A myeloproliferative disorder of unknown etiology, characterized by abnormal proliferation of all hematopoietic bone marrow elements and an absolute increase in red cell mass and total blood volume, associated frequently with splenomegaly, leukocytosis, and thrombocythemia. Hematopoiesis is also reactive in extramedullary sites (liver and spleen). In time myelofibrosis occurs.
An increase in the total red cell mass of the blood. (Dorland, 27th ed)
A clinical syndrome characterized by repeated spontaneous hemorrhages and a remarkable increase in the number of circulating platelets.
A Janus kinase subtype that is involved in signaling from GROWTH HORMONE RECEPTORS; PROLACTIN RECEPTORS; and a variety of CYTOKINE RECEPTORS such as ERYTHROPOIETIN RECEPTORS and INTERLEUKIN RECEPTORS. Dysregulation of Janus kinase 2 due to GENETIC TRANSLOCATIONS have been associated with a variety of MYELOPROLIFERATIVE DISORDERS.
A de novo myeloproliferation arising from an abnormal stem cell. It is characterized by the replacement of bone marrow by fibrous tissue, a process that is mediated by CYTOKINES arising from the abnormal clone.
Conditions which cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. They all involve dysregulation of multipotent MYELOID PROGENITOR CELLS, most often caused by a mutation in the JAK2 PROTEIN TYROSINE KINASE.
Increased numbers of platelets in the peripheral blood. (Dorland, 27th ed)
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.
An antineoplastic agent that acts by alkylation.
The cells in the erythroid series derived from MYELOID PROGENITOR CELLS or from the bi-potential MEGAKARYOCYTE-ERYTHROID PROGENITOR CELLS which eventually give rise to mature RED BLOOD CELLS. The erythroid progenitor cells develop in two phases: erythroid burst-forming units (BFU-E) followed by erythroid colony-forming units (CFU-E); BFU-E differentiate into CFU-E on stimulation by ERYTHROPOIETIN, and then further differentiate into ERYTHROBLASTS when stimulated by other factors.
The techniques used to draw blood from a vein for diagnostic purposes or for treatment of certain blood disorders such as erythrocytosis, hemochromatosis, polycythemia vera, and porphyria cutanea tarda.
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.
Cell surface proteins that bind erythropoietin with high affinity and trigger intracellular changes influencing the behavior of cells.
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.
Cell surface receptors that are specific for THROMBOPOIETIN. They signal through interaction with JANUS KINASES such as JANUS KINASE 2.
Puncture of a vein to draw blood for therapeutic purposes. Bloodletting therapy has been used in Talmudic and Indian medicine since the medieval time, and was still practiced widely in the 18th and 19th centuries. Its modern counterpart is PHLEBOTOMY.
A ubiquitin-protein ligase that mediates OXYGEN-dependent polyubiquitination of HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT. It is inactivated in VON HIPPEL-LINDAU SYNDROME.
The formation and development of blood cells outside the BONE MARROW, as in the SPLEEN; LIVER; or LYMPH NODES.
Leukocytes with abundant granules in the cytoplasm. They are divided into three groups according to the staining properties of the granules: neutrophilic, eosinophilic, and basophilic. Mature granulocytes are the NEUTROPHILS; EOSINOPHILS; and BASOPHILS.
Volume of circulating ERYTHROCYTES . It is usually measured by RADIOISOTOPE DILUTION TECHNIQUE.
A SOMATOSTATIN-secreting tumor derived from the pancreatic delta cells (SOMATOSTATIN-SECRETING CELLS). It is also found in the INTESTINE. Somatostatinomas are associated with DIABETES MELLITUS; CHOLELITHIASIS; STEATORRHEA; and HYPOCHLORHYDRIA. The majority of somatostatinomas have the potential for METASTASIS.
An individual in which both alleles at a given locus are identical.
Formation and development of a thrombus or blood clot in the blood vessel.
A subclass of lipid-linked proteins that contain a GLYCOSYLPHOSPHATIDYLINOSITOL LINKAGE which holds them to the CELL MEMBRANE.
An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase.
A mutation in which a codon is mutated to one directing the incorporation of a different amino acid. This substitution may result in an inactive or unstable product. (From A Dictionary of Genetics, King & Stansfield, 5th ed)
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
The naturally occurring or experimentally induced replacement of one or more AMINO ACIDS in a protein with another. If a functionally equivalent amino acid is substituted, the protein may retain wild-type activity. Substitution may also diminish, enhance, or eliminate protein function. Experimentally induced substitution is often used to study enzyme activities and binding site properties.
Antigens that exist in alternative (allelic) forms in a single species. When an isoantigen is encountered by species members who lack it, an immune response is induced. Typical isoantigens are the BLOOD GROUP ANTIGENS.
A bluish or purplish discoloration of the skin and mucous membranes due to an increase in the amount of deoxygenated hemoglobin in the blood or a structural defect in the hemoglobin molecule.
The series of cells in the red blood cell lineage at various stages of differentiation.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
A cytologic technique for measuring the functional capacity of stem cells by assaying their activity.
Very large BONE MARROW CELLS which release mature BLOOD PLATELETS.
A neural crest tumor usually derived from the chromoreceptor tissue of a paraganglion, such as the carotid body, or medulla of the adrenal gland (usually called a chromaffinoma or pheochromocytoma). It is more common in women than in men. (Stedman, 25th ed; from Segen, Dictionary of Modern Medicine, 1992)
ERYTHROCYTE size and HEMOGLOBIN content or concentration, usually derived from ERYTHROCYTE COUNT; BLOOD hemoglobin concentration; and HEMATOCRIT. The indices include the mean corpuscular volume (MCV), the mean corpuscular hemoglobin (MCH), and the mean corpuscular hemoglobin concentration (MCHC).
The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
A transient increase in the number of leukocytes in a body fluid.
The number of RED BLOOD CELLS per unit volume in a sample of venous BLOOD.
An individual having different alleles at one or more loci regarding a specific character.
A condition in which the hepatic venous outflow is obstructed anywhere from the small HEPATIC VEINS to the junction of the INFERIOR VENA CAVA and the RIGHT ATRIUM. Usually the blockage is extrahepatic and caused by blood clots (THROMBUS) or fibrous webs. Parenchymal FIBROSIS is uncommon.
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.
Progenitor cells from which all blood cells derive.
Multiple symptoms associated with reduced oxygen at high ALTITUDE.
Enlargement of the spleen.
A myelodysplastic/myeloproliferative disorder characterized by myelodysplasia associated with bone marrow and peripheral blood patterns similar to CHRONIC MYELOID LEUKEMIA, but cytogenetically lacking a PHILADELPHIA CHROMOSOME or bcr/abl fusion gene (GENES, ABL).
The short, metacentric human chromosomes, called group F in the human chromosome classification. This group consists of chromosome pairs 19 and 20.
A humoral factor that stimulates the production of thrombocytes (BLOOD PLATELETS). Thrombopoietin stimulates the proliferation of bone marrow MEGAKARYOCYTES and their release of blood platelets. The process is called THROMBOPOIESIS.

Insulin-like growth factor I plays a role in regulating erythropoiesis in patients with end-stage renal disease and erythrocytosis. (1/419)

Erythroid progenitor growth, the serum hormones that regulate erythropoiesis, and the effect of patient's serum on the growth of normal erythroid progenitors were assessed in eight patients with end-stage renal disease (ESRD) and erythrocytosis. All patients were male and had been on maintenance dialysis, they had a hematocrit >50% and/or a red blood cell count >6 x 10(12)/L and an arterial oxygen saturation >95%. Four had acquired cystic disease of the kidney (ACDK), and four other non-ACDK patients did not have known causes of secondary erythrocytosis after appropriate investigations and long-term follow-up. The methylcellulose culture technique was used to assay the erythroid progenitor (BFU-E/CFU-E) growth. Serum erythropoietin (EPO) and insulin-like growth factor I (IGF-I) levels were measured by RIA. Paired experiments were performed to determine the effects of 10% sera from ESRD patients and control subjects on normal marrow CFU-E growth. The numbers of EPO-dependent BFU-E in marrow and/or blood of patients with ESRD and erythrocytosis were higher than those of normal controls. No EPO-independent erythroid colonies were found. Serum EPO levels were constantly normal in one patient and elevated in three patients with ACDK; for non-ACDK patients, EPO levels were normal or low in two patients and persistently increased in one, but fluctuated in the remaining one on serial assays. There was no correlation between serum EPO levels and hematocrit values. The serum IGF-I levels in patients with ESRD and erythrocytosis were significantly increased compared with normal subjects or ESRD patients with anemia. We found an inverse correlation between serum EPO and IGF-I levels. Sera from patients with ESRD and erythrocytosis exhibited a stimulating effect on normal marrow CFU-E growth. The stimulating effect of sera from patients who had a normal serum EPO level and an elevated IGF-I level could be partially blocked by anti-IGF-I. The present study suggests that IGF-I plays an important role in the regulation of erythropoiesis in patients with ESRD and erythrocytosis who did not have an increased EPO production.  (+info)

Pulmonary prostacyclin synthase overexpression in transgenic mice protects against development of hypoxic pulmonary hypertension. (2/419)

Prostacyclin synthase (PGIS) is the final committed enzyme in the metabolic pathway leading to prostacyclin (PGI2) production. Patients with severe pulmonary hypertension have a PGIS deficiency of their precapillary vessels, but the importance of this deficiency for lung vascular remodeling remains unclear. We hypothesized that selective pulmonary overexpression of PGIS may prevent the development of pulmonary hypertension. To study this hypothesis, transgenic mice were created with selective pulmonary PGIS overexpression using a construct of the 3.7-kb human surfactant protein-C (SP-C) promoter and the rat PGIS cDNA. Transgenic mice (Tg+) and nontransgenic littermates (Tg-) were subjected to a simulated altitude of 17,000 ft for 5 weeks, and right ventricular systolic pressure (RVSP) was measured. Histology was performed on the lungs. The Tg+ mice produced 2-fold more pulmonary 6-keto prostaglandin F1alpha (PGF1alpha) levels than did Tg- mice. After exposure to chronic hypobaric hypoxia, Tg+ mice have lower RVSP than do Tg- mice. Histologic examination of the lungs revealed nearly normal arteriolar vessels in the Tg+ mice in comparison with vessel wall hypertrophy in the Tg- mice. These studies demonstrate that Tg+ mice were protected from the development of pulmonary hypertension after exposure to chronic hypobaric hypoxia. We conclude that PGIS plays a major role in modifying the pulmonary vascular response to chronic hypoxia. This has important implications for the pathogenesis and treatment of severe pulmonary hypertension.  (+info)

Localization of the gene responsible for familial benign polycythemia to chromosome 11q23. (3/419)

Familial benign polycythemia (FBP) (OMIM 263400) is a rare autosomal recessive condition characterized by erythrocytosis, normal leukocyte and platelet counts, normal uric acid level, and usually increased erythropoietin production. There is a high incidence of this disorder in Chuvashia (Russian Federation), probably due to a founder effect. In an attempt to locate the gene responsible for this disorder, we have carried out linkage studies in 12 Chuvash families, with 35 affected and 32 unaffected members. Linkage to the erythropoietin and erythropoietin receptor loci was excluded, and the FBP gene was assigned to the region of chromosome 11q23 between D11S4142 and D11S1356, with a maximal lod score of 6.61.  (+info)

Activation of the erythropoietin receptor by the gp55-P viral envelope protein is determined by a single amino acid in its transmembrane domain. (4/419)

The spleen focus forming virus (SFFV) gp55-P envelope glycoprotein specifically binds to and activates murine erythropoietin receptors (EpoRs) coexpressed in the same cell, triggering proliferation of erythroid progenitors and inducing erythroleukemia. Here we demonstrate specific interactions between the single transmembrane domains of the two proteins that are essential for receptor activation. The human EpoR is not activated by gp55-P but by mutation of a single amino acid, L238, in its transmembrane sequence to its murine counterpart serine, resulting in its ability to be activated. The converse mutation in the murine EpoR (S238L) abolishes activation by gp55-P. Computational searches of interactions between the membrane-spanning segments of murine EpoR and gp55-P provide a possible explanation: the face of the EpoR transmembrane domain containing S238 is predicted to interact specifically with gp55-P but not gp55-A, a variant which is much less effective in activating the murine EpoR. Mutational studies on gp55-P M390, which is predicted to interact with S238, provide additional support for this model. Mutation of M390 to isoleucine, the corresponding residue in gp55-A, abolishes activation, but the gp55-P M390L mutation is fully functional. gp55-P is thought to activate signaling by the EpoR by inducing receptor oligomerization through interactions involving specific transmembrane residues.  (+info)

Erythropoietin receptor mutations associated with familial erythrocytosis cause hypersensitivity to erythropoietin in the heterozygous state. (5/419)

Inherited mutations in the erythropoietin receptor (EPOR) causing premature termination of the receptor cytoplasmic region are associated with dominant familial erythrocytosis (FE), a benign clinical condition characterized by hypersensitivity of erythroid progenitor cells to EPO and low serum EPO (S-EPO) levels. We describe a Swedish family with dominant FE in which erythrocytosis segregates with a new truncation in the negative control domain of the EPOR. We show that cells engineered to concomitantly express the wild-type (WT) EPOR and mutant EPORs associated with FE (FE EPORs) are hypersensitive to EPO-stimulated proliferation and activation of Jak2 and Stat5. These results demonstrate that FE is caused by hyperresponsiveness of receptor-mediated signaling pathways and that this is dominant with respect to WT EPOR signaling.  (+info)

Role of the spleen in the exaggerated polycythemic response to hypoxia in chronic mountain sickness in rats. (6/419)

In a rat model of chronic mountain sickness, the excessive polycythemic response to hypoxic exposure is associated with profound splenic erythropoiesis. We studied the uptake and distribution of radioactive iron and red blood cell (RBC) morphology in intact and splenectomized rats over a 30-day hypoxic exposure. Retention of (59)Fe in the plasma was correlated with (59)Fe uptake by both spleen and marrow and the appearance of (59)Fe-labeled RBCs in the blood. (59)Fe uptake in both the spleen and the marrow paralleled the production of nucleated RBCs. Splenic (59)Fe uptake was approximately 10% of the total marrow uptake under normoxic conditions but increased to 60% of the total marrow uptake during hypoxic exposure. Peak splenic (59)Fe uptake and splenomegaly occurred at the most intense phase of erythropoiesis and coincided with the rapid appearance of (59)Fe-labeled RBCs in the blood. The bone marrow remains the most important erythropoietic organ under both resting and stimulated states, but inordinate splenic erythropoiesis in this rat strain accounts in large measure for the excessive polycythemia during the development of chronic mountain sickness in chronic hypoxia.  (+info)

Neutrophil alkaline phosphatase score in chronic granulocytic leukaemia: effects of splenectomy and antileukaemic drugs. (7/419)

Staining with naphthol AS phosphate and Fast Blue BB salt has been used for the estimation of neutrophil alkaline phosphatase (NAP) scores in patients with chronic granulocytic leukaemia (CGL). The very low scores found at diagnosis rise when the disease is treated, and there is some inverse correlation between the NAP score and the absolute neutrophil count. Patients treated intensively developed high NAP scores. Elective splenectomy performed during the chronic phase of CGL is followed by a pronounced but transient neutrophilia and a concurrent striking rise in the NAP score. Similar changes were observed in patients without CGL who underwent splenectomy. These observations can be explained by assuming that newly formed neutrophils in CGL have a normal content of NAP but are rapidly sequestered in non-circulating extramedullary pools, whereas the circulating neutrophil with a typically low NAP content is a relatively aged cell which has lost enzyme activity. In subjects with or without CGL, removal of the spleen, a major site of such pooling, temporarily permits the circulation of newly formed neutrophils but eventually other organs assume the sequestering functions of the spleen. Thus the aberrations of NAP score seen in CGL might be attributable not to an intrinsic cellular defect but to an exaggeration of the granulocyte storage phenomena which also occur in subjects without CGL.  (+info)

Significance of an abnormally low or high hemoglobin concentration during pregnancy: special consideration of iron nutrition. (8/419)

An association between moderate anemia and poor perinatal outcomes has been found through epidemiologic studies, although available evidence cannot establish this relation as causal. Anemia may not be a direct cause of poor pregnancy outcomes, except in the case of maternal mortality resulting directly from severe anemia due to hypoxia and heart failure. Preventing or treating anemia, whether moderate or severe, is desirable. Because iron deficiency is a common cause of maternal anemia, iron supplementation is a common practice to reduce the incidence of maternal anemia. Nevertheless, the effectiveness of large-scale supplementation programs needs to be improved operationally and, where multiple micronutrient deficiencies are common, supplementation beyond iron and folate can be considered. High hemoglobin concentrations are often mistaken as adequate iron status; however, high hemoglobin is independent of iron status and is often associated with poor health outcomes. Very high hemoglobin concentrations cause high blood viscosity, which results in both compromised oxygen delivery to tissues and cerebrovascular complications. Epidemiologic studies have also found an association between high maternal hemoglobin concentrations and an increased risk of poor pregnancy outcomes. Evidence does not suggest that this association is causal; it could be better attributed to hypertensive disorders of pregnancy and to preeclampsia. The pathophysiologic mechanism of these conditions during pregnancy can produce higher hemoglobin concentrations because of reduced normal plasma expansion and cause fetal stress because of reduced placental-fetal perfusion. Accordingly, higher than normal hemoglobin concentrations should be regarded as an indicator of possible pregnancy complications, not necessarily as a sign of adequate iron nutrition, because iron supplementation does not increase hemoglobin higher than the optimal concentration needed for oxygen delivery.  (+info)

The exact cause of polycythemia vera is not known, but it is believed to be due to a genetic mutation in the JAK2 gene, which is involved in the signaling pathways that regulate blood cell production. The condition typically affects adults over the age of 60 and is more common in men than women.

Symptoms of polycythemia vera can include:

* Fatigue
* Weakness
* Shortness of breath
* Headaches
* Dizziness
* Itching
* Night sweats
* Weight loss

Diagnosis of polycythemia vera is typically made based on a combination of physical examination, medical history, and laboratory tests, including:

* Complete blood count (CBC) to measure the levels of red blood cells, white blood cells, and platelets
* Blood chemistry tests to assess liver function and other body chemicals
* Genetic testing to look for the JAK2 mutation
* Bone marrow biopsy to examine the bone marrow tissue for abnormalities

Treatment for polycythemia vera usually involves phlebotomy (the removal of blood from the body) to reduce the number of red blood cells and relieve symptoms such as itching and night sweats. In some cases, medications may be used to reduce the production of blood cells or to treat specific symptoms. Regular monitoring by a healthcare provider is important to detect any changes in the condition and to prevent complications.

Overall, polycythemia vera is a chronic and progressive disease that can have significant impact on quality of life if left untreated. Early diagnosis and appropriate treatment can help manage symptoms and improve outcomes for patients with this condition.

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. Primary essential thrombocythemia (PET): This is the more common form, usually occurring spontaneously without any identifiable cause. Symptoms may include headache, migraine, seizures, and stroke-like episodes.
2. Secondary essential thrombocythemia: This form is caused by another medical condition or medication that stimulates the production of platelets. Symptoms are similar to those of PET, but there may be an underlying cause such as a tumor or an adverse reaction to medication.

Treatment for essential thrombocythemia includes medications to reduce platelet count and prevent blood clots, as well as close monitoring and management of any underlying causes. In some cases, surgery may be necessary to remove a tumor or other contributing factor.

PMF is a chronic disease that worsens over time, and it can lead to complications such as bleeding, infection, and bone damage. Treatment options include medications to reduce symptoms and slow the progression of the disease, as well as blood transfusions and splenectomy (removal of the spleen) in severe cases. The median age at diagnosis is around 60 years old, and the disease affects approximately 2-5 cases per million people per year.

Sources:

* American Cancer Society. (2019). What is primary myelofibrosis? Retrieved from
* Leukemia and Lymphoma Society. (n.d.). Primary Myelofibrosis. Retrieved from

There are several types of MPDs, including:

1. Polycythemia vera (PV): This is a rare disorder characterized by an overproduction of red blood cells, white blood cells, and platelets.
2. Essential thrombocythemia (ET): This is a rare disorder characterized by an overproduction of platelets.
3. Primary myelofibrosis (PMF): This is a rare and severe disorder characterized by the accumulation of scar tissue in the bone marrow, leading to an overproduction of immature white blood cells.
4. Chronic myelogenous leukemia (CML): This is a type of cancer that affects the bone marrow and blood cells, characterized by the overproduction of immature white blood cells.

The symptoms of MPDs can vary depending on the specific disorder, but may include:

* Fatigue
* Weakness
* Shortness of breath
* Headaches
* Dizziness
* Pale skin
* Easy bruising or bleeding
* Swollen spleen
* Bone pain

The exact cause of MPDs is not known, but they are thought to be due to genetic mutations that occur in the bone marrow cells. Treatment options for MPDs include:

* Chemotherapy: This is a type of drug that kills cancer cells.
* Radiation therapy: This is a type of treatment that uses high-energy X-rays to kill cancer cells.
* Stem cell transplantation: This is a procedure in which healthy stem cells are transplanted into the body to replace damaged or diseased bone marrow cells.

Overall, MPDs are rare and complex disorders that can have a significant impact on quality of life. While there is no cure for these conditions, treatment options are available to help manage symptoms and improve outcomes.

In healthy individuals, the normal platelet count ranges from 150,000 to 450,000 platelets per microliter of blood. In thrombocytosis, the platelet count is significantly higher than this range, often above 600,000 platelets/μL.

Thrombocytosis can be caused by a variety of factors, including:

1. Bone marrow disorders: Disorders such as essential thrombocythemia, polycythemia vera, and myelofibrosis can lead to an overproduction of platelets in the bone marrow.
2. Infection: Sepsis and other infections can cause a temporary increase in platelet production.
3. Inflammation: Certain inflammatory conditions, such as appendicitis and pancreatitis, can also lead to thrombocytosis.
4. Cancer: Some types of cancer, such as leukemia and lymphoma, can cause an overproduction of platelets.
5. Medications: Certain medications, such as estrogens and corticosteroids, can increase platelet production.

Thrombocytosis can lead to a range of complications, including:

1. Blood clots: The excessive number of platelets in the blood can increase the risk of blood clots forming in the veins and arteries.
2. Pulmonary embolism: If a blood clot forms in the lungs, it can cause a pulmonary embolism, which can be life-threatening.
3. Stroke: Thrombocytosis can increase the risk of stroke, especially if there are existing risk factors such as high blood pressure or a history of cardiovascular disease.
4. Heart attack and heart failure: Excessive platelet activity can increase the risk of heart attack and heart failure.
5. Gastrointestinal bleeding: The increased number of platelets in the blood can make it more difficult to control bleeding, especially in the gastrointestinal tract.

Thrombocytosis is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as:

1. Complete blood count (CBC): This test measures the number of platelets in the blood, as well as other components such as red and white blood cells.
2. Blood smear: A sample of blood is examined under a microscope to assess the shape and size of the platelets.
3. Bone marrow aspiration and biopsy: These tests involve removing a small sample of bone marrow tissue to examine the number and type of cells present.
4. Imaging studies: Imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) may be used to look for evidence of blood clots or other complications.

Treatment for thrombocytosis depends on the underlying cause and the severity of the condition. Some common treatments include:

1. Medications: Drugs such as aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners may be used to reduce the risk of blood clots and other complications.
2. Plateletpheresis: This is a procedure in which the patient's blood is removed and the platelets are separated from the rest of the blood components. The remaining blood is then returned to the body.
3. Splenectomy: In some cases, surgical removal of the spleen may be necessary to treat thrombocytosis.
4. Chemotherapy: This is a treatment that uses drugs to kill cancer cells, which can cause thrombocytosis in some cases.

Overall, it is important to seek medical attention if you experience any symptoms of thrombocytosis, as early diagnosis and treatment can help prevent complications and improve outcomes.

Somatostatinomas are relatively rare, accounting for only about 1-2% of all pancreatic tumors. They tend to affect older adults, typically in their 60s or 70s, and are more common in women than men. The exact cause of somatostatinomas is not well understood, but genetic mutations and changes in the DNA of somatostatin-producing cells may play a role in their development.

The diagnosis of a somatostatinoma typically involves a combination of imaging tests such as CT scans, MRI, and PET scans, along with blood tests to measure hormone levels and identify genetic mutations. Treatment options for somatostatinomas may include surgery, chemotherapy, and radiation therapy, depending on the size, location, and aggressiveness of the tumor. Prognosis for somatostatinoma patients is generally good if the tumor is diagnosed early and treated appropriately, but the long-term outlook can vary depending on the specific characteristics of the tumor and the individual patient's overall health.

There are several types of thrombosis, including:

1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.

The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:

1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic

Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.

In medicine, cyanosis is often used as an indication of the severity of a patient's condition. For example, a patient with severe cyanosis may have a more serious underlying condition than a patient with mild cyanosis. Additionally, cyanosis can be used to monitor the effectiveness of treatment and to determine when further interventions are necessary.

Cyanosis can be diagnosed through physical examination, blood tests, and other diagnostic procedures such as pulse oximetry or arterial blood gas analysis. Treatment for cyanosis depends on the underlying cause and may include oxygen therapy, medication, or surgical intervention.

In summary, cyanosis is a condition characterized by a bluish discoloration of the skin and mucous membranes due to inadequate oxygenation of the body's tissues. It is an important sign of underlying disease and can be used to assess the severity of a patient's condition and monitor the effectiveness of treatment.

Paragangliomas are rare, accounting for less than 1% of all tumors diagnosed in adults. They can occur at any age but are more common in young adults and middle-aged individuals. These tumors are more common in males than females, and their incidence is higher in certain families with inherited syndromes, such as neurofibromatosis type 1 (NF1) or familial paraganglioma.

The symptoms of paraganglioma depend on their location and size. Small tumors may not cause any symptoms, while larger tumors can press on nearby organs and structures, causing a variety of symptoms such as:

* Pain in the abdomen or pelvis
* Swelling or lump in the neck or abdomen
* High blood pressure
* Headaches
* Blurred vision
* Confusion or seizures (in cases of malignant paraganglioma)

Paragangliomas are difficult to diagnose, as they can be mistaken for other conditions such as appendicitis or pancreatitis. Imaging studies such as CT or MRI scans are often used to help identify the location and size of the tumor, while laboratory tests may be used to evaluate hormone levels and other factors that can help differentiate paraganglioma from other conditions.

Treatment for paraganglioma depends on the type, size, and location of the tumor, as well as the patient's overall health status. Small, benign tumors may not require treatment, while larger or malignant tumors may be treated with surgery, chemotherapy, or radiation therapy. In some cases, a combination of these treatments may be used.

The prognosis for paraganglioma is generally good if the tumor is diagnosed and treated early, but it can be poor if the tumor is large or has spread to other parts of the body. With surgical removal of the tumor, the 5-year survival rate is approximately 90% for patients with benign paraganglioma and 30-50% for those with malignant paraganglioma. However, the overall prognosis can vary depending on individual factors such as the size and location of the tumor, the effectiveness of treatment, and the patient's underlying health status.

White blood cells are an important part of the immune system and play a crucial role in fighting off infections and diseases. However, when there is an excessive increase in their numbers, it can lead to various complications, including:

1. Increased risk of infection: With too many white blood cells in the bloodstream, there is a higher chance of developing infections.
2. Inflammation: Excessive production of white blood cells can cause inflammation in various parts of the body.
3. Blood clotting disorders: White blood cells can clump together and form clots, which can lead to blockages in blood vessels.
4. Tissue damage: The excessive growth of white blood cells can cause damage to tissues and organs.
5. Bone marrow failure: Prolonged leukocytosis can lead to bone marrow failure, which can result in a decrease in the production of other blood cells, such as red blood cells and platelets.

There are several types of leukocytosis, including:

1. Reactive leukocytosis: This is the most common type and is caused by an infection or inflammation.
2. Chronic leukocytosis: This type is characterized by a persistent increase in white blood cells over a long period of time.
3. Acute leukocytosis: This type is characterized by a sudden and severe increase in white blood cells, often accompanied by other symptoms such as fever and fatigue.
4. Leukemia: This is a type of cancer that affects the bone marrow and blood cells. It can cause an abnormal increase in white blood cells.

Diagnosis of leukocytosis typically involves a physical examination, medical history, and laboratory tests such as complete blood count (CBC) and bone marrow biopsy. Treatment depends on the underlying cause and may include antibiotics for infections, steroids to reduce inflammation, or chemotherapy for leukemia. In some cases, no treatment is necessary if the condition resolves on its own.

The condition is named after the German physician Hans von Budde and the Italian physician Giorgio Chiari, who independently described it in the late 19th century. It is also known as Budd-Chiari syndrome or venous sinus thrombosis.

The exact cause of Budd-Chiari Syndrome is not known, but it is thought to be related to a combination of genetic and environmental factors. Some cases have been linked to autoimmune disorders, such as lupus, or to infections, such as endocarditis.

Symptoms of Budd-Chiari Syndrome can vary in severity and may include:

* Headaches
* Facial swelling
* Difficulty swallowing
* Numbness or tingling in the face or limbs
* Vision problems
* Fatigue
* Shortness of breath

If you suspect that you or someone else may have Budd-Chiari Syndrome, it is important to seek medical attention as soon as possible. A healthcare provider can perform a physical examination and order diagnostic tests, such as imaging studies or blood tests, to confirm the diagnosis and determine the underlying cause.

Treatment for Budd-Chiari Syndrome typically involves addressing the underlying cause of the condition, such as antibiotics for an infection or medication to treat an autoimmune disorder. In some cases, a procedure called thrombectomy may be necessary to remove a blood clot that is blocking the veins.

In severe cases, Budd-Chiari Syndrome can lead to complications such as stroke or heart failure, so it is important to seek medical attention promptly if symptoms persist or worsen over time. With timely and appropriate treatment, however, many people with this condition are able to recover and manage their symptoms effectively.

The symptoms of altitude sickness can vary in severity and may include:

* Headache
* Dizziness and lightheadedness
* Nausea and vomiting
* Fatigue and weakness
* Shortness of breath
* Coughing and chest tightness
* Swelling of the hands, feet, and face

In severe cases, altitude sickness can lead to more serious complications such as:

* High-altitude pulmonary edema (HAPE): fluid buildup in the lungs that can be life-threatening
* High-altitude cerebral edema (HACE): fluid buildup in the brain that can be life-threatening

To prevent altitude sickness, it is recommended to ascend gradually and give your body time to acclimate to the higher altitude. This can be done by spending a few days at a lower altitude before ascending to a higher altitude. It is also important to stay hydrated by drinking plenty of water and avoid alcohol and sedatives, which can increase the risk of altitude sickness.

If you experience any symptoms of altitude sickness, it is important to descend to a lower altitude as soon as possible. Medications such as acetazolamide (Diamox) can also be used to help prevent and treat altitude sickness. In severe cases, hospitalization may be necessary to receive oxygen therapy and other medical treatment.

The term splenomegaly is used to describe any condition that results in an increase in the size of the spleen, regardless of the underlying cause. This can be caused by a variety of factors, such as infection, inflammation, cancer, or genetic disorders.

Splenomegaly can be diagnosed through a physical examination, where the doctor may feel the enlarged spleen during an abdominal palpation. Imaging tests, such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI), may also be used to confirm the diagnosis and evaluate the extent of the splenomegaly.

Treatment for splenomegaly depends on the underlying cause. For example, infections such as malaria or mononucleosis are treated with antibiotics, while cancerous conditions may require surgical intervention or chemotherapy. In some cases, the spleen may need to be removed, a procedure known as splenectomy.

In conclusion, splenomegaly is an abnormal enlargement of the spleen that can be caused by various factors and requires prompt medical attention for proper diagnosis and treatment.

This type of leukemia is considered "chronic" because it progresses slowly over time, and it is "atypical" because the cancer cells do not fit into any of the standard subtypes of myeloid leukemia. It is also "BCR-ABL negative," meaning that there is no evidence of a specific genetic abnormality (the BCR-ABL fusion gene) that is present in other types of chronic myeloid leukemia.

This type of leukemia is relatively rare and tends to affect older adults. It can cause symptoms such as fatigue, fever, night sweats, and an enlarged spleen, and it can increase the risk of infections and bleeding. Treatment typically involves chemotherapy and, in some cases, bone marrow transplantation.

The management of polycythemia varies based on its etiology: See polycythemia vera for management of primary polycythemia, ... "relative polycythemia"). Absolute polycythemia can be due to genetic mutations in the bone marrow ("primary polycythemia"), ... Polycythemia vera (PCV) (a.k.a. polycythemia rubra vera (PRV)) occurs when excess red blood cells are produced as a result of ... Polycythemia has many causes. It can describe an increase in the number of red blood cells ("absolute polycythemia") or to a ...
"Polycythemia vera - MayoClinic.com". Polycythemia vera: Definition. Mayo Clinic. Retrieved 2011-09-03. "What Is Polycythemia ... People with polycythemia vera can be asymptomatic. A classic symptom of polycythemia vera is pruritus or itching, particularly ... JAK2-positive polycythemia vera - diagnosis requires both criteria to be present: JAK2-negative polycythemia vera - diagnosis ... "Polycythemia Vera Follow-up". Retrieved 2011-09-03. "Highlights in Polycythemia Vera From the 2016 EHA Congres". Retrieved 2016 ...
... (TAPS) is a form of chronic inter-twin transfusion.[excessive citations] It is distinguished ... "Twin Anemia Polycythemia Sequence". NORD (National Organization for Rare Disorders). Retrieved 2021-10-04. Genova, L.; ... "Twin Anemia-Polycythemia Sequence in Two Monochorionic Twin Pairs Without Oligo-Polyhydramnios Sequence". Placenta. 28 (1): 47- ... "Twin Anemia-Polycythemia Sequence: Diagnostic Criteria, Classification, Perinatal Management and Outcome". Fetal Diagnosis and ...
FST Polycythemia vera; 263300; JAK2 Polycythemia, benign familial; 263400; VHL Polydactyly, postaxial, types A1 and B; 174200; ...
Anemia and polycythemia. in: Braunwald E, et al. Harrison's Principles of Internal Medicine. (15th Edition). McGraw Hill (New ...
See polycythemia vera.) "Obituary notice. Scott Murphy". philly.com. April 2006. Sandler, S. Gerald (November 2007). "Obituary ... "Polycythemia Vera: Stem-Cell and Probable Clonal Origin of the Disease". N Engl J Med. 295 (17): 913-916. doi:10.1056/ ...
Polycythemia can also occur. In children, chronic hypoxemia may manifest as delayed growth, neurological development and motor ...
Polycythemia, a condition in which the number of red cells in the blood is too high, is usually diagnosed when the hematocrit ... Polycythemia can make the blood thicker than normal and therefore lead to complications. Partial exchange transfusion has been ... In conditions such as neonatal polycythemia, a specific amount of the child's blood is removed and replaced with normal saline ... Partial exchange might be required for polycythemia. Nearly all exchange transfusions are allogeneic (that is, the new blood or ...
Causes include polycythemia and hyperfibrinogenemia. To help with diagnosis, the clinician can watch out for predisposing ...
Polycythemia vera definition, mayoclinic.org; accessed July 30, 2021. Yetter, Deborah (May 16, 2020). "Phyllis George, former ... George died of complications from polycythemia vera, a blood cancer, on May 14, 2020, aged 70, at the Albert B. Chandler ...
Aerts has polycythemia, a fatal blood disease.[clarification needed] He is also the former owner and operator of the largest ... Aerts has a rare blood disease called polycythemia, which causes the body to produce excess red blood cells. Although the ...
No evidence of polycythemia vera hematocrit < midpoint of normal range or normal red cell mass in presence of normal iron ... Vannucchi, AM (June 2010). "Insights into the pathogenesis and management of thrombosis in polycythemia vera and essential ... Campbell PJ, Green AR (2005). "Management of Polycythemia Vera and Essential Thrombocythemia" (PDF). Hematology. 2005: 201-8. ... polycythemia vera and essential thrombocythemia: 2011 update on diagnosis, risk-stratification, and management". American ...
... including polycythaemia vera. In patients with polycythaemia, the reduction of mutant JAK2 concentrations by givinostat is ... polycythaemia vera. and Duchenne muscular dystrophy. A preclinical study produced early results suggesting the molecule might ... "Treatment options for essential thrombocythemia and polycythemia vera". Expert Review of Hematology. 2 (1): 41-55. doi:10.1586/ ... Givinostat for the treatment of polycythaemia vera" (PDF). European Medicines Agency. "Potential treatment for diastolic ...
Burgess, J. H.; Bishop, J. M. (1963). "Pulmonary Diffusing Capacity and ITS Subdivisions in Polycythemia Vera". Journal of ... polycythemia, left to right intracardiac shunts, due increase in volume of blood exposed to inspired gas. Asthma due to better ... More hemoglobin is present in polycythemia, and so D L C O {\displaystyle D_{L_{CO}}} is elevated. In anemia, the opposite is ...
Reikvam H, Tiu RV (April 2012). "Venous thromboembolism in patients with essential thrombocythemia and polycythemia vera". ... polycythemia vera, essential thrombocythemia, intravenous drug use, and smoking. Some risk factors influence the location of ...
"Regulated expression of microRNAs in normal and polycythemia vera erythropoiesis". Experimental Hematology. 35 (11): 1657-67. ...
In addition, these neuroendocrine tumors release erythropoietin (EPO) into circulating blood, and lead to polycythemia. ... leading to polycythemia, paragangliomas, and somatostatinomas". Blood. 121 (13): 2563-6. doi:10.1182/blood-2012-10-460972. PMC ... "Somatic HIF2A gain-of-function mutations in paraganglioma with polycythemia". The New England Journal of Medicine. 367 (10): ...
In polycythaemia vera, the most common side effects include anemia (low red blood cell counts) and thrombocytopenia (low blood ... It is also indicated for the treatment of adults with polycythaemia vera who are resistant to or intolerant of hydroxyurea. ... In 2014, it was approved in polycythemia vera (PCV) when there has been an inadequate response to or intolerance of hydroxyurea ... January 2015). "Ruxolitinib versus standard therapy for the treatment of polycythemia vera". The New England Journal of ...
Laboratory findings in neonates may indicate polycythemia, leukopenia, or neutropenia. As they age, neurological deficits begin ...
... complications from polycythemia vera. Mun Jong-nam, North Korean diplomat, ambassador to Italy (2017) and Syria (since 2018), ...
"Anemia and Polycythemia", Harrison's Principles of Internal Medicine (19 ed.), New York, NY: McGraw-Hill Education, retrieved ...
... polycythemia vera, essential thrombocytosis, and primary myelofibrosis. In one review of adult-AMKL, 25% of 49 cases were ... polycythemia vera, essential thrombocytosis, primary myelofibrosis, or mediastinal germ cell tumor. AMKL associated with ...
It can also be associated with lupus, polycythemia vera and homocystinuria. Malar flush is a plum-red discolouration of the ... It can also be associated with other conditions, such as lupus, polycythemia vera and homocystinuria. Malar rash Topol, Eric J ...
December 1988). "[Therapeutic effect of ranimustine (MCNU) on essential thrombocythemia and polycythemia vera]". Gan To Kagaku ... is a nitrosourea alkylating agent approved in Japan for the treatment of chronic myelogenous leukemia and polycythemia vera. It ...
... , sold under the brand name Besremi, is a medication used to treat polycythemia vera. It is an ... Ropeginterferon alfa-2b is the first medication approved by the U.S. Food and Drug Administration (FDA) to treat polycythemia ... In this trial, 51 adults with polycythemia vera received ropeginterferon alfa-2b for an average of about five years. The ... In the European Union, ropeginterferon alfa-2b is indicated as monotherapy in adults for the treatment of polycythemia vera ...
The cause of death was polycythemia, a kind of chronic leucosis. It is mentioned in a book Isaak Lipnitsky by Vadim Teplitsky ( ...
Passamonti F, Lazzarino M (September 2003). "Treatment of polycythemia vera and essential thrombocythemia: the role of ...
... can begin with a blood picture similar to that found in polycythemia vera or chronic myeloid leukemia. ... Najean Y, Rain JD (November 1997). "Treatment of polycythemia vera: the use of hydroxyurea and pipobroman in 292 patients under ... November 2010). "Oxidative stress is increased in primary and post-polycythemia vera myelofibrosis". Experimental Hematology. ... such as polycythemia vera, and less commonly, essential thrombocythemia. In these cases, myelofibrosis occurs as a result of ...
When the hematocrit rises to 60 or 70%, which it often does in polycythemia, the blood viscosity can become as great as 10 ... Tefferi A (May 2003). "A contemporary approach to the diagnosis and management of polycythemia vera". Curr. Hematol. Rep. 2 (3 ...
September 2012). "Somatic HIF2A gain-of-function mutations in paraganglioma with polycythemia". The New England Journal of ... May 2013). "New syndrome of paraganglioma and somatostatinoma associated with polycythemia". Journal of Clinical Oncology. 31 ( ... March 2013). "Novel HIF2A mutations disrupt oxygen sensing, leading to polycythemia, paragangliomas, and somatostatinomas". ... Polycythemia Duodenal somatostatinoma Retinal and choroidal vascular changes Paraganglioma/Pheochromocytoma Pheochromocytoma ...
Polycythemia vera is a rare blood cancer that affects the bone marrow and causes the body to make too many red blood cells, ... The definition of polycythemia vera has changed in recent years. Once considered a blood disorder only, polycythemia vera is ... You can also find patient information on polycythemia vera on the National Center for Advancing Translational Sciences website ... For more detailed information on polycythemia vera, the National Cancer Institute provides patient information on its Chronic ...
Find symptoms and other information about Polycythemia vera. ... Polycythemia vera is a condition characterized by an increased ... Polycythemia vera. Other Names: Acquired primary erythrocytosis; Osler-Vaquez disease; PV; Polycythemia rubra vera; Vaquez ... When Do Symptoms of Polycythemia vera Begin?. Symptoms of this disease may start to appear at any time in life.. The age ... About Polycythemia vera. Many rare diseases have limited information. Currently GARD aims to provide the following information ...
Polycythemia vera is a condition characterized by an increased number of red blood cells in the bloodstream. Explore symptoms, ... Individuals with polycythemia vera have an increased risk of deep vein thrombosis. (DVT), a type of blood clot that occurs in ... Mutations in the JAK2 and TET2 genes are associated with polycythemia vera. Although it remains unclear exactly what initiates ... In rare instances, polycythemia vera has been found to run in families. In some of these families, the risk of developing ...
Update - Polycythemia Vera Research in Pennsylvania-Schuylkill, Luzerne, and Carbon Counties (September 2012) Cdc-pdf. [PDF - ... Determination of accuracy of Polycythemia Vera diagnoses and use of the JAK2V617F test in the diagnostic scheme Cdc-pdf. [PDF ... Updated and expanded study of polycythemia vera and other myeloproliferative neoplasms in the tri-county area Cdc-pdf. [PDF - ... Fact sheet: Geographic study of polycythemia vera occurrence in central Pennsylvania (2001-2007) Cdc-pdf. [PDF - 105 KB] ...
Polycythemia can be caused by polycythemia vera, a type of blood cancer that results when bone marrow makes too many red blood ... Polycythemia can be caused by polycythemia vera, a type of blood cancer that results when bone marrow makes too many red blood ... Polycythemia can be caused by polycythemia vera, a type of blood cancer that results when bone marrow makes too many red blood ... There are two main causes of polycythemia, which determine each type.. *Primary polycythemia vera: Occurs due to a hereditary ...
Thirty-six patients with polycythemia vera were treated with hydroxyurea for 12 to 67 months. Nineteen patients were previously ... Therapeutic recommendations in polycythemia vera based on Polycythemia Vera Study Group protocols. Berk PD, Goldberg JD, ... Treatment of polycythemia vera with hydroxyurea R Sharon et al. Cancer. 1986. . ... Anesthesia for polycythemia vera. Sosis MB. Sosis MB. J Clin Anesth. 1990 Jan-Feb;2(1):31-4. doi: 10.1016/0952-8180(90)90046-6. ...
polycythaemia vera. Polycythaemia has gained the dubious distinction of being a haematological disorder with an inordinately ... Polycythaemia and chorea improved rapidly with venesections and follow up showed no recurrence of polycythaemia or neurological ... Laboratory investigations confirmed the diagnosis of polycythaemia according to current Polycythemia Vera Study Group ... Most cases of polycythaemia chorea have occurred in elderly women, usually with acute onset or sudden aggravation. In some ...
... and polycythemia vera (PV) are BCR-ABL1-negative myeloproliferative neoplasms associated with somatic hematopoietic stem cell ... Overcoming treatment challenges in myelofibrosis and polycythemia vera: the role of ruxolitinib Jeffrey C Bryan 1 , Srdan ... Overcoming treatment challenges in myelofibrosis and polycythemia vera: the role of ruxolitinib Jeffrey C Bryan et al. Cancer ... Mean change from baseline in EORTC-QLQ-C30 QoL and functioning scores at week 32 in patients with polycythemia vera in the ...
Polycythemia vera (PV) is a rare blood disease. The disease affects people of all ages, but its most common in adults who are ... Risk Factors of Polycythemia Vera. Polycythemia vera (PV) is a rare blood disease. The disease affects people of all ages, but ...
A New Syndrome of Paraganglioma and Somatostatinoma Associated with Polycythemia: Genetic and Other Findings ... A New Syndrome of Paraganglioma and Somatostatinoma Associated with Polycythemia: Clinical Findings (2) ... CC Grand Rounds: (1) A New Syndrome of Paraganglioma and Somatostatinoma Associated with Polycythemia: Clinical Findings (2) A ... CC Grand Rounds: (1) A New Syndrome of Paraganglioma and Somatostatinoma Associated with Polycythemia: Clinical Findings (2) A ...
Polycythemia vera (PV) is a type of blood cancer known as a myeloproliferative neoplasm. It involves the abnormal development ... Polycythemia vera (PV) is a type of blood cancer known as a myeloproliferative neoplasm. It involves the abnormal development ... Areas of active investigation aimed at improving the treatment of polycythemia vera include the following:. JAK inhibitors: ... 3 Hensley B, Geyer H, Mesa R. Polycythemia vera: current pharmacotherapy and future directions. Expert Opinion in ...
A publicly available article also appearing in PubMed about Secondary Polycythemia ... Chuvash Polycythemia (CP). This endemic and recessively inherited congenital polycythemia is named after the Chuvash people in ... Relative Polycythemia (Gaisbock Syndrome, Spurious, or Stress Erythrocytosis). Relative polycythemia is an elevated hematocrit ... Secondary polycythemia lacks specific management recommendations as opposed to polycythemia vera. Many of the recommendations ...
Polycythemia vera (PV) is a myeloproliferative neoplasm associated with increased thrombotic and cardiovascular risk, which are ... From efficacy to safety: a Polycythemia Vera Study Group report on hydroxyurea in patients with polycythemia vera. Semin ... PV, polycythemia vera. * ≥ 12 months. †Patients were followed up from the index date until the date of the earliest event: ... Polycythemia vera (PV) is a myeloproliferative neoplasm (MPN) [1] that affects , 140,000 patients in the United States [2]. In ...
Secondary Polycythemia. Whenever the tissues becomehypoxic because of too little oxygen in the breathed air, such as at high ... