Hemoglobins
Hemoglobin A
Hemoglobins, Abnormal
Fetal Hemoglobin
Hemoglobin, Sickle
Hemoglobin C
Oxyhemoglobins
Hemoglobin A, Glycosylated
Hemoglobin E
Hemoglobin A2
Truncated Hemoglobins
Hemoglobinopathies
Oxygen
Hemoglobin C Disease
Blood Substitutes
Hemoglobin J
Hemoglobin H
Anemia, Sickle Cell
Erythrocytes
2,3-Diphosphoglycerate
Globins
Heme
Thalassemia
Iron
Hematocrit
Erythropoietin
Hemoglobin SC Disease
Carbon Monoxide
Hematinics
Erythrocyte Indices
Anemia, Iron-Deficiency
Phytic Acid
Haptoglobins
beta-Thalassemia
Hemoglobin M
Antisickling Agents
alpha-Thalassemia
Ferritins
alpha-Globins
Erythrocytes, Abnormal
Myoglobin
Hemolysis
beta-Globins
Hydrogen-Ion Concentration
Anemia, Hypochromic
Erythropoiesis
Hemoglobinuria
Hemin
Spectrophotometry
Electrophoresis, Cellulose Acetate
Pregnancy Complications, Hematologic
Heinz Bodies
Exchange Transfusion, Whole Blood
Annelida
Reticulocyte Count
Oligochaeta
Hemeproteins
Blood Transfusion
Iron Isotopes
Diabetes Mellitus
Spectroscopy, Near-Infrared
Reticulocytes
Diabetes Mellitus, Type 2
Fructosamine
Electrophoresis, Starch Gel
Anemia, Hemolytic
Isoelectric Focusing
Macromolecular Substances
Blood Cell Count
Protein Conformation
Erythrocyte Transfusion
Protein Binding
Allosteric Regulation
Renal Dialysis
Chromatography, High Pressure Liquid
Vitreoscilla
Erythrocyte Volume
Erythrocyte Aging
Partial Pressure
Polychaeta
Hemodilution
Oxidation-Reduction
Bivalvia
Chironomidae
gamma-Globins
Oximetry
Phenylhydrazines
Kidney Failure, Chronic
Nitric Oxide
Hydroxyurea
Iron, Dietary
Protoporphyrins
Amino Acid Sequence
Spectrum Analysis, Raman
Erythrocyte Membrane
Erythrocruorins
Treatment Outcome
Spectrum Analysis
Prospective Studies
Biological Markers
Whales
Chromatography, Ion Exchange
Diabetes Mellitus, Type 1
Leghemoglobin
Risk Factors
Altitude
Leukemia, Erythroblastic, Acute
Transferrin
Serum Albumin
Molecular Sequence Data
Retrospective Studies
Osmotic Fragility
Pregnancy
Bloodletting
Reference Values
Erythroblasts
Erythroid Precursor Cells
Oxygen Consumption
Chromium Isotopes
Methemoglobinemia
Amino Acids
Dicrocoelium
Blood Proteins
Binding Sites
The determination of hemoglobin and myoglogin residues as a parameter for testing heat exposure in back bacon. (1/8574)
The use of an extraction of the heme pigments hemoglobin and myoglobin as a test for the heat exposure of back bacon was investigated by treating back bacon at varying temperatures of 50-70 degrees C and times of two to 180 minutes and observing the effect on the absorbance of heme pigment residue after nitrite oxidation. Absorbance at 409 nm was used in place of the more usual 540 nm to provide greater sensitivity in the detection of heme. A decrease in residual heme pigments was time-dependent, particularly at lower temperatures. In view of this factor and the complex nature of the heat exposure of a large block of back bacon, the application of this test would require a calibration of each process. Alternatively, limits to the amounts of heme pigment residue could be set. The heme pigment test is useful in its simplicity and overcomes difficulties associated with the coagulation and enzyme tests. (+info)Thiamine deficiency is prevalent in a selected group of urban Indonesian elderly people. (2/8574)
This cross-sectional study involved 204 elderly individuals (93 males and 111 females). Subjects were randomly recruited using a list on which all 60-75 y-old-people living in seven sub-villages in Jakarta were included. The usual food intake was estimated using semiquantitative food frequency questionnaires. Hemoglobin, plasma retinol, vitamin B-12, red blood cell folate and the percentage stimulation of erythrocyte transketolase (ETK), as an indicator of thiamine status, were analyzed. Median energy intake was below the assessed requirement. More than 75% of the subjects had iron and thiamine intakes of approximately 2/3 of the recommended daily intake, and 20.2% of the study population had folate intake of approximately 2/3 of the recommended daily intake. Intakes of vitamins A and B-12 were adequate. Biochemical assessments demonstrated that 36.6% of the subjects had low thiamine levels (ETK stimulation > 25%). The elderly men tended to have lower thiamine levels than the elderly women. The overall prevalence of anemia was 28.9%, and the elderly women were affected more than the elderly men. Low biochemical status of vitamins A, B-12 and RBC folate was found in 5.4%, 8.8 % and 2.9% of the subjects, respectively. Dietary intakes of thiamine and folate were associated with ETK stimulation and plasma vitamin B-12 concentration (r = 0.176, P = 0.012 and r = 0.77, P = 0.001), respectively. Results of this study suggest that anemia, thiamine and possibly vitamin B-12 deficiency are prevalent in the elderly living in Indonesia. Clearly, micronutrient supplementation may be beneficial for the Indonesian elderly population living in underprivileged areas. (+info)Subunit dissociation in fish hemoglobins. (3/8574)
The tetramer-dimer dissociation equilibria (K 4,2) of several fish hemoglobins have been examined by sedimentation velocity measurements with a scanner-computer system for the ultracentrifuge and by flash photolysis measurements using rapid kinetic methods. Samples studied in detail included hemoglobins from a marine teleost, Brevoortia tyrannus (common name, menhaden); a fresh water teleost, Cyprinus carpio, (common name, carp); and an elasmobranch Prionace glauca (common name, blue shark). For all three species in the CO form at pH 7, in 0.1 M phosphate buffer, sedimentation coefficients of 4.3 S (typical of tetrameric hemoglobin) are observed in the micromolar concentration range. In contrast, mammalian hemoglobins dissociate appreciably to dimers under these conditions. The inability to detect dissociation in three fish hemoglobins at the lowest concentrations examined indicates that K 4,2 must have a value of 10(-8) M or less. In flash photolysis experiments on very dilute solutions in long path length cells, two kinetic components were detected with their proportions varying as expected for an equilibrium between tetramers (the slower component) and dimers (the faster component); values of K 4,2 for the three fish hemoglobins in the range 10(-9) to 10(-8) M were calculated from these data. Thus, the values of K 4,2 for liganded forms of the fish hemoglobins appear to be midway between the value for liganded human hemoglobin (K 4,2 approximately 10(-6) M) and unliganded human hemoglobin (K 4,2 approximately 10(-12) M). This conclusion is supported by measurements on solutions containing guanidine hydrochloride to enhance the degree of dissociation. All three fish hemoglobins are appreciably dissociated at guanidine concentrations of about 0.8 M, which is roughly midway between the guanidine concentrations needed to cause comparable dissociation of liganded human hemoglobin (about 0.4 M) and unliganded human hemoglobin (about 1.6 M). Kinetic measurements on solutions containing guanidine hydrochloride indicated that there are changes in both the absolute rates and the proportions of the fast and slow components, which along with other factors complicated the analysis of the data in terms of dissociation constants. Measurements were also made in solutions containing urea to promote dissociation, but with this agent very high concentrations (about 6 M) were required to give measureable dissociation and the fish hemoglobins were unstable under these conditions, with appreciable loss of absorbance spectra in both the sedimentation and kinetic experiments. (+info)Reactivity of cyanate with valine-1 (alpha) of hemoglobin. A probe of conformational change and anion binding. (4/8574)
The 3-fold increase in the carbamylation rate of Val-1 (alpha) of hemoglobin upon deoxygenation described earlier is now shown to be a sensitive probe of conformational change. Thus, whereas this residue in methemoglobin A is carbamylated at the same rate as in liganded hemoglobin, upon addition of inositol hexaphosphate its carbamylation rate is enhanced 30% as much as the total change in the rate between the CO and deoxy states. For CO-hemoglobin Kansas in the presence of the organic phosphate, the relative increase in the carbamylation rate of this residue is about 50%. These results indicate that methemoglobin A and hemoglobin Kansas in the presence of inositol hexaphosphate do not assume a conformation identical with deoxyhemoglobin but rather form either a mixture of R and T states or an intermediate conformation in the region around Val-1 (alpha). Studies on the mechanism for the rate enhancement in deoxyhemoglobin suggest that the cyanate anion binds to groups in the vicinity of Val-1 (alpha) prior to proton transfer and carbamylation of this NH2-terminal residue. Thus, specific removal with carboxypeptidase B of Arg-141 (alpha), which is close to Val-1 (alpha) in deoxyhemoglobin, abolishes the enhancement in carbamylation. Chloride, which has the same valency as cyanate, is a better competitive inhibitor of the carbamylation of deoxyhemoglobin (Ki = 50 mM) compared with liganded hemoglobin. Nitrate and iodide are also effective inhibitors of the carbamylation of Val-1 (alpha) of deoxyhemoglobin (Ki = 35 mM); inorganic phosphate, sulfate, and fluoride are poor competitive inhibitors. The change in pKa of Val-1 (alpha) upon deoxygenation may be due to its differential interaction with chloride. (+info)Aggregation of deoxyhemoglobin S at low concentrations. (5/8574)
The self-association of deoxyhemoglobin S was measured in dilute solutions (0 to 5 g/dl) by Rayleigh light scattering at 630 nm and osmometry in 0.05 M potassium phosphate buffer (pH 7.35). Weight and number average molecular weights (Mw and Mn, respectively) and the second or higher virial coefficients, B' were determined. No experimentally significant differences were observed between oxy- and deoxy-Hb S up to the concentration of 2 g/dl; their apparent average molecular weights were within experimental error. Above that concentration, both Mn and Mw of deoxy-Hb S were significantly different from that of oxy-Hb S. The negative second viral coefficent of deoxy-Hb S, observed by both techniques, is consistent with the self-association of this protein. The lack of effect of 0.4 M propylurea on the state of aggregation and the significant influence of 0.1 M NaCl suggests that polar interactions are involved in formation of these aggregates. (+info)O-raffinose cross-linking markedly reduces systemic and renal vasoconstrictor effects of unmodified human hemoglobin. (6/8574)
The hemodynamic effects of a 20% exchange-transfusion with different solutions of highly purified human hemoglobin A-zero (A0) were evaluated. We compared unmodified hemoglobin with hemoglobin cross-linked with O-raffinose. Unmodified hemoglobin increased systemic vascular resistance and mean arterial pressure more than the O-raffinose cross-linked hemoglobin solution (by approximately 45% and approximately 14%, respectively). Unmodified hemoglobin markedly reduced cardiac output (CO) by approximately 21%, whereas CO was unaffected by the O-raffinose cross-linked hemoglobin solution. Unmodified and O-raffinose cross-linked hemoglobin solutions increased mean arterial pressure to comparable extents ( approximately 14% and approximately 9%, respectively). Unmodified hemoglobin increased renal vascular resistance 2-fold and reduced the glomerular filtration rate by 58%. In marked contrast, the O-raffinose cross-linked hemoglobin had no deleterious effect on the glomerular filtration rate, renal blood flow, or renal vascular resistance. The extents to which unmodified and O-raffinose cross-linked hemoglobin solutions inactivated nitric oxide also were compared using three separate in vitro assays: platelet nitric oxide release, nitric oxide-stimulated platelet cGMP production, and endothelium-derived relaxing factor-mediated inhibition of platelet aggregation. Unmodified hemoglobin inactivated or oxidized nitric oxide to a greater extent than the O-raffinose cross-linked hemoglobin solutions in all three assays. In summary, O-raffinose cross-linking substantially reduced the systemic vasoconstriction and the decrease in CO induced by unmodified hemoglobin and eliminated the deleterious effects of unmodified hemoglobin on renal hemodynamics and function. We hypothesize that O-raffinose cross-linking reduces the degree of oxidation of nitric oxide and that this contributes to the reduced vasoactivity of this modified hemoglobin. (+info)Detection of viruses and body fluids which may contain viruses in the domestic environment. (7/8574)
The domestic environment was investigated for the presence of viruses and body fluids that may contain viruses. A range of surfaces in 39 homes (17 visited on 2 occasions) were sampled by swabbing and analysed using cell culture, reverse transcription polymerase chain reaction for enteroviral RNA, haemoglobin as a marker for blood, amylase as an indicator of urine, saliva and sweat, and protein as an indicator of general hygiene. Haemoglobin was found on 1.9% of surfaces sampled and of the positive samples 30% were from articles frequently handled. Amylase (> 5 U/l) was found in 29.3% of samples tested. Protein was found in 97.8% of samples tested. Enteroviral RNA, indicating the presence of virus, was detected in 3 out of 448 samples tested; they were from a tap handle, telephone handpiece and a toilet bowl. No viruses were isolated in cell culture, however significant problems were encountered with bacterial and fungal contamination. This work demonstrates that only testing environmental samples for bacteria and ATP may not give a total view of the microbiological problem in the home. A range of test methods is useful to gain a broad view of the problems of hygiene in the home and to allow comparative studies of specific areas such as the kitchen and bathroom. (+info)Amino acid sequences of the alpha and beta chains of adult hemoglobin of the slender loris, Loris tardigradus. (8/8574)
alpha and beta chains from adult hemoglobin of the slender loris (Loris tardigradus) were isolated by Amberlite CG-50 column chromatography. After S-aminoethylation, both chains were digested with trypsin and the amino acid sequences of the tryptic peptides obtained were analyzed. Further, the order of these tryptic peptides in each chain was deduced from their homology with the primary structures of alpha and beta chains of human adult hemoglobin. Comparing the primary structures of the alpha and beta chains of adult hemoglobin of the slender loris thus obtained with those of adult hemoglobin of the slow loris, 4 amino acid substitutions in the alpha chains and 2 in the beta chains were recognized. (+info)There are many different types of anemia, each with its own set of causes and symptoms. Some common types of anemia include:
1. Iron-deficiency anemia: This is the most common type of anemia and is caused by a lack of iron in the diet or a problem with the body's ability to absorb iron. Iron is essential for making hemoglobin.
2. Vitamin deficiency anemia: This type of anemia is caused by a lack of vitamins, such as vitamin B12 or folate, that are necessary for red blood cell production.
3. Anemia of chronic disease: This type of anemia is seen in people with chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer.
4. Sickle cell anemia: This is a genetic disorder that affects the structure of hemoglobin and causes red blood cells to be shaped like crescents or sickles.
5. Thalassemia: This is a genetic disorder that affects the production of hemoglobin and can cause anemia, fatigue, and other health problems.
The symptoms of anemia can vary depending on the type and severity of the condition. Common symptoms include fatigue, weakness, pale skin, shortness of breath, and dizziness or lightheadedness. Anemia can be diagnosed with a blood test that measures the number and size of red blood cells, as well as the levels of hemoglobin and other nutrients.
Treatment for anemia depends on the underlying cause of the condition. In some cases, dietary changes or supplements may be sufficient to treat anemia. For example, people with iron-deficiency anemia may need to increase their intake of iron-rich foods or take iron supplements. In other cases, medical treatment may be necessary to address underlying conditions such as kidney disease or cancer.
Preventing anemia is important for maintaining good health and preventing complications. To prevent anemia, it is important to eat a balanced diet that includes plenty of iron-rich foods, vitamin C-rich foods, and other essential nutrients. It is also important to avoid certain substances that can interfere with the absorption of nutrients, such as alcohol and caffeine. Additionally, it is important to manage any underlying medical conditions and seek medical attention if symptoms of anemia persist or worsen over time.
In conclusion, anemia is a common blood disorder that can have significant health implications if left untreated. It is important to be aware of the different types of anemia, their causes, and symptoms in order to seek medical attention if necessary. With proper diagnosis and treatment, many cases of anemia can be successfully managed and prevented.
The most common types of hemoglobinopathies include:
1. Sickle cell disease: This is caused by a point mutation in the HBB gene that codes for the beta-globin subunit of hemoglobin. It results in the production of sickle-shaped red blood cells, which can cause anemia, infections, and other complications.
2. Thalassemia: This is a group of genetic disorders that affect the production of hemoglobin and can result in anemia, fatigue, and other complications.
3. Hemophilia A: This is caused by a defect in the F8 gene that codes for coagulation factor VIII, which is essential for blood clotting. It can cause bleeding episodes, especially in males.
4. Glucose-6-phosphate dehydrogenase (G6PD) deficiency: This is caused by a point mutation in the G6PD gene that codes for an enzyme involved in red blood cell production. It can cause hemolytic anemia, especially in individuals who consume certain foods or medications.
5. Hereditary spherocytosis: This is caused by point mutations in the ANK1 or SPTA1 genes that code for proteins involved in red blood cell membrane structure. It can cause hemolytic anemia and other complications.
Hemoglobinopathies can be diagnosed through genetic testing, such as DNA sequencing or molecular genetic analysis. Treatment options vary depending on the specific disorder but may include blood transfusions, medications, and in some cases, bone marrow transplantation.
Hemoglobin C disease is characterized by the presence of both normal hemoglobin (HbA) and abnormal hemoglobin (HbC) in red blood cells, which leads to a variety of symptoms and complications. The severity of the disease can range from mild to severe, depending on the specific mutations present and the percentage of HbC in the blood.
Symptoms of Hemoglobin C Disease:
The symptoms of hemoglobin C disease can vary in severity and may include:
1. Anemia: People with HbC disease often have lower than normal levels of red blood cells, which can lead to fatigue, weakness, and shortness of breath.
2. Jaundice: Yellowing of the skin and eyes due to high bilirubin levels can occur in severe cases of HbC disease.
3. Enlarged spleen: The spleen may become enlarged due to the accumulation of abnormal red blood cells.
4. Gallstones: People with HbC disease are at increased risk of developing gallstones.
5. Pain: Pain in the abdomen, joints, and other parts of the body can occur due to the abnormal hemoglobin.
6. Increased risk of infections: People with HbC disease may be more susceptible to infections due to their anemia and weakened immune system.
7. Delayed development: Children with HbC disease may experience delayed development and growth.
Complications of Hemoglobin C Disease:
Hemoglobin C disease can lead to a number of complications, including:
1. Stroke: People with HbC disease are at increased risk of stroke due to the abnormal hemoglobin.
2. Heart failure: The heart may become enlarged and fail to pump blood effectively due to the strain placed on it by the abnormal red blood cells.
3. Kidney damage: The kidneys may be damaged due to the accumulation of abnormal red blood cells.
4. Anemia: People with HbC disease may develop anemia, which can lead to fatigue, weakness, and shortness of breath.
5. Blood transfusions: Regular blood transfusions may be necessary to maintain healthy red blood cell levels.
6. Iron overload: The frequent blood transfusions can lead to iron overload, which can cause liver damage and other complications.
7. Increased risk of cancer: People with HbC disease may be at increased risk of developing certain types of cancer, such as leukemia.
8. Increased risk of thrombosis: The abnormal hemoglobin can increase the risk of blood clots and thrombosis.
9. Shortened lifespan: People with HbC disease may have a shorter lifespan compared to those without the condition.
10. Reduced quality of life: HbC disease can significantly impact an individual's quality of life, leading to fatigue, pain, and other symptoms that can affect daily activities and relationships.
It is important to note that these complications can be managed with proper medical care and attention. Regular monitoring and follow-up with a healthcare provider are crucial for managing the disease and preventing or minimizing these complications.
Sickle cell anemia is caused by mutations in the HBB gene that codes for hemoglobin. The most common mutation is a point mutation at position 6, which replaces the glutamic acid amino acid with a valine (Glu6Val). This substitution causes the hemoglobin molecule to be unstable and prone to forming sickle-shaped cells.
The hallmark symptom of sickle cell anemia is anemia, which is a low number of healthy red blood cells. People with the condition may also experience fatigue, weakness, jaundice (yellowing of the skin and eyes), infections, and episodes of severe pain. Sickle cell anemia can also increase the risk of stroke, heart disease, and other complications.
Sickle cell anemia is diagnosed through blood tests that measure hemoglobin levels and the presence of sickle cells. Treatment typically involves managing symptoms and preventing complications with medications, blood transfusions, and antibiotics. In some cases, bone marrow transplantation may be recommended.
Prevention of sickle cell anemia primarily involves avoiding the genetic mutations that cause the condition. This can be done through genetic counseling and testing for individuals who have a family history of the condition or are at risk of inheriting it. Prenatal testing is also available for pregnant women who may be carriers of the condition.
Overall, sickle cell anemia is a serious genetic disorder that can significantly impact quality of life and life expectancy if left untreated. However, with proper management and care, individuals with the condition can lead fulfilling lives and manage their symptoms effectively.
There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.
Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.
There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.
Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.
Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.
The disease is classified into two main types: Hemoglobin SC disease and Hemoglobin SE disease. Hemoglobin SC disease is the most common type of hemoglobinopathy and affects approximately 1 in 10,000 people worldwide. It is more common in certain ethnic groups, such as people of African, Mediterranean, and Southeast Asian descent.
Hemoglobin SC disease can cause a range of symptoms, including anemia, fatigue, jaundice, and infections. The disease can also lead to complications such as splenomegaly (enlargement of the spleen), gallstones, and heart problems. Treatment for Hemoglobin SC disease typically involves blood transfusions and management of related complications.
In summary, Hemoglobin SC disease is a genetic disorder that affects the production of hemoglobin and can cause a range of symptoms and complications. It is more common in certain ethnic groups and can be managed with blood transfusions and other treatments.
Prevalence: Iron deficiency anemia is one of the most common nutritional disorders worldwide, affecting approximately 1.6 billion people, with women being more likely to be affected than men.
Causes: The main cause of iron deficiency anemia is a diet that does not provide enough iron. Other causes include:
* Poor absorption of iron from the diet
* Increased demand for iron due to growth or pregnancy
* Blood loss due to menstruation, internal bleeding, or surgery
* Chronic diseases such as kidney disease, cancer, and rheumatoid arthritis
Signs and symptoms: The signs and symptoms of iron deficiency anemia may include:
* Fatigue and weakness
* Pale skin
* Shortness of breath
* Dizziness or lightheadedness
* Headaches
* Cold hands and feet
Diagnosis: Iron deficiency anemia is diagnosed based on a physical exam, medical history, and laboratory tests, including:
* Complete blood count (CBC) to check for low red blood cell count and low hemoglobin level
* Serum iron and transferrin tests to check for low iron levels
* Ferritin test to check for low iron stores
Treatment: Treatment of iron deficiency anemia involves correcting the underlying cause, which may include:
* Dietary changes to increase iron intake
* Iron supplements to replenish iron stores
* Addressing any underlying causes such as bleeding or malabsorption
Complications: Iron deficiency anemia can lead to complications such as:
* Heart failure
* Increased risk of infections
* Poor cognitive function and development in children
Prevention: Preventing iron deficiency anemia involves consuming enough iron through a balanced diet, avoiding foods that inhibit iron absorption, and addressing any underlying causes. It is also important to maintain good overall health, including managing chronic conditions such as bleeding or malabsorption.
There are two main types of beta-thalassemia:
1. Beta-thalassemia major (also known as Cooley's anemia): This is the most severe form of the condition, and it can cause serious health problems and a shortened lifespan if left untreated. Children with this condition are typically diagnosed at birth or in early childhood, and they may require regular blood transfusions and other medical interventions to manage their symptoms and prevent complications.
2. Beta-thalassemia minor (also known as thalassemia trait): This is a milder form of the condition, and it may not cause any noticeable symptoms. People with beta-thalassemia minor have one mutated copy of the HBB gene and one healthy copy, which allows them to produce some normal hemoglobin. However, they may still be at risk for complications such as anemia, fatigue, and a higher risk of infections.
The symptoms of beta-thalassemia can vary depending on the severity of the condition and the age of onset. Common symptoms include:
* Fatigue
* Weakness
* Pale skin
* Shortness of breath
* Frequent infections
* Yellowing of the skin and eyes (jaundice)
* Enlarged spleen
Beta-thalassemia is most commonly found in people of Mediterranean, African, and Southeast Asian ancestry. It is caused by mutations in the HBB gene, which is inherited from one's parents. There is no cure for beta-thalassemia, but it can be managed with blood transfusions, chelation therapy, and other medical interventions. Bone marrow transplantation may also be a viable option for some patients.
In conclusion, beta-thalassemia is a genetic disorder that affects the production of hemoglobin, leading to anemia, fatigue, and other complications. While there is no cure for the condition, it can be managed with medical interventions and bone marrow transplantation may be a viable option for some patients. Early diagnosis and management are crucial in preventing or minimizing the complications of beta-thalassemia.
Sickle cell trait is relatively common in certain populations, such as people of African, Mediterranean, or Middle Eastern descent. It is estimated that about 1 in 12 African Americans carry the sickle cell gene, and 1 in 500 are homozygous for the trait (meaning they have two copies of the sickle cell gene).
Although people with sickle cell trait do not develop sickle cell anemia, they can experience certain complications related to the trait. For example, they may experience episodes of hemolytic crisis, which is a condition in which red blood cells are destroyed faster than they can be replaced. This can occur under certain conditions, such as dehydration or infection.
There are several ways that sickle cell trait can affect an individual's life. For example, some people with the trait may experience discrimination or stigma based on their genetic status. Additionally, individuals with sickle cell trait may be more likely to experience certain health problems, such as kidney disease or eye damage, although these risks are generally low.
There is no cure for sickle cell trait, but it can be managed through proper medical care and self-care. Individuals with the trait should work closely with their healthcare provider to monitor their health and address any complications that arise.
Overall, sickle cell trait is a relatively common genetic condition that can have significant implications for an individual's life. It is important for individuals with the trait to understand their risk factors and take steps to manage their health and well-being.
There are two main forms of alpha-Thalassemia:
1. Alpha-thalassemia major (also known as Hemoglobin Bart's hydrops fetalis): This is a severe form of the disorder that can cause severe anemia, enlarged spleen, and death in infancy. It is caused by a complete absence of one or both of the HBA1 or HBA2 genes.
2. Alpha-thalassemia minor (also known as Hemoglobin carrier state): This form of the disorder is milder and may not cause any symptoms at all. It is caused by a partial deletion of one or both of the HBA1 or HBA2 genes.
People with alpha-thalassemia minor may have slightly lower levels of hemoglobin and may be more susceptible to anemia, but they do not typically experience any severe symptoms. Those with alpha-thalassemia major, on the other hand, are at risk for serious complications such as anemia, infections, and organ failure.
There is no cure for alpha-thalassemia, but treatment options include blood transfusions, iron chelation therapy, and management of associated complications. Screening for alpha-thalassemia is recommended for individuals who are carriers of the disorder, as well as for those who have a family history of the condition.
There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
In hypochromic anemia, the RBCs are smaller than normal and have a lower concentration of hemoglobin. This can lead to a decrease in the amount of oxygen being carried to the body's tissues, which can cause fatigue, weakness, and shortness of breath.
There are several possible causes of hypochromic anemia, including:
1. Iron deficiency: Iron is essential for the production of hemoglobin, so a lack of iron can lead to a decrease in hemoglobin levels and the development of hypochromic anemia.
2. Vitamin deficiency: Vitamins such as vitamin B12 and folate are important for the production of red blood cells, so a deficiency in these vitamins can lead to hypochromic anemia.
3. Chronic disease: Certain chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer, can lead to hypochromic anemia.
4. Inherited disorders: Certain inherited disorders, such as thalassemia and sickle cell anemia, can cause hypochromic anemia.
5. Autoimmune disorders: Autoimmune disorders, such as autoimmune hemolytic anemia, can cause hypochromic anemia by destroying red blood cells.
Hypochromic anemia is typically diagnosed through a combination of physical examination, medical history, and laboratory tests such as complete blood counts (CBCs) and serum iron studies. Treatment depends on the underlying cause of the anemia and may include dietary changes, supplements, medication, or blood transfusions.
Hemoglobinuria can be caused by a variety of factors, including:
1. Blood disorders such as sickle cell disease, thalassemia, and von Willebrand disease.
2. Inherited genetic disorders such as hemophilia.
3. Autoimmune disorders such as autoimmune hemolytic anemia.
4. Infections such as septicemia or meningococcemia.
5. Toxins such as lead, which can damage red blood cells and cause hemoglobinuria.
6. Certain medications such as antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).
7. Kidney disease or failure.
8. Transfusion-related acute lung injury (TRALI), which can occur after blood transfusions.
9. Hemolytic uremic syndrome (HUS), a condition that occurs when red blood cells are damaged and broken down, leading to kidney failure.
The symptoms of hemoglobinuria may include:
1. Red or brown-colored urine
2. Frequent urination
3. Pale or yellowish skin
4. Fatigue
5. Shortness of breath
6. Nausea and vomiting
7. Headache
8. Dizziness or lightheadedness
9. Confusion or loss of consciousness in severe cases.
Diagnosis of hemoglobinuria is typically made through urine testing, such as a urinalysis, which can detect the presence of hemoglobin in the urine. Additional tests may be ordered to determine the underlying cause of hemoglobinuria, such as blood tests, imaging studies, or biopsies.
Treatment of hemoglobinuria depends on the underlying cause and severity of the condition. In some cases, treatment may involve addressing the underlying condition that is causing the hemoglobinuria, such as managing an infection or stopping certain medications. Other treatments may include:
1. Fluid and electrolyte replacement to prevent dehydration and maintain proper fluid balance.
2. Medications to help remove excess iron from the body.
3. Blood transfusions to increase the number of red blood cells in the body and improve oxygen delivery.
4. Dialysis to filter waste products from the blood when the kidneys are unable to do so.
5. Supportive care, such as oxygen therapy and pain management.
In severe cases of hemoglobinuria, complications can include:
1. Kidney damage or failure
2. Septicemia (blood infection)
3. Respiratory failure
4. Heart problems
5. Increased risk of infections and other complications.
Prevention of hemoglobinuria involves managing any underlying medical conditions, such as diabetes or infections, and avoiding certain medications that can cause the condition. It is also important to seek medical attention if symptoms of hemoglobinuria develop, as early treatment can help prevent complications and improve outcomes.
There are three main types of polycythemia:
1. Polycythemia vera (PV): This is the most common type and is characterized by an overproduction of red blood cells, white blood cells, and platelets. It is a slowly progressing disease that can lead to complications such as blood clots, bleeding, and an increased risk of cancer.
2. Essential thrombocythemia (ET): This type is characterized by an overproduction of platelets, which can increase the risk of blood clots and other cardiovascular problems.
3. Primary myelofibrosis (PMF): This type is characterized by bone marrow scarring, anemia, fatigue, and an increased risk of blood clots.
Symptoms of polycythemia may include:
* Headache
* Dizziness
* Fatigue
* Shortness of breath
* Pale skin
* Swelling in the spleen or liver
Diagnosis is based on a physical examination, medical history, and laboratory tests such as complete blood counts (CBCs) and bone marrow biopsies. Treatment options for polycythemia include:
1. Phlebotomy (removal of blood): This is the most common treatment for PV and ET, which involves removing excess blood to reduce the number of red blood cells, white blood cells, and platelets.
2. Chemotherapy: This may be used in combination with phlebotomy to treat PV and PMF.
3. Hydroxyurea: This medication is used to reduce the production of blood cells and relieve symptoms such as headache and dizziness.
4. Interferons: These medications are used to treat ET and may be effective in reducing the number of platelets.
5. Stem cell transplantation: In severe cases of PV or PMF, a stem cell transplant may be necessary.
It is important to note that these treatments do not cure polycythemia, but they can help manage symptoms and slow the progression of the disease. Regular monitoring and follow-up with a healthcare provider is essential to ensure the best possible outcomes.
1. Iron deficiency anemia: This is the most common hematologic complication of pregnancy, caused by the increased demand for iron and the potential for poor dietary intake or gastrointestinal blood loss.
2. Thrombocytopenia: A decrease in platelet count, which can be mild and resolve spontaneously or severe and require treatment.
3. Leukemia: Rare but potentially serious, leukemia can occur during pregnancy and may require prompt intervention to ensure the health of both the mother and the fetus.
4. Thrombosis: The formation of a blood clot in a blood vessel, which can be life-threatening for both the mother and the baby if left untreated.
5. Hemorrhage: Excessive bleeding during pregnancy, which can be caused by various factors such as placenta previa or abruption.
6. Preeclampsia: A condition characterized by high blood pressure and damage to organs such as the kidneys and liver, which can increase the risk of hemorrhage and other complications.
7. Ectopic pregnancy: A pregnancy that develops outside of the uterus, often in the fallopian tube, which can cause severe bleeding and be life-threatening if left untreated.
There are several types of diabetes mellitus, including:
1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.
The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:
1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds
If left untreated, diabetes mellitus can lead to a range of complications, including:
1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.
It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.
Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.
Common symptoms of type 2 diabetes include:
* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections
If left untreated, type 2 diabetes can lead to a range of complications, including:
* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation
The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:
* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.
There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.
Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, dizziness, headaches, and pale or yellowish skin. Treatment options depend on the underlying cause but may include blood transfusions, medication to suppress the immune system, antibiotics for infections, and removal of the spleen (splenectomy) in severe cases.
Prevention strategies for hemolytic anemia include avoiding triggers such as certain medications or infections, maintaining good hygiene practices, and seeking early medical attention if symptoms persist or worsen over time.
It is important to note that while hemolytic anemia can be managed with proper treatment, it may not be curable in all cases, and ongoing monitoring and care are necessary to prevent complications and improve quality of life.
Pallor is often used as an indicator of underlying disease, particularly in conditions where there is a decrease in the amount of hemoglobin in the blood, such as anemia or blood loss. It can also be a sign of other diseases such as liver cirrhosis, kidney failure, and some types of cancer.
There are different types of pallor, including:
1. Anemic pallor: This is the most common type of pallor and is caused by a decrease in the number of red blood cells or hemoglobin in the blood. It can be seen in conditions such as iron deficiency anemia, vitamin deficiency anemia, and sickle cell anemia.
2. Post-inflammatory pallor: This type of pallor is caused by inflammation that leads to a decrease in blood flow to the skin. It can be seen in conditions such as erythema migrans (Lyme disease), and other inflammatory conditions.
3. Cirrhotic pallor: This type of pallor is caused by liver cirrhosis and is characterized by a pale, washed-out appearance of the skin.
4. Renal pallor: This type of pallor is caused by kidney failure and is characterized by a pale, washed-out appearance of the skin.
5. Cancer pallor: This type of pallor is caused by certain types of cancer, such as carcinomas and lymphomas, and is characterized by a pale, washed-out appearance of the skin.
In summary, pallor is a term used to describe an abnormal paleness or whiteness of the skin that can be caused by a variety of underlying medical conditions. It is often used as an indicator of illness and can be seen in a wide range of conditions, including anemia, inflammation, liver cirrhosis, kidney failure, and certain types of cancer.
A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).
Prevalence:
Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.
Causes:
The causes of chronic kidney failure are numerous and include:
1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.
Symptoms:
Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:
1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.
Diagnosis:
Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:
1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.
Imaging studies may include:
1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.
Treatment:
Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:
1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.
Complications:
Chronic kidney failure can lead to several complications, including:
1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.
Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.
Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.
Erythroleukemia typically affects adults in their 50s and 60s, although it can occur at any age. Symptoms may include fever, night sweats, weight loss, and fatigue. The cancer cells can spread to other parts of the body, including the spleen, liver, and lymph nodes.
Erythroleukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore normal blood cell production. In some cases, a bone marrow transplant may be necessary. The prognosis for erythroleukemia is generally poor, with a five-year survival rate of about 20%.
Erythroleukemia is classified as an acute leukemia, meaning it progresses rapidly and can lead to life-threatening complications if left untreated. It is important for patients to receive prompt and appropriate treatment to improve their chances of survival and quality of life.
Prevalence: Anemia, hemolytic, congenital is a rare disorder, affecting approximately 1 in 100,000 to 1 in 200,000 births.
Causes: The condition is caused by mutations in genes that code for proteins involved in hemoglobin synthesis or red blood cell membrane structure. These mutations can lead to abnormal hemoglobin formation, red blood cell membrane instability, and increased susceptibility to oxidative stress, which can result in hemolytic anemia.
Symptoms: Symptoms of anemia, hemolytic, congenital may include jaundice (yellowing of the skin and eyes), fatigue, weakness, pale skin, and shortness of breath. In severe cases, the condition can lead to life-threatening complications such as anemia, infections, and kidney failure.
Diagnosis: Anemia, hemolytic, congenital is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, including blood smear examination, hemoglobin electrophoresis, and mutation analysis.
Treatment: Treatment for anemia, hemolytic, congenital depends on the specific underlying genetic cause and may include blood transfusions, folic acid supplements, antibiotics, and/or surgery to remove the spleen. In some cases, bone marrow transplantation may be necessary.
Prognosis: The prognosis for anemia, hemolytic, congenital varies depending on the specific underlying genetic cause and the severity of the condition. With appropriate treatment, many individuals with this condition can lead relatively normal lives, but in severe cases, the condition can be life-threatening.
There are several possible causes of methemoglobinemia, including:
1. Exposure to certain medications or chemicals, such as nitrates or aniline dyes.
2. Genetic disorders that affect the production or function of hemoglobin.
3. Infections, such as bacterial infections of the blood or respiratory tract.
4. Poor nutrition or malnutrition.
5. Certain chronic medical conditions, such as sickle cell anemia or thalassemia.
Methemoglobinemia can be diagnosed through a variety of tests, including:
1. Complete blood count (CBC) to measure the levels of methemoglobin in the blood.
2. Blood gas analysis to measure the partial pressure of oxygen and carbon dioxide in the blood.
3. Co-oximetry to measure the levels of methemoglobin and other forms of hemoglobin.
4. Urine tests to check for the presence of abnormal hemoglobin.
5. Genetic testing to identify inherited disorders that may be causing the condition.
Treatment of methemoglobinemia depends on the underlying cause and may include:
1. Administration of oxygen therapy to increase the amount of oxygen in the blood.
2. Use of medications to reduce the levels of methemoglobin and increase the levels of normal hemoglobin.
3. Transfusions of red blood cells to replace abnormal hemoglobin with normal hemoglobin.
4. Management of underlying medical conditions, such as infections or genetic disorders.
5. Dietary changes to address any nutritional deficiencies that may be contributing to the condition.
In severe cases of methemoglobinemia, hospitalization may be necessary to provide oxygen therapy and other treatments. In some cases, patients with methemoglobinemia may require long-term management and follow-up care to prevent complications and manage the underlying cause of the condition.
Hemoglobin
Embryonic hemoglobin
Hemoglobin O
Glycated hemoglobin
Hemoglobin electrophoresis
Hemoglobin variants
VHb (hemoglobin)
Fetal hemoglobin
Hemoglobin A3
Hemoglobin E
Hemoglobin A2
Hemoglobin A
Hemoglobin-G
F-Hemoglobin
Mu hemoglobin
Hemoglobin Barts
Hemoglobin J
Hemoglobin C
Hemoglobin subunit beta
Hemoglobin subunit zeta
Hemoglobin Hopkins-2
Hemoglobin Constant Spring
Hemoglobin D-Punjab
Hemoglobin M disease
Hemoglobin Lepore syndrome
Hemoglobin O-Arab
Hemoglobin subunit alpha
Hemoglobin H disease
Mean corpuscular hemoglobin
Hemoglobin, alpha 2
Definition: Glycosylated Hemoglobin Test (Hemoglobin A1c) (for Teens) - East Tenneesee Children's
Learn the Facts and Benefits of Hemoglobin Tests - Bright Hub
PRIME PubMed | Spectrophotometry of hemoglobin and hemoglobin derivatives
Kidshealth: Blood Test: Hemoglobin A1c | Akron Children's Hospital
Hemoglobin: MedlinePlus Medical Encyclopedia
Weekly Epoetin Ups Hemoglobin Levels, QOL in Anemic Patients
NY R00328 - The tariff classification of Hemoglobin Powder from Germany - United States International Trade Commision Rulings
Compliance with the Clinical Laboratory Improvement
Amendments of 1988 for Hemoglobin Screening -- California, 1995
Hemoglobin Level Variability: Associations with Mortality : Clinical Journal of the American Society of Nephrology
Browsing by Subject "Hemoglobin E"
Does low haemoglobin affect the chances of conception?
The Amino Acid Sequence of the γ Chain of Human Fetal Hemoglobin - CaltechAUTHORS
Hemoglobin C disease
Masimo - Webinar: Hemoglobin, Coagulation & Oxygenation in COVID-19 Patients
High prevalence of haemoglobin S in the closed Egyptian community of Siwa Oasis | Journal of Clinical Pathology
1206.0412] Importance of many body effects in the kernel of hemoglobin for ligand binding
Hemoglobin-based oxygen carriers. Structural alterations that affect free radical formation | Scholars@Duke
Haemoglobin Binding Science Fair Project
KAKEN - Research Projects | Analysis of parasitophorous vacuole membrane protein in hemoglobin transport and metabolism of...
Inhibition of haemoglobin-mediated lipid oxidation in washed cod muscle and cod protein isolates by Fucus vesiculosus extract...
WHO EMRO | International collaborative assessment study of the AHD575 method for the measurement of blood haemoglobin | Volume...
HEMOGLOBIN, SERUM - Warde Medical Laboratory
2021 - Hemoglobin Level
Glycated haemoglobin and metabolic control of diabetes mellitus: External versus locally established clinical targets for...
What is HbA1c - Glycated Haemoglobin?
www.iristech.net. Diabetes Hemoglobin Testing
Alere HemoPoint H2 System - Hemoglobin Testing
Lower Your Hemoglobin A1C Naturally - GMFEA
Abnormal5
- Hemoglobinopathies are a group of common, inherited disorders of hemoglobin (Hb), resulting in the synthesis of structurally abnormal globin subunits. (arupconsult.com)
- The hemoglobin evaluation reflexive cascade initially tests for abnormal hemoglobin. (arupconsult.com)
- Hemoglobin C is an abnormal type of hemoglobin, the protein in red blood cells that carries oxygen. (adam.com)
- Hemoglobin electrophoresis is abnormal in HbM disease, but normal with NADH-methemoglobin reductase deficiency [McKenzie 2010]. (cdc.gov)
- Abnormal haemoglobin. (who.int)
Anemia7
- In 1995, in conjunction with an assessment of county-specific variations in prevalence rates of anemia, the California Department of Health Services conducted a mail survey of CHDP providers to assess compliance with CLIA regulations for hemoglobin screening. (cdc.gov)
- Anemia can occur if the body's hemoglobin levels are too low. (brighthub.com)
- In the early 1990s, anemia correction was viewed simply as treatment with EPO along with correction of iron deficiency to increase hemoglobin levels from below 10 g/dl to within the initial label target range of 10 to 11 g/dl. (lww.com)
- As experience with anemia correction grew and the potential side effects, including seizures and hypertension, occurred less frequently than anticipated from the initial trials, the United States Food and Drug Administration increased the target hemoglobin range to 10 to 12 g/dl. (lww.com)
- High Hemoglobin Meaning: The problem of low blood is called anemia, but the excessive amount of blood in the body is also a disease, which is named polycythemia. (hemolevel.com)
- Non-invasive hemoglobin estimation for preoperative anemia screening. (bvsalud.org)
- A decrease in haptoglobin can support a diagnosis of hemolytic anemia when seen with an increased reticulocyte count, decreased erythrocyte count, decreased hemoglobin and hematocrit. (cdc.gov)
Rather than hemoglobin2
- of these, 16 providers were excluded from analysis because nine used a contracted commercial laboratory to perform their hemoglobin measurements, and seven used hematocrit rather than hemoglobin assessment. (cdc.gov)
- Conclusions: Number of months with hemoglobin values below the target range, rather than hemoglobin variability itself, may be the primary driver of increased risk of death. (lww.com)
Outcomes1
- This study evaluated the association of packed red blood cell (PRBC) transfusion with mortality outcomes across hemoglobin levels amongst emergency center (EC) patients presenting with medical pathology in Kigali, Rwanda . (bvsalud.org)
Person's3
- As a person's blood sugar becomes higher, more of the person's hemoglobin becomes glycosylated. (kidshealth.org)
- The glycosylated hemoglobin test shows what a person's average blood glucose level was for the 2 to 3 months before the test. (kidshealth.org)
- A hemoglobin A1c test measures how much a person's glucose levels have been in and out of the healthy (or target) range during the last 2-3 months. (akronchildrens.org)
Oxygen saturation2
SpHb2
- The Masimo Pronto Pulse CO-Oximeter was utilized to estimate blood hemoglobin concentrations (SpHb), which were then compared with hemoglobin concentrations obtained via complete blood count . (bvsalud.org)
- SpHb generally overestimated hemoglobin with a mean (± 1.96 × standard deviation) difference of 0.8 (-2.2, 3.9) g/dL. (bvsalud.org)
Haptoglobin3
- A typical cyanosis workup includes CBC with differential and peripheral blood smear, free serum hemoglobin and haptoglobin, ABGs and pulse oximetry. (cdc.gov)
- Tests to rule out hemolysis include CBC with differential, reticulocyte count, peripheral blood smear, lactate dehydrogenase (LDH), bilirubin, serum haptoglobin, free serum hemoglobin and Heinz body preparation. (cdc.gov)
- Free serum hemoglobin and haptoglobin levels are drawn to assess for hemolytic anemias. (cdc.gov)
Umbilical4
- The fetal hemoglobin for this investigation was isolated chromatographically from umbilical cord blood. (caltech.edu)
- to assess the effect of delayed clamping of the umbilical cord on hemoglobin concentrations in infants up to three months of age born to anemic and non anemic mothers. (bvsalud.org)
- Maternal hemoglobin concentration at delivery, umbilical cord hemoglobin and ferritin were collected. (bvsalud.org)
- The dependent and explanatory variables include ([hemoglobin at three months - umbilical cord hemoglobin / umbilical cord hemoglobin]*100) and immediate/delayed cord clamping, respectively. (bvsalud.org)
Metalloprotein2
- We support this model using linear-scaling first-principles calculations, in combination with dynamical mean-field theory, applied to heme, the kernel of the hemoglobin metalloprotein central to human respiration. (arxiv.org)
- Hemoglobin is the iron-containing oxygen-transport metalloprotein in the red blood cells of vertebrates, and the tissues of some invertebrates. (sciencefairadventure.com)
HbA1c2
- Glucose (a type of sugar) molecules in the blood normally become stuck to hemoglobin molecules - this means the hemoglobin has become glycosylated (also referred to as hemoglobin A1c, or HbA1c). (kidshealth.org)
- HbA1c (Glycated haemoglobin) is made when glucose (sugar) in your body sticks to your red blood cells. (letsgetchecked.com)
Ligand1
- By plotting a graph, absorbance vs. wave length we can identify haemoglobin (no bound ligand), oxyhaemoglobin and carboxyhaemoglobin. (sciencefairadventure.com)
Measurements1
- Patients â ¥15 years of age, treated for medical emergencies during 2013-16, with EC hemoglobin measurements were included. (bvsalud.org)
Polycythemia1
- When the hemoglobin levels in the blood are elevated, polycythemia vera can occur. (brighthub.com)
Concentrations2
- Assessment of hemoglobin concentrations may facilitate optimization prior to surgery . (bvsalud.org)
- At approximately three months of age, 210 (64.6%) infants had their hemoglobin concentrations, socioeconomic, anthropometric and infant feeding practices collected. (bvsalud.org)
Hemoglobinopathies1
- Hemoglobin and hemoglobinopathies. (adam.com)
Binds3
- If too much glucose builds up in blood, it binds to hemoglobin. (akronchildrens.org)
- At lungs oxygen binds to haemoglobin to form the oxygen-haemoglobin complex called oxyhaemoglobin. (sciencefairadventure.com)
- But carbon monoxide binds to haemoglobin irreversibly and 200 times faster than oxygen to form a very bright red compound called carboxyhaemoglobin, meaning that small amounts of CO dramatically reduce hemoglobin's ability to transport oxygen. (sciencefairadventure.com)
Mortality2
- In this retrospective, national study of associations between the degree of hemoglobin level variability in the first 6 mo of 2004 and subsequent mortality rates in the following 6 mo, 159,720 hemodialysis patients receiving epoetin therapy were studied. (lww.com)
- The relationship between EC PRBC transfusion and patient mortality was evaluated using logistic regression , with stratified analyses performed at hemoglobin levels of 7 mg/dL and 5 mg/dL. (bvsalud.org)
Screening4
- This report summarizes the results of that survey, which indicate that, in California, many CHDP providers do not comply with CLIA-mandated quality-assurance practices for hemoglobin screening in their clinical laboratories. (cdc.gov)
- The questionnaires assessed the type of health-care practice, the method used for hemoglobin screening, and quality-assurance practices. (cdc.gov)
- Methods of hemoglobin screening were classified as waived or nonwaived based on CLIA standards. (cdc.gov)
- Rates of compliance with CLIA regulations varied by type of health-care practice and hemoglobin screening method. (cdc.gov)
Lipid1
- The effects of Fucus vesiculosus extract and fractions towards haemoglobin- (Hb-) catalysed lipid oxidation in washed cod muscle system and cod protein isolates during ice storage were examined. (matis.is)
Glucose2
- The glucose remains attached to the hemoglobin for the life of the red blood cell, or about 2 to 3 months. (kidshealth.org)
- Hemoglobin A1c (HbA 1c ) levels should be measured every 3 months and treatment adjusted if goals for both HbA 1c and blood glucose are not met. (medscape.com)
Cyanide3
- In 1967, the International Council for Standardization in Haematology (ICSH) recommended the haemoglobin cyanide (HiCN) method as the reference method for use [1]. (who.int)
- In 1985 WHO established the second haemoglobin cyanide reference material [5] and recommended the HiCN method be given the status of an international reference procedure. (who.int)
- In heavy smokers, up to 20% of the oxygen-active sites can be blocked by CO. In similar fashion, hemoglobin also has competitive binding affinity for cyanide (CN-), sulfur monoxide(SO), nitrogen dioxide (NO2), and sulfide(S2-), including hydrogen sulfide (H2S). (sciencefairadventure.com)
Level6
- High hemoglobin level is most often caused by low oxygen levels in the blood (hypoxia), present over a long period of time. (medlineplus.gov)
- A high hemoglobin A1c level may mean that a child's medicines need to be adjusted. (akronchildrens.org)
- In this open-label study, HIV-positive patients with a hemoglobin level of 12 g/dL or less were randomized to receive 100 U/kg of epoetin three times a week or 40,000 U once a week for 16 weeks. (cancernetwork.com)
- Background/objectives: Awareness of hemoglobin level variability in dialysis patients is increasing, as is interest in its potential implications. (lww.com)
- Anaemia is inadequate level of haemoglobin appropriate for age & sex. (ndtv.com)
- Simple analytical instruments for haemoglobin measurement using the HiCN method, appropriate at the primary level, are not available. (who.int)
Diabetes1
- Doctors check hemoglobin A1c tests in kids with diabetes. (akronchildrens.org)
Africa1
- Reports from Africa reveal that haemoglobin measurement has the poorest precision and reproducibility among all common laboratory indicators [6]. (who.int)
Patients2
- CHICAGO-Once-a-week dosing of recombinant human erythropoietin (epoetin alfa, Epogen, Procrit) is as effective as thrice-weekly dosing in improving hemoglobin (Hb) levels in HIV-positive patients who are anemic, Howard A. Grossman, MD, said at the Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC abstract 254). (cancernetwork.com)
- Findings from an interim analysis of 156 patients indicate that HIV-positive individuals receiving epoetin once a week achieve the same degree of improvement in hemoglobin levels and quality of life assessments as those who take the medication three times weekly. (cancernetwork.com)
Anemic1
- The delayed cord clamping benefits the hemoglobin status of infants, especially those born to non anemic mothers. (bvsalud.org)
Monitoring2
- Monitoring the bloods hemoglobin levels can help test for many medical disorders. (brighthub.com)
- During a meeting in Geneva on September 2002, the World Health Organization (WHO) Working Group on Anaemia noted that blood haemoglobin determination for diagnosing and monitoring treatment of anaemia in populations of countries with limited resources is still an unsolved problem. (who.int)
Search1
- Results of search for 'su:{Hemoglobins. (who.int)
Reveal1
- Hemoglobin testing can reveal numerous aspects of the blood. (brighthub.com)
Spray2
- After collection, the hemoglobin is spray dried at a low temperature, in accordance with the EU regulation for animal proteins, and put up packed in 25 kg bags. (faqs.org)
- Blood samples from 15 spray painters applying HDI-containing paint were analyzed for hemoglobin HDA (HDA-Hb) and N-acetyl-1,6-hexamethylene diamine (monoacetyl-HDA-Hb) by GC-MS. HDA-Hb was detected in the majority of workers (≤1.2-37ng/g Hb), whereas monoacetyl-HDA-Hb was detected in one worker (0.06 ng/g Hb). (cdc.gov)
Symptoms1
- Contact your health care provider if you have symptoms of hemoglobin C disease. (adam.com)
Main1
- Hemoglobin tests are done for three main reasons. (brighthub.com)
Tests2
- Why Are Hemoglobin A1c Tests Done? (akronchildrens.org)
- Methemoglobinemia can be acquired (exposure to oxidants) or inherited (i.e. decreased enzyme activity or presence of hemoglobin M). Acquired methemoglobinemia will have normal enzyme assay activity tests and normal Hb electrophoresis. (cdc.gov)
Consists1
- According to your letter, the subject product, Hemoglobin Powder, consists of hemoglobin collected from fresh pork blood, from animals slaughtered at EU-approved slaughterhouses under veterinarian control. (faqs.org)
High2
- High hemoglobin A1c levels can happen when someone's blood sugars have been higher than their healthy range. (akronchildrens.org)
- transiently and persistently high hemoglobin levels were not associated with increased risk of death. (lww.com)
Laboratories3
- ABSTRACT Accurate, economical methods for haemoglobin determination by laboratories in countries with limited resources are not available. (who.int)
- The results indicate that the AHD575 method is suitable for measuring haemoglobin in laboratories at all levels. (who.int)
- Despite its deficiencies, the use of the HiCN method improved haemoglobin measurement in laboratories using automated techniques. (who.int)
Persons1
- Testing hemoglobin levels can also be used to view a persons overall health. (brighthub.com)
Body2
- Hemoglobin is the substance inside red blood cells that carries oxygen to the cells of the body. (kidshealth.org)
- Hemoglobin is needed in the body to carry oxygen through out the body. (brighthub.com)
Tissues1
- A light sensor containing two light sources (red and infra-red) transmits light through tissues, is absorbed by haemoglobin and detected by a photo sensor. (who.int)
Test12
- The hemoglobin test measures how much hemoglobin is in your blood. (medlineplus.gov)
- The hemoglobin test is a common test and is almost always done as part of a complete blood count (CBC). (medlineplus.gov)
- A blood test can measure the amount of glycosylated hemoglobin in the blood. (kidshealth.org)
- Hemoglobin test are often given to test for underlying health conditions. (brighthub.com)
- This test measures the body's blood levels of hemoglobin. (brighthub.com)
- Why is a Hemoglobin Test Used? (brighthub.com)
- One reason a test may be done to measure hemoglobin levels is to monitor previous medical conditions. (brighthub.com)
- In order to diagnose many medical conditions, a hemoglobin test is often conducted. (brighthub.com)
- The test for measuring hemoglobin levels is relatively simple. (brighthub.com)
- What Is a Hemoglobin A1c Test? (akronchildrens.org)
- Sometimes a hemoglobin A1c test is done as part of a routine checkup to screen for problems. (akronchildrens.org)
- If you have questions about the hemoglobin A1c test or what the test results mean, talk to your doctor. (akronchildrens.org)
Carbon1
- To demonstrate the ability of oxygen and carbon monoxide to bind with haemoglobin. (sciencefairadventure.com)
Testing1
- Although not required under CLIA, 75 (31.4%) of these providers reported participation in a proficiency testing program for hemoglobin. (cdc.gov)
Months1
- Questionnaires were mailed to each of the 418 CHDP providers that submitted hemoglobin data for greater than or equal to 100 children aged 6-59 months to the Pediatric Nutrition Surveillance System (PedNSS) during 1993. (cdc.gov)
Human2
- The 146 amino acid residues of the γ chain of human fetal hemoglobin have been placed in sequence. (caltech.edu)
- The differences between the γ chains of human fetal hemoglobin and the β chains of human adult hemoglobin are responsible for the differences in the properties of the two molecules. (caltech.edu)