and certain medical conditions such as cancer or blood disorders.
Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, pale skin, jaundice (yellowing of the skin and eyes), dark urine, and a rapid heartbeat. Treatment for hemolytic anemia depends on the underlying cause and may include medications, blood transfusions, or surgery.
Protoporphyrins are organic compounds that are the immediate precursors to heme in the porphyrin synthesis pathway. They are composed of a porphyrin ring, which is a large, complex ring made up of four pyrrole rings joined together, with an acetate and a propionate side chain at each pyrrole. Protoporphyrins are commonly found in nature and are important components of many biological systems, including hemoglobin, the protein in red blood cells that carries oxygen throughout the body.
There are several different types of protoporphyrins, including protoporphyrin IX, which is the most common form found in humans and other animals. Protoporphyrins can be measured in the blood or other tissues as a way to diagnose or monitor certain medical conditions, such as lead poisoning or porphyrias, which are rare genetic disorders that affect the production of heme. Elevated levels of protoporphyrins in the blood or tissues can indicate the presence of these conditions and may require further evaluation and treatment.
Transferrin is a glycoprotein that plays a crucial role in the transport and homeostasis of iron in the body. It's produced mainly in the liver and has the ability to bind two ferric (Fe3+) ions in its N-lobe and C-lobe, thus creating transferrin saturation.
This protein is essential for delivering iron to cells while preventing the harmful effects of free iron, which can catalyze the formation of reactive oxygen species through Fenton reactions. Transferrin interacts with specific transferrin receptors on the surface of cells, particularly in erythroid precursors and brain endothelial cells, to facilitate iron uptake via receptor-mediated endocytosis.
In addition to its role in iron transport, transferrin also has antimicrobial properties due to its ability to sequester free iron, making it less available for bacterial growth and survival. Transferrin levels can be used as a clinical marker of iron status, with decreased levels indicating iron deficiency anemia and increased levels potentially signaling inflammation or liver disease.
Reticulocytes are immature red blood cells that still contain remnants of organelles, such as ribosomes and mitochondria, which are typically found in developing cells. These organelles are involved in the process of protein synthesis and energy production, respectively. Reticulocytes are released from the bone marrow into the bloodstream, where they continue to mature into fully developed red blood cells called erythrocytes.
Reticulocytes can be identified under a microscope by their staining characteristics, which reveal a network of fine filaments or granules known as the reticular apparatus. This apparatus is composed of residual ribosomal RNA and other proteins that have not yet been completely eliminated during the maturation process.
The percentage of reticulocytes in the blood can be used as a measure of bone marrow function and erythropoiesis, or red blood cell production. An increased reticulocyte count may indicate an appropriate response to blood loss, hemolysis, or other conditions that cause anemia, while a decreased count may suggest impaired bone marrow function or a deficiency in erythropoietin, the hormone responsible for stimulating red blood cell production.
Abnormal erythrocytes refer to red blood cells that have an abnormal shape, size, or other characteristics. This can include various types of abnormalities such as:
1. Anisocytosis: Variation in the size of erythrocytes.
2. Poikilocytosis: Variation in the shape of erythrocytes, including but not limited to teardrop-shaped cells (dacrocytes), crescent-shaped cells (sickle cells), and spherical cells (spherocytes).
3. Anemia: A decrease in the total number of erythrocytes or a reduction in hemoglobin concentration, which can result from various underlying conditions such as iron deficiency, chronic disease, or blood loss.
4. Hemoglobinopathies: Abnormalities in the structure or function of hemoglobin, the protein responsible for carrying oxygen in erythrocytes, such as sickle cell anemia and thalassemia.
5. Inclusion bodies: Abnormal structures within erythrocytes, such as Heinz bodies (denatured hemoglobin) or Howell-Jolly bodies (nuclear remnants).
These abnormalities can be detected through a complete blood count (CBC) and peripheral blood smear examination. The presence of abnormal erythrocytes may indicate an underlying medical condition, and further evaluation is often necessary to determine the cause and appropriate treatment.
Fanconi anemia is a rare, inherited disorder that affects the body's ability to produce healthy blood cells. It is characterized by bone marrow failure, congenital abnormalities, and an increased risk of developing certain types of cancer. The condition is caused by mutations in genes responsible for repairing damaged DNA, leading to chromosomal instability and cell death.
The classic form of Fanconi anemia (type A) is typically diagnosed in childhood and is associated with various physical abnormalities such as short stature, skin pigmentation changes, thumb and radial ray anomalies, kidney and genitourinary malformations, and developmental delays. Other types of Fanconi anemia (B-G) may have different clinical presentations but share the common feature of bone marrow failure and cancer predisposition.
Bone marrow failure in Fanconi anemia results in decreased production of all three types of blood cells: red blood cells, white blood cells, and platelets. This can lead to anemia (low red blood cell count), neutropenia (low white blood cell count), and thrombocytopenia (low platelet count). These conditions increase the risk of infections, fatigue, and bleeding.
Individuals with Fanconi anemia have a significantly higher risk of developing various types of cancer, particularly acute myeloid leukemia (AML) and solid tumors such as squamous cell carcinomas of the head, neck, esophagus, and anogenital region.
Treatment for Fanconi anemia typically involves managing symptoms related to bone marrow failure, such as transfusions, growth factors, and antibiotics. Hematopoietic stem cell transplantation (HSCT) is the only curative treatment option for bone marrow failure but carries risks of its own, including graft-versus-host disease and transplant-related mortality. Regular cancer surveillance is essential due to the increased risk of malignancies in these patients.
Thalassemia is a group of inherited genetic disorders that affect the production of hemoglobin, a protein in red blood cells responsible for carrying oxygen throughout the body. The disorder results in less efficient or abnormal hemoglobin, which can lead to anemia, an insufficient supply of oxygen-rich red blood cells.
There are two main types of Thalassemia: alpha and beta. Alpha thalassemia occurs when there is a problem with the alpha globin chain production, while beta thalassemia results from issues in beta globin chain synthesis. These disorders can range from mild to severe, depending on the number of genes affected and their specific mutations.
Severe forms of Thalassemia may require regular blood transfusions, iron chelation therapy, or even a bone marrow transplant to manage symptoms and prevent complications.
Hemoglobin H (Hb H) is a type of abnormal hemoglobin that can occur in individuals with certain genetic disorders, such as hemoglobinopathies. It is formed when four beta-globin chains come together, instead of the usual two alpha and two beta chains found in normal adult hemoglobin (Hb A).
This abnormal structure can result from a mutation that causes the absence or deficiency of alpha-globin chains, leading to an excess of beta-globin chains. Hemoglobin H is often associated with conditions such as thalassemia, particularly when there is a severe deficiency of alpha-globin chain production (alpha-thalassemia).
Hemoglobin H can cause hemolytic anemia, which means that the red blood cells are destroyed prematurely. The severity of the condition depends on the degree of imbalance between alpha and beta chains and other genetic factors. Symptoms may include fatigue, jaundice, and splenomegaly (enlarged spleen).
Erythrocytes, also known as red blood cells (RBCs), are the most common type of blood cell in circulating blood in mammals. They are responsible for transporting oxygen from the lungs to the body's tissues and carbon dioxide from the tissues to the lungs.
Erythrocytes are formed in the bone marrow and have a biconcave shape, which allows them to fold and bend easily as they pass through narrow blood vessels. They do not have a nucleus or mitochondria, which makes them more flexible but also limits their ability to reproduce or repair themselves.
In humans, erythrocytes are typically disc-shaped and measure about 7 micrometers in diameter. They contain the protein hemoglobin, which binds to oxygen and gives blood its red color. The lifespan of an erythrocyte is approximately 120 days, after which it is broken down in the liver and spleen.
Abnormalities in erythrocyte count or function can lead to various medical conditions, such as anemia, polycythemia, and sickle cell disease.
Hemolytic anemia, autoimmune is a type of anemia characterized by the premature destruction of red blood cells (RBCs) in which the immune system mistakenly attacks and destroys its own RBCs. This occurs when the body produces autoantibodies that bind to the surface of RBCs, leading to their rupture (hemolysis). The symptoms may include fatigue, weakness, shortness of breath, and dark colored urine. The diagnosis is made through blood tests that measure the number and size of RBCs, reticulocyte count, and the presence of autoantibodies. Treatment typically involves suppressing the immune system with medications such as corticosteroids or immunosuppressive drugs, and sometimes removal of the spleen (splenectomy) may be necessary.
Hepcidin is a peptide hormone primarily produced in the liver that plays a crucial role in regulating iron homeostasis within the body. It acts by inhibiting the absorption of dietary iron in the intestines and the release of iron from storage sites, such as macrophages, into the bloodstream. By reducing the amount of iron available for use, hepcidin helps prevent excessive iron accumulation in tissues, which can be harmful and contribute to the development of various diseases, including iron overload disorders and certain types of anemia. The production of hepcidin is regulated by several factors, including iron levels, inflammation, and erythropoiesis (the production of red blood cells).
Transferrin receptors are membrane-bound proteins found on the surface of many cell types, including red and white blood cells, as well as various tissues such as the liver, brain, and placenta. These receptors play a crucial role in iron homeostasis by regulating the uptake of transferrin, an iron-binding protein, into the cells.
Transferrin binds to two ferric ions (Fe3+) in the bloodstream, forming a complex known as holo-transferrin. This complex then interacts with the transferrin receptors on the cell surface, leading to endocytosis of the transferrin-receptor complex into the cell. Once inside the cell, the acidic environment within the endosome causes the release of iron ions from the transferrin molecule, which can then be transported into the cytoplasm for use in various metabolic processes.
After releasing the iron, the apo-transferrin (iron-free transferrin) is recycled back to the cell surface and released back into the bloodstream, where it can bind to more ferric ions and repeat the cycle. This process helps maintain appropriate iron levels within the body and ensures that cells have access to the iron they need for essential functions such as DNA synthesis, energy production, and oxygen transport.
In summary, transferrin receptors are membrane-bound proteins responsible for recognizing and facilitating the uptake of transferrin-bound iron into cells, playing a critical role in maintaining iron homeostasis within the body.
Macrocytic anemia is a type of anemia in which the red blood cells are larger than normal in size (macrocytic). This condition can be caused by various factors such as deficiency of vitamin B12 or folate, alcohol abuse, certain medications, bone marrow disorders, and some inherited genetic conditions.
The large red blood cells may not function properly, leading to symptoms such as fatigue, weakness, shortness of breath, pale skin, and a rapid heartbeat. Macrocytic anemia can be diagnosed through a complete blood count (CBC) test, which measures the size and number of red blood cells in the blood.
Treatment for macrocytic anemia depends on the underlying cause. In cases of vitamin B12 or folate deficiency, supplements or dietary changes may be recommended. If the anemia is caused by medication, a different medication may be prescribed. In severe cases, blood transfusions or injections of vitamin B12 may be necessary.
Pernicious anemia is a specific type of vitamin B12 deficiency anemia that is caused by a lack of intrinsic factor, a protein made in the stomach that is needed to absorb vitamin B12. The absence of intrinsic factor leads to poor absorption of vitamin B12 from food and results in its deficiency.
Vitamin B12 is essential for the production of healthy red blood cells, which carry oxygen throughout the body. Without enough vitamin B12, the body cannot produce enough red blood cells, leading to anemia. Pernicious anemia typically develops slowly over several years and can cause symptoms such as fatigue, weakness, pale skin, shortness of breath, and a decreased appetite.
Pernicious anemia is an autoimmune disorder, which means that the body's immune system mistakenly attacks healthy cells in the stomach lining, leading to a loss of intrinsic factor production. It is more common in older adults, particularly those over 60 years old, and can also be associated with other autoimmune disorders such as type 1 diabetes, Hashimoto's thyroiditis, and Addison's disease.
Treatment for pernicious anemia typically involves vitamin B12 replacement therapy, either through oral supplements or injections of the vitamin. In some cases, dietary changes may also be recommended to ensure adequate intake of vitamin B12-rich foods such as meat, fish, poultry, and dairy products.
Renal dialysis is a medical procedure that is used to artificially remove waste products, toxins, and excess fluids from the blood when the kidneys are no longer able to perform these functions effectively. This process is also known as hemodialysis.
During renal dialysis, the patient's blood is circulated through a special machine called a dialyzer or an artificial kidney, which contains a semi-permeable membrane that filters out waste products and excess fluids from the blood. The cleaned blood is then returned to the patient's body.
