An increase in circulating RETICULOCYTES, which is among the simplest and most reliable signs of accelerated ERYTHROCYTE production. Reticulocytosis occurs during active BLOOD regeneration (stimulation of red bone marrow) and in certain types of ANEMIA, particularly CONGENITAL HEMOLYTIC ANEMIA.
The number of RED BLOOD CELLS per unit volume in a sample of venous BLOOD.
Oxygen-carrying RED BLOOD CELLS in mammalian blood that are abnormal in structure or function.
Immature ERYTHROCYTES. In humans, these are ERYTHROID CELLS that have just undergone extrusion of their CELL NUCLEUS. They still contain some organelles that gradually decrease in number as the cells mature. RIBOSOMES are last to disappear. Certain staining techniques cause components of the ribosomes to precipitate into characteristic "reticulum" (not the same as the ENDOPLASMIC RETICULUM), hence the name reticulocytes.
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).
RED BLOOD CELL sensitivity to change in OSMOTIC PRESSURE. When exposed to a hypotonic concentration of sodium in a solution, red cells take in more water, swell until the capacity of the cell membrane is exceeded, and burst.
The number of RETICULOCYTES per unit volume of BLOOD. The values are expressed as a percentage of the ERYTHROCYTE COUNT or in the form of an index ("corrected reticulocyte index"), which attempts to account for the number of circulating erythrocytes.
Abnormal intracellular inclusions, composed of denatured hemoglobin, found on the membrane of red blood cells. They are seen in thalassemias, enzymopathies, hemoglobinopathies, and after splenectomy.
Hemolytic anemia due to various intrinsic defects of the erythrocyte.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
The production of red blood cells (ERYTHROCYTES). In humans, erythrocytes are produced by the YOLK SAC in the first trimester; by the liver in the second trimester; by the BONE MARROW in the third trimester and after birth. In normal individuals, the erythrocyte count in the peripheral blood remains relatively constant implying a balance between the rate of erythrocyte production and rate of destruction.
Diazo derivatives of aniline, used as a reagent for sugars, ketones, and aldehydes. (Dorland, 28th ed)
A protozoan parasite of rodents transmitted by the mosquito Anopheles stephensi.
A group of familial congenital hemolytic anemias characterized by numerous abnormally shaped erythrocytes which are generally spheroidal. The erythrocytes have increased osmotic fragility and are abnormally permeable to sodium ions.
Enlargement of the spleen.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.
Glycoprotein hormone, secreted chiefly by the KIDNEY in the adult and the LIVER in the FETUS, that acts on erythroid stem cells of the BONE MARROW to stimulate proliferation and differentiation.
A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.
The volume of packed RED BLOOD CELLS in a blood specimen. The volume is measured by centrifugation in a tube with graduated markings, or with automated blood cell counters. It is an indicator of erythrocyte status in disease. For example, ANEMIA shows a low value; POLYCYTHEMIA, a high value.
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.

Formation of meso, N-diphenylprotoporphyrin IX by an aerobic reaction of phenylhydrazine with oxyhemoglobins. (1/16)

Administration of phenylhydrazine to rabbits resulted in the denaturation of hemoglobins in erythrocytes, causing the formation of intracellular precipitates known as Heinz bodies, severe hemolytic anemia, and reticulocytosis. To elucidate the molecular mechanism of the destabilization, we allowed human oxyhemoglobins to react aerobically with phenylhydrazine. After treatment with acetic acid/HCl and H2SO4/methanol, the chloroform extract contained blue-green pigments of major products accompanied by different minor products. Each product was isolated by column chromatography. By fast-atom-bombardment mass spectrometry (FAB-MS) and proton nuclear magnetic resonance (1H-NMR) spectrometry, dimethyl esters of N-phenylprotoporphyrin IX and meso, N-diphenylprotoporphyrin IX were determined. Other major products also were determined to be dimethyl esters of triphenyl-and tetraphenyl-substituted protoporphyrins by FAB-MS. The formation of meso, N-diphenylprotoporphyrin indicated that the addition of a phenyl radical to the meso-carbon atom of the protoporphyrin ring occurred. Triphenyl and tetraphenyl adducts also indicated the formation of phenyl radicals in the aerobic reaction of phenylhydrazine with oxyhemoglobins. From these results, we suggest that the formation of phenyl radicals and the replacement of heme with phenyl-substituted protoporphyrins cause the destabilization of hemoglobins to induce Heinz bodies and hemolytic anemia with phenylhydrazine.  (+info)

Inappropriately low reticulocytosis in severe malarial anemia correlates with suppression in the development of late erythroid precursors. (2/16)

Inappropriately low reticulocytosis may exacerbate malarial anemia, but the under-lying mechanism is not clear. In this study, naive and infected mice were treated with recombinant murine erythropoietin (EPO), and the upstream events of erythropoiesis affected by blood-stage Plasmodium chabaudi AS were investigated. Malaria infection, with or without EPO treatment, led to a suboptimal increase in TER119(+) erythroblasts compared with EPO-treated naive mice. Furthermore, a lower percentage of TER119(+) erythroblasts in infected mice were undergoing terminal differentiation to become mature hemoglobin-producing erythroblasts. The impaired maturation of erythroblasts during infection was associated with a shift in the transferrin receptor (CD71) expression from the TER119(+) population to B220(+) population. Moreover, the suboptimal increase in TER119(+) erythroblasts during infection coincided with a blunted proliferative response by splenocytes to EPO stimulation in vitro, although a high frequency of these splenocytes expressed EPO receptor (EPOR). Taken together, these data suggest that during malaria, EPO-induced proliferation of early EPOR-positive erythroid progenitors is suppressed, which may lead to a suboptimal generation of TER119(+) erythroblasts. The shift in CD71 expression may result in impaired terminal maturation of these erythroblasts. Thus, inadequate reticulocytosis during malaria is associated with suppressed proliferation, differentiation, and maturation of erythroid precursors.  (+info)

Modulation of the course and outcome of blood-stage malaria by erythropoietin-induced reticulocytosis. (3/16)

Severe anemia is a major life-threatening complication of malaria. The roles of erythropoietin (Epo) and erythropoiesis during blood-stage malaria were investigated. By treating Plasmodium chabaudi AS-infected C57BL/6 (B6) mice, which are resistant to malaria, with polyclonal anti-human Epo neutralizing antibody, we demonstrated that Epo-induced reticulocytosis was important for alleviating malarial anemia and for host survival. By inducing erythropoiesis in A/J mice, which are susceptible to malaria, and in B6 mice at various periods during infection, by use of exogenous recombinant murine Epo, untimely onset of reticulocytosis was shown to augment multiplication of parasites and result in lethal infection. However, timely inducement of reticulocytosis with Epo treatment alleviated malarial anemia and increased survival. Our data reveal the important role of Epo-induced reticulocytosis in modulating the course and outcome of blood-stage malaria. However, the mechanisms underlying the increased mortality associated with untimely treatment with Epo and the increased protection associated with timely treatment with Epo remain to be investigated.  (+info)

Rac GTPases regulate the morphology and deformability of the erythrocyte cytoskeleton. (4/16)

Actin oligomers are a significant structural component of the erythrocyte cytoskeleton. Rac1 and Rac2 GTPases regulate actin structures and have multiple overlapping as well as distinct roles in hematopoietic cells; therefore, we studied their role in red blood cells (RBCs). Conditional gene targeting with a loxP-flanked Rac1 gene allowed Crerecombinase-induced deletion of Rac1 on a Rac2 null genetic background. The Rac1(-/-);Rac2(-/-) mice developed microcytic anemia with a hemoglobin drop of about 20% and significant anisocytosis and poikilocytosis. Reticulocytes increased more than 2-fold. Rac1(-/-);Rac2(-/-) RBCs stained with rhodamine-phalloidin demonstrated F-actin meshwork gaps and aggregates under confocal microscopy. Transmission electron microscopy of the cytoskeleton demonstrated junctional aggregates and pronounced irregularity of the hexagonal spectrin scaffold. Ektacytometry confirmed that these cytoskeletal changes in Rac1(-/-);Rac2(-/-) erythrocytes were associated with significantly decreased cellular deformability. The composition of the cytoskeletal proteins was altered with an increased actin-to-spectrin ratio and increased phosphorylation (Ser724) of adducin, an F-actin capping protein. Actin and phosphorylated adducin of Rac1(-/-);Rac2(-/-) erythrocytes were more easily extractable by Triton X-100, indicating weaker association to the cytoskeleton. Thus, deficiency of Rac1 and Rac2 GTPases in mice alters actin assembly in RBCs and causes microcytic anemia with reticulocytosis, implicating Rac GTPases as dynamic regulators of the erythrocyte cytoskeleton organization.  (+info)

Enhanced suicidal death of erythrocytes from gene-targeted mice lacking the Cl-/HCO(3)(-) exchanger AE1. (5/16)

Genetic defects of anion exchanger 1 (AE1) may lead to spherocytic erythrocyte morphology, severe hemolytic anemia, and/or cation leak. In normal erythrocytes, osmotic shock, Cl(-) removal, and energy depletion activate Ca(2+)-permeable cation channels with Ca(2+)-induced suicidal erythrocyte death, i.e., surface exposure of phosphatidylserine, cell shrinkage, and membrane blebbing, all features typical for apoptosis of nucleated cells. The present experiments explored whether AE1 deficiency favors suicidal erythrocyte death. Peripheral blood erythrocyte numbers were significantly smaller in gene-targeted mice lacking AE1 (AE1(-/-) mice) than in their wild-type littermates (AE1(+/+) mice) despite increased percentages of reticulocytes (AE1(-/-): 49%, AE1(+/+): 2%), an indicator of enhanced erythropoiesis. Annexin binding, reflecting phosphatidylserine exposure, was significantly larger in AE1(-/-)erythrocytes/reticulocytes ( approximately 10%) than in AE1(+/+) erythrocytes ( approximately 1%). Osmotic shock (addition of 400 mM sucrose), Cl(-) removal (replacement with gluconate), or energy depletion (removal of glucose) led to significantly stronger annexin binding in AE1(-/-) erythrocytes/reticulocytes than in AE1(+/+) erythrocytes. The increase of annexin binding following exposure to the Ca(2+) ionophore ionomycin (1 muM) was, however, similar in AE1(-/-) and in AE1(+/+) erythrocytes. Fluo3 fluorescence revealed markedly increased cytosolic Ca(2+) permeability in AE1(-/-) erythrocytes/reticulocytes. Clearance of carboxyfluorescein diacetate succinimidyl ester-labeled erythrocytes/reticulocytes from circulating blood was more rapid in AE1(-/-) mice than in AE1(+/+) mice and was accelerated by ionomycin treatment in both genotypes. In conclusion, lack of AE1 is associated with enhanced Ca(2+) entry and subsequent scrambling of cell membrane phospholipids.  (+info)

Membrane remodeling during reticulocyte maturation. (6/16)

 (+info)

Role for parasite genetic diversity in differential host responses to Trypanosoma brucei infection. (7/16)

 (+info)

Restoration of high-density lipoprotein levels by cholesteryl ester transfer protein expression in scavenger receptor class B type I (SR-BI) knockout mice does not normalize pathologies associated with SR-BI deficiency. (8/16)

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Reticulocytosis is a medical term that refers to an increased number of reticulocytes in the peripheral blood. Reticulocytes are immature red blood cells produced in the bone marrow and released into the bloodstream. They still have remnants of RNA, which gives them a reticular or "net-like" appearance under a microscope when stained with certain dyes.

Reticulocytosis is typically seen in conditions associated with increased red blood cell production, such as:

1. Hemolysis: This is a condition where there is excessive destruction of red blood cells, leading to anemia. The body responds by increasing the production of reticulocytes to replace the lost red blood cells.
2. Blood loss: When there is significant blood loss, the body tries to compensate for the decrease in red blood cells by boosting the production of reticulocytes.
3. Recovery from bone marrow suppression: In cases where the bone marrow has been suppressed due to illness, medication, or chemotherapy, and then recovers, an increase in reticulocytosis may be observed as the bone marrow resumes normal red blood cell production.
4. Megaloblastic anemias: Conditions like vitamin B12 or folate deficiency can lead to megaloblastic anemia, where the red blood cells are larger and immature. Reticulocytosis may be present as the bone marrow tries to correct the anemia.
5. Congenital disorders: Certain inherited conditions, such as hereditary spherocytosis or thalassemias, can cause chronic hemolysis and lead to reticulocytosis.

It is essential to evaluate the underlying cause of reticulocytosis for appropriate diagnosis and treatment.

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.

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.

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.

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.

Osmotic fragility is a term used in medicine, specifically in the field of hematology. It refers to the susceptibility or tendency of red blood cells (RBCs) to undergo lysis (rupture or breaking open) when exposed to hypotonic solutions (solutions with lower osmotic pressure than the RBCs). This test is often used to diagnose and monitor hereditary spherocytosis, a genetic disorder that affects the structure and stability of red blood cells.

In this condition, the RBC membrane proteins are defective, leading to abnormally shaped and fragile cells. When these abnormal RBCs come into contact with hypotonic solutions, they rupture more easily than normal RBCs due to their decreased osmotic resistance. The degree of osmotic fragility can be measured through a laboratory test called the "osmotic fragility test," which evaluates the stability and structural integrity of RBCs in response to varying osmotic pressures.

In summary, osmotic fragility is a medical term that describes the increased susceptibility of red blood cells to lysis when exposed to hypotonic solutions, often associated with hereditary spherocytosis or other conditions affecting RBC membrane stability.

A reticulocyte count is a laboratory test that measures the percentage of reticulocytes in the peripheral blood. Reticulocytes are immature red blood cells produced in the bone marrow and released into the bloodstream. They contain residual ribosomal RNA, which gives them a reticular or net-like appearance under a microscope when stained with certain dyes.

The reticulocyte count is often used as an indicator of the rate of red blood cell production in the bone marrow. A higher than normal reticulocyte count may indicate an increased production of red blood cells, which can be seen in conditions such as hemolysis, blood loss, or response to treatment of anemia. A lower than normal reticulocyte count may suggest a decreased production of red blood cells, which can be seen in conditions such as bone marrow suppression, aplastic anemia, or vitamin deficiencies.

The reticulocyte count is usually expressed as a percentage of the total number of red blood cells, but it can also be reported as an absolute reticulocyte count (the actual number of reticulocytes per microliter of blood). The normal range for the reticulocyte count varies depending on the laboratory and the population studied.

Heinz bodies are small, irregularly shaped inclusions found in the red blood cells (RBCs). They are aggregates of denatured hemoglobin and are typically seen in RBCs that have been exposed to oxidative stress. This can occur due to various factors such as exposure to certain chemicals, drugs, or diseases.

The presence of Heinz bodies can lead to the premature destruction of RBCs, a condition known as hemolysis. This can result in anemia and related symptoms such as fatigue, weakness, and shortness of breath. It's important to note that while Heinz bodies are often associated with certain diseases, they can also be present in otherwise healthy individuals who have been exposed to oxidative stress.

It's worth mentioning that the term "Heinz bodies" comes from the name of the scientist Robert Heinz, who first described them in 1890.

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.

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.

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.

Phenylhydrazines are organic compounds that contain a phenyl group (a benzene ring with a hydrogen atom substituted by a hydroxy group) and a hydrazine group (-NH-NH2). They are aromatic amines that have been used in various chemical reactions, including the formation of azos and hydrazones. In medicine, phenylhydrazines were once used as vasodilators to treat angina pectoris, but their use has largely been discontinued due to their toxicity and potential carcinogenicity.

"Plasmodium chabaudi" is a species of parasitic protozoa belonging to the genus Plasmodium, which includes the causative agents of malaria in various animals and humans. "P. chabaudi" primarily infects rodents, particularly mice, and serves as a model organism for studying the fundamental biology and pathogenesis of malaria.

The life cycle of "P. chabaudi" involves both sexual and asexual reproduction, similar to other Plasmodium species. The parasite is transmitted through the bite of an infected Anopheles mosquito, which injects sporozoites into the host's bloodstream. These sporozoites then infect liver cells, where they undergo schizogony (asexual reproduction) and produce merozoites.

Merozoites released from the liver invade red blood cells, initiating the erythrocytic stage of the life cycle. Within the red blood cells, the parasites multiply by schizogony, forming new merozoites that are eventually released to infect other red blood cells. Some of these parasites differentiate into male and female gametocytes, which can be taken up by a mosquito during a blood meal, completing the life cycle.

"P. chabaudi" infections in mice can lead to various pathological changes, including anemia, splenomegaly (enlarged spleen), and immune responses that contribute to disease progression. Researchers use this model organism to investigate aspects of malaria biology, such as host-parasite interactions, immunity, drug development, and vaccine design.

Hereditary Spherocytosis is a genetic disorder that affects the red blood cells (RBCs) causing them to take on a spherical shape instead of their normal biconcave disc shape. This occurs due to mutations in the genes responsible for the proteins that maintain the structure and flexibility of RBCs, such as ankyrin, band 3, spectrin, and protein 4.2.

The abnormally shaped RBCs are fragile and prone to hemolysis (premature destruction), which can lead to anemia, jaundice, and gallstones. Symptoms can vary from mild to severe and may include fatigue, weakness, shortness of breath, and a yellowing of the skin and eyes (jaundice). Diagnosis is typically made through a combination of family history, physical examination, complete blood count (CBC), and specialized tests such as osmotic fragility test, eosin-5'-maleimide binding test, or direct antiglobulin test. Treatment may include monitoring, supplementation with folic acid, and in severe cases, splenectomy (surgical removal of the spleen) to reduce RBC destruction.

Splenomegaly is a medical term that refers to an enlargement or expansion of the spleen beyond its normal size. The spleen is a vital organ located in the upper left quadrant of the abdomen, behind the stomach and below the diaphragm. It plays a crucial role in filtering the blood, fighting infections, and storing red and white blood cells and platelets.

Splenomegaly can occur due to various underlying medical conditions, including infections, liver diseases, blood disorders, cancer, and inflammatory diseases. The enlarged spleen may put pressure on surrounding organs, causing discomfort or pain in the abdomen, and it may also lead to a decrease in red and white blood cells and platelets, increasing the risk of anemia, infections, and bleeding.

The diagnosis of splenomegaly typically involves a physical examination, medical history, and imaging tests such as ultrasound, CT scan, or MRI. Treatment depends on the underlying cause and may include medications, surgery, or other interventions to manage the underlying condition.

Hemolysis is the destruction or breakdown of red blood cells, resulting in the release of hemoglobin into the surrounding fluid (plasma). This process can occur due to various reasons such as chemical agents, infections, autoimmune disorders, mechanical trauma, or genetic abnormalities. Hemolysis may lead to anemia and jaundice, among other complications. It is essential to monitor hemolysis levels in patients undergoing medical treatments that might cause this condition.

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.

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.

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.

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.

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.

... is a condition where there is an increase in reticulocytes, immature red blood cells. It is commonly seen in ...
The fetus can develop reticulocytosis and anemia. The intensity of this fetal disease ranges from mild to very severe, and ... In the presence of significant hemolysis the smear will show schistocytes (fragmented red blood cells), reticulocytosis, and in ...
Reticulocytosis may not be apparent in the acute phase or when there is viral-induced myelosuppression. Once the clinical ... Reticulocytosis may be subtle in the acute phase. Peripheral blood smear may show corresponding polychromasia. Neutrophil ...
It is much easier to test for polychromasia in blood cells than to perform special staining for reticulocytosis. If ... There is a slight correlation between polychromasia and reticulocytosis. ...
The child had mild anemia and reticulocytosis, which is commonly seen in anemia. There were, however, no sickled cells found in ...
Reticulocytosis, or an increase in circulating immature red blood cells, may be seen. The causes of AIHA are poorly understood ... Reticulocytosis Erythroid hyperplasia of the bone marrow Specific investigations Positive direct Coombs test Steroids are the ...
anemia (14.7%), reticulocytosis (56%), thrombocytopenia (17.6%), an increase in D-dimer and fever were also reported. A study ...
M. haemofelis infection is suspected in cats with regenerative anemia, in which polychromasia and reticulocytosis are noted. ...
hypothyroidism chronic obstructive pulmonary disease (COPD) aplastic anemia reticulocytosis (commonly from hemolysis or a ...
In contrast, non-megaloblastic macrocytic anemias associated with a high reticulocyte count (reticulocytosis) may be caused by ...
... and reticulocytosis. Hemolytic crises are a major concern with sickle-cell disease and G6PD deficiency. Paxillus involutus ...
It increases the erythrocyte production (reticulocytosis) because reticulocytes are immature red blood cells that still contain ...
... reticulocytosis MeSH G09.188.250.840 - thrombin time MeSH G09.188.250.960 - whole blood coagulation time MeSH G09.188.261.145 ...
... arterial blood gases 790.92 Abnormal coagulation profile 790.93 Abnormal prostate specific antigen 790.99 Other Reticulocytosis ...
... and the absence of reticulocytosis (elevated reticulocytes in the blood would usually be observed in haemolytic anaemia).[ ...
Reticulocytosis is a condition where there is an increase in reticulocytes, immature red blood cells. It is commonly seen in ...
Reticulocytosis occurs during active BLOOD regeneration (stimulation of red bone marrow) and in certain types of ANEMIA, ... "Reticulocytosis" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Reticulocytosis" by people in this website by year, and ... Below are the most recent publications written about "Reticulocytosis" by people in Profiles. ...
Reticulocytosis * Increased mean corpuscular hemoglobin concentration (MCHC) * Spherocytes on the peripheral blood smear ...
Normochromic, normocytic, or macrocytic anemia, together with reticulocytosis in the absence of blood loss, is suggestive of ...
A mild reticulocytosis (5- 6%) without anemia, is even more prevalent. The laboratory findings are occasionally accompanied by ... However, most patients developed a mild reticulocytosis. The untoward reactions have reverted to normal following cessation of ...
... with brisk reticulocytosis. Signs of intravascular coagulation are characteristically absent in patients with TTP. ...
Reticulocytosis. HP:0001923. HPO. Human Phenotype Ontology. Sickle Cell Anemia. ORPHA:232. HPO. ...
Blood testing indicated decreased hemoglobinemia (5.2 g/dL; reference 9-14 g/dL) and reticulocytosis (260,000 × 109 cells/L; ...
Postmarketing reports: Unspecified hemorrhage, purpura, reticulocytosis, prolongation of prothrombin time, disseminated ...
The anemia of lead intoxication is hypochromic and normo -or microcytic with associated reticulocytosis. ...
Anemia, jaundice, and reticulocytosis develop during hemolysis. The peripheral smear may reveal RBCs that appear to have a ...
If your results show a higher than normal amount of reticulocytes (reticulocytosis), it may mean:. *You have hemolytic anemia, ...
Erythroblastosis and reticulocytosis in anemic fetuses. Am J Obstet Gynecol 1988; 159:1063. ...
The initial reduction of hemoglobin (2-3g) is common, but it is usually compensated by reticulocytosis.33 Jacques CMC. ...
Reticulocytosis is diagnosed from the characteristic histology of a skin biopsy, showing:. *Multiple multinucleated giant cells ... In many patients, multicentric reticulocytosis can go into remission after an average course of 8 years; however, by this time ... Multicentric reticulohistiocytosis is a very rare multisystem arthropathic form of reticulocytosis. Reticulohistiocytoses are a ...
These anemias have non-regenerative peripheral blood patterns (absence of increased polychromasia/reticulocytosis) but ...
The observation of reticulocytosis which usually occurs between the third and tenth day of therapy confirms the diagnosis of ...
... and adequate reticulocytosis (largely ,100,000/μL). In contrast, all patients share a novel phenomenon which is the ... even patients with normal hemoglobin levels exhibit massive reticulocytosis with increased bilirubin) (31, 64, 71). The ... and compensatory reticulocytosis adequate to hemoglobin levels). Nevertheless, sometimes clinically significant hemolytic ...
2004b) Modulation of the course and outcome of blood-stage malaria by erythropoietin-induced reticulocytosis The Journal of ... 2004a) Inappropriately low reticulocytosis in severe malarial anemia correlates with suppression in the development of late ... Previous studies have shown the induction of reticulocytosis during the course of P. yoelii infection (Martín-Jaular et al., ... whether the lower parasitemia causes the lower reticulocytosis. Using a P. falciparum growth inhibition assay, we could ...
Megakaryocytic/erythroid progenitor (MEP) reductions in Hoxa7(-/-) mice correlated with reticulocytosis and thrombocytopenia ...
... if reticulocytosis is present, consider a workup for hemolysis (including lactate dehydrogenase and bilirubin tests). ...
... reticulocytosis and polychromasia). The therapeutic protocol is mainly based on the immunosuppression. A two-year old poodle ... In the full blood exam it was observed a regenerative anemia with reticulocytosis and the presence of spherocytosis, indicating ...
Any anemic cat, especially one with an anemia showing evidence of regeneration (polychromasia and/or reticulocytosis), may be ...
Initial blood tests revealed a normochromic normocytic anaemia (haemoglobin, 81 g/L) with reticulocytosis, marked ...
Reticulocytosis and polychromatophilia may be present; teardrop-shaped RBCs (dacryocytes) are characteristic morphologic ...
  • Normochromic, normocytic, or macrocytic anemia, together with reticulocytosis in the absence of blood loss, is suggestive of hemolysis. (medscape.com)
  • Reticulocytosis occurs during active BLOOD regeneration (stimulation of red bone marrow) and in certain types of ANEMIA, particularly CONGENITAL HEMOLYTIC ANEMIA. (rush.edu)
  • Initial blood tests revealed a normochromic normocytic anaemia (haemoglobin, 81 g/L) with reticulocytosis, marked thrombocytopenia, and moderate renal impairment. (hkmj.org)
  • The laboratory finding frequently observed is the moderate anemia with characteristics of regeneration (macrocytosis, reticulocytosis and polychromasia). (vin.com)
  • Reticulocytosis occurs with resolution of the antibody. (medscape.com)
  • Reticulocytosis is a condition where there is an increase in reticulocytes, immature red blood cells. (wikipedia.org)
  • Reticulocytosis is a condition where there is an increase in reticulocytes, immature red blood cells. (wikipedia.org)
  • 4. A direct correlation between the mean corpuscular volume of the red cell and the per cent reticulocytes was found within the limits of 0 to 80 per cent reticulocytosis. (ashpublications.org)
  • As reticulocytes are the preferred target cells for the strain of P yoelii used (P yoelii yoelii 265 BY), it was postulated that the inhibition of reticulocytosis in IFN-alpha-treated mice was causally related to the observed decreased blood parasite load. (pasteur.fr)
  • Compared with other hereditary hemolytic anemias, PKD is associated with a far greater post-splenectomy reticulocytosis, with reticulocytes reaching 50% or more over pre-splenectomy counts. (thebloodproject.com)
  • Gerbils have a high proportion of RBCs with polychromasia, basophilic stippling, and reticulocytosis. (merckvetmanual.com)
  • 2 A mild to severe regenerative anemia is present (reticulocytosis, nucleated RBCs, polychromasia, increased MCV). (vin.com)
  • caused by turnover of a higher number of RBCs), and reticulocytosis and increased peripheral nucleated RBCs (caused by increased erythropoiesis secondary to fetal hypoxia). (merckmanuals.com)
  • Reticulocytosis and anemia are associated with an increased risk of death and stroke in the newborn cohort of the Cooperative Study of Sickle Cell Disease. (nih.gov)
  • These data suggest that reticulocytosis among asymptomatic infants with sickle cell anemia is associated with an increased risk of death or stroke during childhood. (nih.gov)
  • 2. Five swine responded to the drug in the usual manner with progressive anemia, reticulocytosis, and erythrocytic hyperplasia of the bone marrow. (ashpublications.org)
  • Se produce reticulocitosis durante la regeneración activa de la SANGRE (estimulación de la médula ósea) y en ciertos tipos de ANEMIA, particularmente en la ANEMIA HEMOLÍTICA CONGÉNITA. (bvsalud.org)
  • Reticulocytosis occurs during active BLOOD regeneration (stimulation of red bone marrow) and in certain types of ANEMIA , particularly CONGENITAL HEMOLYTIC ANEMIA . (bvsalud.org)
  • It's not that any one of the following are indicative of Lyme, but taken together you may see results on labs indicating hemolytic anemia with reticulocytosis, thrombocytopenia, elevated bilirubin, elevated liver enzymes and/or reduced or absent haptoglobin. (suzycohen.com)
  • Tine f5.Lactamase-resistamt penicillins tend to experience an increase in comorbidity burden chapter inappropriate medication use in chronic disease thalassemias reticulocytosis sideroblastic normal reticulocyte count high low edition b13 level may be resistant to sterilisation processes, replacing the compressor to remove and caused personality changes in skin hygiene products due to bacterial lyte and fluid and protein s. (stonecottagegardens.com)
  • A blood film showed features consistent with haemolysis with spherocytes, polychromasia and a reticulocytosis. (scirp.org)
  • The reduced blood parasite load in IFN-alpha-treated mice was associated with reduced erythropoiesis and reticulocytosis. (pasteur.fr)
  • Beta-thalassemia - X-linked thrombocytopenia is a form of beta-thalassemia (see this term) characterized by splenomegaly and petechiae, moderate thrombocytopenia, prolonged bleeding time due to platelet dysfunction, reticulocytosis and mild beta-thalassemia. (orpha.net)
  • Reticulocytosis was also associated with severe disease. (nih.gov)