Renal dialysis is typically recommended for patients with advanced kidney disease or kidney failure, such as those with end-stage renal disease (ESRD). It is a life-sustaining treatment that helps to maintain the balance of fluids and electrolytes in the body, prevent the buildup of waste products and toxins, and control blood pressure.
There are two main types of renal dialysis: hemodialysis and peritoneal dialysis. Hemodialysis is the most common type and involves using a dialyzer to filter the blood outside the body. Peritoneal dialysis, on the other hand, involves placing a catheter in the abdomen and using the lining of the abdomen (peritoneum) as a natural filter to remove waste products and excess fluids from the body.
Overall, renal dialysis is an essential treatment option for patients with kidney failure, helping them to maintain their quality of life and prolong their survival.
Sickle cell anemia is a genetic disorder that affects the hemoglobin in red blood cells. Hemoglobin is responsible for carrying oxygen throughout the body. In sickle cell anemia, the hemoglobin is abnormal and causes the red blood cells to take on a sickle shape, rather than the normal disc shape. These sickled cells are stiff and sticky, and they can block blood vessels, causing tissue damage and pain. They also die more quickly than normal red blood cells, leading to anemia.
People with sickle cell anemia often experience fatigue, chronic pain, and jaundice. They may also have a higher risk of infections and complications such as stroke, acute chest syndrome, and priapism. The disease is inherited from both parents, who must both be carriers of the sickle cell gene. It primarily affects people of African descent, but it can also affect people from other ethnic backgrounds.
There is no cure for sickle cell anemia, but treatments such as blood transfusions, medications to manage pain and prevent complications, and bone marrow transplantation can help improve quality of life for affected individuals. Regular medical care and monitoring are essential for managing the disease effectively.
Megaloblastic anemia is a type of macrocytic anemia, which is characterized by the presence of large, structurally abnormal, and immature red blood cells called megaloblasts in the bone marrow. This condition arises due to impaired DNA synthesis during erythropoiesis (the process of red blood cell production), often as a result of deficiencies in vitamin B12 or folate, or from the use of certain medications that interfere with DNA synthesis.
The hallmark feature of megaloblastic anemia is the presence of megaloblasts in the bone marrow, which exhibit an asynchrony between nuclear and cytoplasmic maturation. This means that although the cytoplasm of these cells may appear well-developed, their nuclei remain underdeveloped and fragmented. As a result, the peripheral blood shows an increase in mean corpuscular volume (MCV), reflecting the larger size of the red blood cells.
Additional hematological findings include decreased reticulocyte counts, neutrophil hypersegmentation, and occasionally thrombocytopenia or leukopenia. Neurological symptoms may also be present due to the involvement of the nervous system in vitamin B12 deficiency.
Megaloblastic anemia is typically treated with supplementation of the deficient vitamin (B12 or folate), which helps restore normal erythropoiesis and alleviate symptoms over time.
Equine Infectious Anemia (EIA) is a viral disease that affects horses and other equine animals. The causative agent of this disease is the Equine Infectious Anemia Virus (EIAV), which belongs to the family Retroviridae and genus Lentivirus. This virus is primarily transmitted through the transfer of infected blood, most commonly through biting insects such as horseflies and deerflies.
The EIAV attacks the immune system of the infected animal, causing a variety of symptoms including fever, weakness, weight loss, anemia, and edema. The virus has a unique ability to integrate its genetic material into the host's DNA, which can lead to a lifelong infection. Some animals may become chronic carriers of the virus, showing no signs of disease but remaining infectious to others.
There is currently no cure for EIA, and infected animals must be isolated to prevent the spread of the disease. Vaccines are available in some countries, but they do not provide complete protection against infection and may only help reduce the severity of the disease. Regular testing and monitoring of equine populations are essential to control the spread of this virus.
Hemolytic anemia, congenital is a type of anemia that is present at birth and characterized by the abnormal breakdown (hemolysis) of red blood cells. This can occur due to various genetic defects that affect the structure or function of the red blood cells, making them more susceptible to damage and destruction.
There are several types of congenital hemolytic anemias, including:
1. Congenital spherocytosis: A condition caused by mutations in genes that affect the shape and stability of red blood cells, leading to the formation of abnormally shaped and fragile cells that are prone to hemolysis.
2. G6PD deficiency: A genetic disorder that affects the enzyme glucose-6-phosphate dehydrogenase (G6PD), which is essential for protecting red blood cells from damage. People with this condition have low levels of G6PD, making their red blood cells more susceptible to hemolysis when exposed to certain triggers such as infections or certain medications.
3. Hereditary elliptocytosis: A condition caused by mutations in genes that affect the structure and flexibility of red blood cells, leading to the formation of abnormally shaped and fragile cells that are prone to hemolysis.
4. Pyruvate kinase deficiency: A rare genetic disorder that affects an enzyme called pyruvate kinase, which is essential for the production of energy in red blood cells. People with this condition have low levels of pyruvate kinase, leading to the formation of fragile and abnormally shaped red blood cells that are prone to hemolysis.
Symptoms of congenital hemolytic anemia can vary depending on the severity of the condition but may include fatigue, weakness, pale skin, jaundice, dark urine, and an enlarged spleen. Treatment may involve blood transfusions, medications to manage symptoms, and in some cases, surgery to remove the spleen.
Recombinant proteins are artificially created proteins produced through the use of recombinant DNA technology. This process involves combining DNA molecules from different sources to create a new set of genes that encode for a specific protein. The resulting recombinant protein can then be expressed, purified, and used for various applications in research, medicine, and industry.
Recombinant proteins are widely used in biomedical research to study protein function, structure, and interactions. They are also used in the development of diagnostic tests, vaccines, and therapeutic drugs. For example, recombinant insulin is a common treatment for diabetes, while recombinant human growth hormone is used to treat growth disorders.
The production of recombinant proteins typically involves the use of host cells, such as bacteria, yeast, or mammalian cells, which are engineered to express the desired protein. The host cells are transformed with a plasmid vector containing the gene of interest, along with regulatory elements that control its expression. Once the host cells are cultured and the protein is expressed, it can be purified using various chromatography techniques.
Overall, recombinant proteins have revolutionized many areas of biology and medicine, enabling researchers to study and manipulate proteins in ways that were previously impossible.
Equine infectious anemia (EIA) is a viral disease that affects horses and other equine animals. It is caused by the Equine Infectious Anemia Virus (EIAV), which is transmitted through the bloodstream of infected animals, often through biting insects such as horseflies and deerflies.
The symptoms of EIA can vary widely, but often include fever, weakness, weight loss, anemia, and edema. In severe cases, the disease can cause death. There is no cure for EIA, and infected animals must be isolated to prevent the spread of the virus.
EIA is diagnosed through blood tests that detect the presence of antibodies to the virus. Horses that test positive for EIA are typically euthanized or permanently quarantined. Prevention measures include testing horses before they are bought, sold, or moved, as well as controlling insect populations and using insect repellents. Vaccines are not available for EIA in most countries.
Chicken anemia virus (CAV) is a small, non-enveloped DNA virus that belongs to the family *Circoviridae* and genus *Gyrovirus*. It primarily infects chickens and causes a variety of clinical signs, including severe anemia, immunosuppression, and runting in young birds.
The virus is highly contagious and can be spread through horizontal transmission via feces, contaminated equipment, or vertically from infected breeder hens to their offspring. CAV infection can lead to significant economic losses in the poultry industry due to decreased growth rates, increased mortality, and reduced egg production.
In addition to its impact on the poultry industry, CAV has also been used as a vector for gene delivery in biomedical research. Its small genome size and ability to infect a wide range of avian species make it an attractive candidate for vaccine development and gene therapy applications.
Dyserythropoietic anemia, congenital is a rare type of inherited anemia characterized by ineffective red blood cell production (erythropoiesis) in the bone marrow. This means that the body has difficulty producing healthy and fully mature red blood cells. The condition is caused by mutations in genes responsible for the development and maturation of red blood cells, leading to the production of abnormally shaped and dysfunctional red blood cells.
There are two main types of congenital dyserythropoietic anemia (CDA), type I and type II, each caused by different genetic mutations:
1. CDA Type I (HEMPAS): This form is caused by a mutation in the SEC23B gene. It typically presents in early childhood with mild to moderate anemia, jaundice, and splenomegaly (enlarged spleen). The severity of the condition can vary widely among affected individuals.
2. CDA Type II (HIEM): This form is caused by a mutation in the KIF23 gene or, less commonly, the TCIRG1 gene. It typically presents in infancy with moderate to severe anemia, hepatomegaly (enlarged liver), and splenomegaly. The condition can lead to iron overload due to repeated blood transfusions, which may require chelation therapy to manage.
Both types of congenital dyserythropoietic anemia are characterized by ineffective erythropoiesis, abnormal red blood cell morphology, and increased destruction of red blood cells (hemolysis). Treatment typically involves supportive care, such as blood transfusions to manage anemia, and occasionally chelation therapy to address iron overload. In some cases, bone marrow transplantation may be considered as a curative option.
Diamond-Blackfan anemia is a rare, congenital bone marrow failure disorder characterized by a decreased production of red blood cells (erythroblasts) in the bone marrow. This results in a reduced number of circulating red blood cells, leading to anemia and related symptoms such as fatigue, weakness, and pallor. The disorder is typically diagnosed in infancy or early childhood and can also be associated with physical abnormalities.
The exact cause of Diamond-Blackfan anemia is not fully understood, but it is believed to involve genetic mutations that affect the development and function of the bone marrow. In many cases, the disorder is inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the mutated gene from an affected parent. However, some cases may arise spontaneously due to new genetic mutations.
Treatment for Diamond-Blackfan anemia typically involves regular blood transfusions to maintain adequate red blood cell levels and alleviate symptoms. Corticosteroid therapy may also be used to stimulate red blood cell production in some cases. In severe or refractory cases, stem cell transplantation may be considered as a curative treatment option.
Fanconi anemia (FA) is a genetic disorder characterized by various developmental abnormalities, bone marrow failure, and increased risk of malignancies. It is caused by mutations in genes involved in the FA complementation group, which are responsible for repairing damaged DNA.
The FA complementation group proteins include FANCA, FANCB, FANCC, FANCD1/BRCA2, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ/BRIP1, FANCL, FANCM, and FAAP100. These proteins work together to form the FA core complex, which is responsible for monoubiquitinating FANCD2 and FANCI in response to DNA damage. This modification allows for the recruitment of downstream effectors that facilitate DNA repair and maintain genomic stability.
Defects in any of these FA complementation group proteins can lead to Fanconi anemia, with varying clinical manifestations depending on the specific gene involved and the severity of the mutation.
Hematologic pregnancy complications refer to disorders related to the blood and blood-forming tissues that occur during pregnancy. These complications can have serious consequences for both the mother and the fetus if not properly managed. Some common hematologic pregnancy complications include:
1. Anemia: A condition characterized by a decrease in the number of red blood cells or hemoglobin in the blood, which can lead to fatigue, weakness, and shortness of breath. Iron-deficiency anemia is the most common type of anemia during pregnancy.
2. Thrombocytopenia: A condition characterized by a decrease in the number of platelets (cells that help blood clot) in the blood. Mild thrombocytopenia is relatively common during pregnancy, but severe thrombocytopenia can increase the risk of bleeding during delivery.
3. Gestational thrombotic thrombocytopenic purpura (GTTP): A rare but serious disorder that can cause blood clots to form in small blood vessels throughout the body, leading to a decrease in the number of platelets and red blood cells. GTTP can cause serious complications such as stroke, kidney failure, and even death if not promptly diagnosed and treated.
4. Disseminated intravascular coagulation (DIC): A condition characterized by abnormal clotting and bleeding throughout the body. DIC can be triggered by various conditions such as severe infections, pregnancy complications, or cancer.
5. Hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome: A serious complication of pregnancy that can cause damage to the liver and lead to bleeding. HELLP syndrome is often associated with preeclampsia, a condition characterized by high blood pressure and damage to organs such as the liver and kidneys.
It's important for pregnant women to receive regular prenatal care to monitor for these and other potential complications, and to seek prompt medical attention if any concerning symptoms arise.
Neonatal anemia is a condition characterized by a lower-than-normal number of red blood cells or lower-than-normal levels of hemoglobin in the blood of a newborn infant. Hemoglobin is the protein in red blood cells that carries oxygen to the body's tissues.
There are several types and causes of neonatal anemia, including:
1. Anemia of prematurity: This is the most common type of anemia in newborns, especially those born before 34 weeks of gestation. It occurs due to a decrease in red blood cell production and a shorter lifespan of red blood cells in premature infants.
2. Hemolytic anemia: This type of anemia is caused by the destruction of red blood cells at a faster rate than they can be produced. It can result from various factors, such as incompatibility between the mother's and baby's blood types, genetic disorders like G6PD deficiency, or infections.
3. Fetomaternal hemorrhage: This condition occurs when there is a significant transfer of fetal blood into the maternal circulation during pregnancy or childbirth, leading to anemia in the newborn.
4. Iron-deficiency anemia: Although rare in newborns, iron-deficiency anemia can occur if the mother has low iron levels during pregnancy, and the infant does not receive adequate iron supplementation after birth.
5. Anemia due to nutritional deficiencies: Rarely, neonatal anemia may result from a lack of essential vitamins or minerals like folate, vitamin B12, or copper in the newborn's diet.
Symptoms of neonatal anemia can vary but may include pallor, lethargy, poor feeding, rapid heartbeat, and difficulty breathing. Diagnosis typically involves a complete blood count (CBC) to measure red blood cell count, hemoglobin levels, and other parameters. Treatment depends on the underlying cause of anemia and may include iron supplementation, transfusions, or management of any underlying conditions.
Hematinics are a class of medications and dietary supplements that are used to enhance the production of red blood cells or hemoglobin in the body. They typically contain iron, vitamin B12, folic acid, or other nutrients that are essential for the synthesis of hemoglobin and the formation of red blood cells.
Iron is a critical component of hematinics because it plays a central role in the production of hemoglobin, which is the protein in red blood cells that carries oxygen throughout the body. Vitamin B12 and folic acid are also important nutrients for red blood cell production, as they help to regulate the growth and division of red blood cells in the bone marrow.
Hematinics are often prescribed to treat anemia, which is a condition characterized by a low red blood cell count or abnormally low levels of hemoglobin in the blood. Anemia can be caused by a variety of factors, including nutritional deficiencies, chronic diseases, and inherited genetic disorders.
Examples of hematinics include ferrous sulfate (an iron supplement), cyanocobalamin (vitamin B12), and folic acid. These medications are available in various forms, such as tablets, capsules, and liquids, and can be taken orally or by injection. It is important to follow the dosage instructions carefully and to inform your healthcare provider of any other medications you are taking, as hematinics can interact with certain drugs and may cause side effects.
Refractory anemia with excess blasts is a type of blood disorder that is characterized by the presence of increased numbers of immature blood cells, or "blasts," in the bone marrow and peripheral blood. This condition is considered a subtype of myelodysplastic syndrome (MDS), which is a group of disorders caused by abnormalities in the production of blood cells in the bone marrow.
In refractory anemia with excess blasts, the bone marrow fails to produce sufficient numbers of healthy red blood cells, white blood cells, and platelets. This results in anemia (low red blood cell count), neutropenia (low white blood cell count), and thrombocytopenia (low platelet count). Additionally, there is an increased number of blasts in the bone marrow and peripheral blood, which can indicate the development of acute myeloid leukemia (AML), a more aggressive form of blood cancer.
Refractory anemia with excess blasts is considered "refractory" because it does not respond well to treatment, including chemotherapy and stem cell transplantation. The prognosis for this condition varies depending on the severity of the disease and other individual factors, but it is generally poor, with many patients progressing to AML within a few years.
Fanconi anemia complementation group C protein, also known as FANCC protein, is a component of the Fanconi anemia (FA) DNA repair pathway. This protein plays a critical role in protecting cells from oxidative stress and maintaining genomic stability. Mutations in the FANCC gene can lead to Fanconi anemia, a rare genetic disorder characterized by bone marrow failure, congenital abnormalities, and increased risk of cancer.
FANCC protein functions as part of a complex that includes other FA proteins, which work together to repair DNA damage caused by interstrand crosslinks (ICLs) - a type of DNA lesion that can lead to genomic instability and cancer. When the FA pathway is activated in response to ICLs, FANCC protein undergoes monoubiquitination, which allows it to interact with other proteins involved in DNA repair and chromatin remodeling.
Defects in the FANCC protein can result in impaired DNA repair and increased sensitivity to DNA-damaging agents, leading to the characteristic features of Fanconi anemia. Additionally, mutations in the FANCC gene have been associated with an increased risk of developing acute myeloid leukemia (AML) and other cancers.
Fanconi Anemia Complementation Group D2 Protein, also known as FANCD2 protein, is a key player in the Fanconi anemia (FA) pathway, which is a DNA repair pathway that helps to maintain genomic stability. The FA pathway is responsible for the repair of DNA interstrand cross-links (ICLs), which are harmful lesions that can lead to genomic instability and cancer.
FANCD2 protein is part of the E3 ubiquitin ligase complex that monoubiquitinates FANCI protein, forming a heterodimeric complex known as ID2. The monoubiquitination of FANCD2/FANCI is a critical step in the FA pathway and is required for the recruitment of downstream repair factors to the site of DNA damage.
Mutations in the gene that encodes FANCD2 protein can lead to Fanconi anemia, a rare genetic disorder characterized by bone marrow failure, congenital abnormalities, and an increased risk of cancer. The disease is typically inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.
Hematocrit is a medical term that refers to the percentage of total blood volume that is made up of red blood cells. It is typically measured as part of a complete blood count (CBC) test. A high hematocrit may indicate conditions such as dehydration, polycythemia, or living at high altitudes, while a low hematocrit may be a sign of anemia, bleeding, or overhydration. It is important to note that hematocrit values can vary depending on factors such as age, gender, and pregnancy status.
Fanconi anemia complementation group A protein (FANCA) is a protein encoded by the FANCA gene in humans. It is a part of the Fanconi anemia (FA) pathway, which is a group of proteins that play a critical role in maintaining genomic stability and preventing cancer.
The FA pathway is involved in the repair of DNA interstrand crosslinks (ICLs), which are harmful lesions that can block replication and transcription of DNA. FANCA protein, along with other FA proteins, forms a complex called the "FA core complex" that monoubiquitinates another FA protein called FANCD2. This monoubiquitination event is essential for the recruitment of downstream repair factors to damaged DNA and restoration of normal DNA structure.
Mutations in the FANCA gene can lead to Fanconi anemia, a rare genetic disorder characterized by congenital abnormalities, bone marrow failure, and increased risk of cancer. The disease is typically inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.
Pallor is a medical term that refers to an abnormal pale appearance of the skin, mucous membranes, or nail beds. It can be a sign of various underlying medical conditions such as anemia (a decrease in red blood cells or hemoglobin), blood loss, malnutrition, vitamin deficiencies, or certain diseases that affect circulation or oxygenation of the blood. Pallor can also occur due to emotional distress or fear, leading to a temporary reduction in blood flow to the skin. It is important to note that pallor should be evaluated in conjunction with other symptoms and medical history for an accurate diagnosis.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Hypochromic anemia
Non-sideropenic hypochromic anaemia
List of OMIM disorder codes
Iron supplement
Orotate phosphoribosyltransferase
Mean corpuscular hemoglobin
Iron(II) gluconate
Microcytic anemia
Head injury
Microprius rufulus
Hemoglobin subunit alpha
Necatoriasis
Codocyte
Plummer-Vinson syndrome
Benjamin syndrome
Nephrotic syndrome
Atransferrinemia
Anemia
Angiostrongylus vasorum
Microcytosis
Nutritional anemia
Uncinaria stenocephala
Koilonychia
Iron-deficiency anemia
Green children of Woolpit
Hemoglobin
Molsheim Charterhouse
Hidradenitis suppurativa
Erik Adolf von Willebrand
Sertindole
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Showed hypochromic-microcytic1
- testing showed hypochromic-microcytic anemia (hemoglobin 8.2 g/dL). (cdc.gov)
Microcytic hypochromic indices2
- however, microcytic hypochromic indices also can be associated with anemia of chronic disease. (medscape.com)
- A hemoglobinopathy work up was done due to the microcytic hypochromic indices. (ispub.com)
Thalassemia4
- The most common causes of this kind of anemia are iron deficiency and thalassemia. (wikipedia.org)
- Of all the hemolytic anemias, thalassemia is associated with ineffective erythropoiesis and normal reticulocyte count. (pediatriconcall.com)
- Kanokwan Sanchaisuriya This community-based study investigated anemia prevalence and certain hematologic features and their possible relationships to thalassemia and iron deficiency (ID) in a population of older people in Northeastern Thailand. (karger.com)
- Frank P. Schelp Background and Aims: Information about the extent to which anemia is related to thalassemia and iron deficiency (ID. (karger.com)
Indices1
- The α-thalassaemia testing was requested predominantly to explain microcytic hypochromic haematological indices. (samj.org.za)
Normochromic1
- Anaemia was diagnosed in 75 patients (37.5%) overall: 45 had microcytic hypochromic anaemia, 18 normocytic normochromic and 12 macrocytic hy- perchromic. (who.int)
Pallor2
- In hypochromic cells, this area of central pallor is increased. (wikipedia.org)
- Hypochromic microcytic anemia with iron overload can lead to pale skin (pallor), tiredness (fatigue), and slow growth. (checkorphan.org)
Deficiency32
- Hypochromic anemia may be caused by iron deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. (umassmed.edu)
- Colloque INSERM-ISTA/CNAM : Groupes à risque de carence en fer dans les pays industrialisés = Groups with high risk of iron deficiency in industrialized countries, Paris, 27-28 mai 1983 / publié sous la responsabilité de Henri Dupin et Serge Hercberg. (who.int)
- Anemia, particularly the iron deficiency kind, has been linked to mental health conditions like depression and anxiety. (psychcentral.com)
- A Japanese study from 2018 with 11,876 participants identified a link between self-reported depression and self-reported iron-deficiency anemia. (psychcentral.com)
- The most common form of this condition, iron deficiency anemia, has the added impact of insufficient iron. (psychcentral.com)
- For example, iron-deficiency anemia results from inadequate amounts of iron in your body. (psychcentral.com)
- Iron deficiency anemia (IDA) occurs when you don't have enough iron to make the blood hemoglobin you need to transport oxygen. (psychcentral.com)
- This type of anemia is caused by a deficiency in vitamin B12, which is required to produce healthy red blood cells. (psychcentral.com)
- The diagnosis was 'mild iron deficiency anemia,' and iron therapy was prescribed. (cdc.gov)
- Benaya Rozen-Zvi Iron deficiency anemia is a common complication of chronic kidney disease (CKD). (karger.com)
- As such, multiple parameters are used for the diagnosis of iron deficiency anaemia in IBD. (karger.com)
- If it is not treated, this can lead to a disorder called iron deficiency anemia . (ucsfbenioffchildrens.org)
- In the past three decades, increased iron intake among infants has resulted in a decline in childhood iron-deficiency anemia in the United States. (cdc.gov)
- As a consequence, the use of screening tests for anemia has become a less efficient means of detecting iron deficiency in some populations. (cdc.gov)
- These recommendations update the 1989 'CDC Criteria for Anemia in Children and Childbearing-Aged Women' (MMWR 1989;38(22):400-4) and are the first comprehensive CDC recommendations to prevent and control iron deficiency. (cdc.gov)
- In the United States, the prevalence of iron-deficiency anemia among children declined during the 1970s in association with increased iron intake during infancy (1-3). (cdc.gov)
- Because of this decline, the value of anemia as a predictor of iron deficiency has also declined, thus decreasing the effectiveness of routine anemia screening among children. (cdc.gov)
- CDC requested the Institute of Medicine to convene an expert committee to develop recommendations for preventing, detecting, and treating iron-deficiency anemia among U.S. children and U.S. women of childbearing age. (cdc.gov)
- Besides iron deficiency and ACD, metabolic disturbances and vitamin deficiencies as well as commonly used IBD drugs can aggravate anemia in IBD. (haematologica.org)
- Therefore, IBD-associated anemia is the prototype of iron deficiency combined with ACD. (haematologica.org)
- Vitamin B6 deficiency can cause hypochromic microcytic anemia without iron deficiency and central nervous system disturbances. (vitamins-minerals-supplements.org)
- A common reason for the two peaks to merge is iron deficiency anemia. (vin.com)
- In iron deficiency anemia, the erythrocytes are smaller (microcytic) and there is often thrombocytosis with large platelets so the two cell types merge in size and may overlap. (vin.com)
- Iron deficiency anemia is perhaps the best example of where instrument graphics improve diagnosis. (vin.com)
- Weiser revealed that 70% of five -week-old kittens had iron deficiency anemia but needed improved instrumentation to show what percentage of erythrocytes were smaller than normal. (vin.com)
- These mean (average) values are too insensitive to reveal iron deficiency in kittens as well as the early stages of iron deficiency anemia in dogs. (vin.com)
- Bayer RBC cytograms and histograms are very sensitive in detecting iron deficiency anemia. (vin.com)
- Iron deficiency anemia is detected earliest by the Bayer system because very few microcytic hypochromic RBCs are needed in the patient's blood to be seen on the RBC cytogram. (vin.com)
- Also known as iron deficiency anemia and the most common type found in the elderly due to nutritional deficits. (brainynurses.com)
- Possible causes of macrocytic anemia include vitamin B-12 deficiency, folate deficiency, liver disease, and hypothyroidism. (medscape.com)
- The diagnosis of iron deficiency (ID) and iron-deficiency anaemia (IDA) in ill children is complicated by the unreliability of serum ferritin (S-ferritin). (bvsalud.org)
- These general, nonspecific tests may indicate common underlying conditions, including iron deficiency and inherited anemias. (cdc.gov)
Chlorosis1
- Hypochromic anemia was historically known as chlorosis or green sickness for the distinct skin tinge sometimes present in patients, in addition to more general symptoms such as a lack of energy, shortness of breath, dyspepsia, headaches, a capricious or scanty appetite and amenorrhea. (wikipedia.org)
Hemoglobin8
- Anemia characterized by a decrease in the ratio of the weight of hemoglobin to the volume of the erythrocyte, i.e., the mean corpuscular hemoglobin concentration is less than normal. (umassmed.edu)
- Anemia is defined as an absolute reduction in the quantity of the oxygen-carrying pigment hemoglobin (Hgb) in the circulating blood. (medscape.com)
- People with X-linked sideroblastic anemia have mature red blood cells that are smaller than normal (microcytic) and appear pale (hypochromic) because of the shortage of hemoglobin. (medlineplus.gov)
- The signs and symptoms of X-linked sideroblastic anemia result from a combination of reduced hemoglobin and an overload of iron. (medlineplus.gov)
- Low hemoglobin levels and the resulting accumulation of iron in the body's organs lead to the characteristic features of X-linked sideroblastic anemia. (medlineplus.gov)
- Anemia can be caused by increased blood loss, decreased production due to nutritional deficits or bone marrow suppression, or increased destruction due to genetically abnormal hemoglobin or antibodies. (brainynurses.com)
- The hemoglobin is low, signifying anemia. (brainynurses.com)
- Screening should include hemoglobin electrophoresis, particularly in individuals with anemia, red blood cell abnormalities, and/or morbidity suggestive of disease. (cdc.gov)
RBCs1
- The marrow does not respond appropriately to microcytic anemia, leading to decreased production of RBCs. (medscape.com)
Diagnosis4
- Anemia is a manifestation of an underlying disease process and is not a diagnosis in itself. (medscape.com)
- Com- be considered in the differential diagnosis plete blood count was performed on all of anaemia [ 4 ]. (who.int)
- The aim of this study was to record the The cut-off values for the diagnosis of prevalence of anaemia, its type as well as anaemia were based on mean ± 2 SD its possible causes among a group of young values of controls. (who.int)
- For β-thalassaemia and sickle cell anaemia, most testing was performed for prenatal diagnosis purposes. (samj.org.za)
Prevalence1
- The prevalence of maternal anemia in developing countries / Nancy L. Sloan, Elizabeth A. Jordan. (who.int)
Iron11
- Hypochromic microcytic anemia with iron overload is a condition that impairs the normal transport of iron in cells. (checkorphan.org)
- In this condition, red blood cells cannot access iron in the blood, so there is a decrease of red blood cell production (anemia) that is apparent at birth. (checkorphan.org)
- In hypochromic microcytic anemia with iron overload, the iron that is not used by red blood cells accumulates in the liver, which can impair its function over time. (checkorphan.org)
- Mutations in the SLC11A2 gene cause hypochromic microcytic anemia with iron overload. (checkorphan.org)
- The lack of involvement of other tissues in hypochromic microcytic anemia with iron overload is likely because these tissues have other ways to transport iron. (checkorphan.org)
- Your provider may recommend this test if you have signs or symptoms of anemia due to low iron. (mountsinai.org)
- A lower-than-normal level of ferritin occurs if you have anemia caused by low iron levels in the body. (mountsinai.org)
- It is very likely that the doctor who treated the child initially would have given iron supplements for the anemia. (pediatriconcall.com)
- CDC emphasizes sound iron nutrition for infants and young children, screening for anemia among women of childbearing age, and the importance of low-dose iron supplementation for pregnant women. (cdc.gov)
- Iron-deficient anemia (IDA) is one of the most common causes of anemia in refugees. (cdc.gov)
- See Domestic Screening Guidance for Evaluation of Nutritional Status and Growth in Refugee Children for additional information on iron-deficient anemia. (cdc.gov)
Intrinsic1
- People who have pernicious anemia sometimes lack intrinsic factor, which helps the body absorb B12. (psychcentral.com)
Aplastic anemia2
- Anemias with primary bone involvement include aplastic anemia and myelophthisic anemia . (medscape.com)
- Aplastic anemia occurs when something interferes with the production of new blood cells, leading to a blood cell count that is too low. (psychcentral.com)
Hemolytic anemia1
- Cold agglutinin disease or syndrome is a relatively uncommon autoimmune hemolytic anemia presenting in the middle aged or elderly (1). (ispub.com)
Sickle3
- A retrospective file analysis ( N =1 249) was performed for all individuals who had molecular genetic testing for α-thalassaemia, β-thalassaemia and sickle cell anaemia to examine indications for testing, population origins of patients and molecular genetics findings. (samj.org.za)
- For sickle cell anaemia, most prenatal tests were requested by African families. (samj.org.za)
- This type of anemia includes sickle cell anemia, thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome, aortic valve prosthesis, disseminated intravascular coagulation (DIC), cold agglutinin disease, and paroxysmal cold hemoglobinuria (PCH). (medscape.com)
Etiology3
- The etiology of myelophthisic anemia involves interruption of normal hematopoiesis due to the accumulation of malignant or reactive cells or cell products. (medscape.com)
- children's age group are allowed to con- tinue follow-up indefinitely if they wish, in The etiology of anaemia in type 1 diabetes order not to change the protocol of therapy. (who.int)
- Also malena due to Gl losses causing severe anemia without frank blood in stools is a rare etiology especially since the child also has hepatosplenomegaly. (pediatriconcall.com)
Smear2
- Also peripheral smear may show presence of hypochromic, microcytic anemia. (pediatriconcall.com)
- After incubation and the smear revealed a microcytic hypochromic picture with polychromasia and target cells (Fig.3). (ispub.com)
Disturbances1
- The use of an organic solvent containing 50 percent pseudocumene, 30 percent mesitylene, and traces of hemimellitene caused hypochromic anemia, hemopoietic disturbances, chronic asthmatic bronchitis, and central nervous system depression in humans. (cdc.gov)
Pregnancy2
- The prevention of hypochromic anaemia in pregnancy. (jameslindlibrary.org)
- In contrast, the rate of anemia among low-income women during pregnancy is high, and no improvement has been noted since the 1970s (4). (cdc.gov)
Sideroblastic3
- Mutations in the ALAS2 gene cause X-linked sideroblastic anemia. (medlineplus.gov)
- People who have a mutation in another gene, HFE , along with a mutation in the ALAS2 gene may experience a more severe form of X-linked sideroblastic anemia. (medlineplus.gov)
- Carriers of an ALAS2 mutation can pass on the mutated gene, but most do not develop any symptoms associated with X-linked sideroblastic anemia. (medlineplus.gov)
Chronic Anemia1
- Go to Anemia and Pediatric Chronic Anemia for complete information on these topics. (medscape.com)
Suggests1
- hypochromic anaemia suggests IDA but is not specific. (bvsalud.org)
Inflammation2
- however, it often manifests in combination with anaemia of inflammation. (karger.com)
- Inflammation affects three major steps essential for normal erythropoiesis and can, therefore, lead to the development of anemia of inflammation. (haematologica.org)
Hematopoiesis1
- Agnogenic myeloid metaplasia, which is characterized by anemia with primary bone marrow involvement, involves gradual bone marrow fibrosis, extramedullary hematopoiesis, and splenomegaly with no known underlying systemic disorder. (medscape.com)
Patients7
- ABSTRACT Over a 2-month period, 200 type 1 diabetic patients attending a paediatric diabetic clinic in Cairo, Egypt were screened for anaemia and other complications of diabetes. (who.int)
- Une anémie a été diagnostiquée chez 75 patients (37,5 %) en tout : 45 avaient une anémie hypochrome microcytaire, 18 une anémie normochrome normocytaire et 12 une anémie hyperchrome macrocytaire. (who.int)
- Sur les 75 patients, 41 (54,7 %) avaient une carence en fer, 14 (18,7 %) avaient une carence en folates et 14 (18,7 %) avaient une thalassémie mineure. (who.int)
- Between January and December 2002, 200 neglect or ignorance, do not follow the patients attending the clinic were screened appropriate dietary regimes, are at-risk of for the presence of anaemia. (who.int)
- They were living in the same with ultimate renal failure is an important area and of the same socioeconomic class cause of anaemia in these patients [ 2 ]. (who.int)
- Manuel Muñoz Preoperative anemia affects 30-40% of patients undergoing major surgery and is an independent risk factor for perioperative blood transfusion, morbidity, and mortality. (karger.com)
- Anemia is seen frequently in many different types of patients. (brainynurses.com)
Diseases1
- A wide array of diseases, including inflammatory, infectious, and malignant disorders, may at some point be associated with anemia. (medscape.com)
Acute1
- Anemia is further broadly subcategorized into acute and chronic. (medscape.com)
Bone marrow2
- Normocytic anemia is further divided into 2 broad categories: anemia with primary bone marrow involvement and anemia secondary to underlying disease. (medscape.com)
- When anemia is present, the bone marrow releases reticulocytes, which then mature in the blood or spleen with the help of folic acid and B 12 . (brainynurses.com)
Affects2
- Anemia is a condition that affects your blood cells and reduces their ability to transport oxygen. (psychcentral.com)
- Hypoxia (reduced oxygen levels) from anemia affects multiple areas of your body, including your brain. (psychcentral.com)
Types3
- Meanwhile, other types of anemia have causes such as genetics or autoimmunity. (psychcentral.com)
- There are several types of anemia, all of which can decrease the amount of oxygen transported in your blood. (psychcentral.com)
- Haematinics are the agents used for formation of blood to treat various types of anemias. (foobrdigital.com)
Common1
- Anemia is far more common in underdeveloped countries than in the United States. (medscape.com)
Uncommon1
- This form of anemia is uncommon. (medlineplus.gov)
Secondary1
- Most cases of anemia in the world are secondary to an underlying disease. (medscape.com)
Grupo2
- Apenas nos experimentos com animais do grupo So4 expostos por 28 dias, verificou-se similaridade entre resultados dos parâmetros acima descritos, além da ocorrência de anemia microcÃtica e hipocrômica. (usp.br)
- Os animais da prole do grupo PF apresentaram hemograma indicativo de anemia megaloblástica. (usp.br)
Inadequate1
- Erythropoietin levels in ACD have been found to be inadequate for the degree of anemia in many but not all conditions including IBD 9 , 10 which may be partly due to interleukin-1- and TNF-α-mediated inhibition of erythropoietin promoter activity and a cytokine-driven formation of toxic radicals, thereby damaging erythropoietin-producing cells and inhibiting erythropoietin formation in the kidney. (haematologica.org)
Suggestive1
- This child has presented with progressive anemia inspite of blood transfusion suggestive of transfusion dependent anemia. (pediatriconcall.com)
Oxygen1
- When you have anemia, your blood can't transport as much oxygen as it should. (psychcentral.com)
Lead1
- A disease may lead to anemia through a combination of mechanisms. (medscape.com)
Destruction1
- Anemia usually is grouped into 3 etiologic categories: decreased red blood cell (RBC) production, increased RBC destruction, and blood loss. (medscape.com)
Differential1
- The CBC with differential is a frequently ordered lab test and provides much information regarding infection, anemia, coagulation, and hydration. (brainynurses.com)
Type1
- Hypochromic anemia is a generic term for any type of anemia in which the red blood cells are paler than normal. (wikipedia.org)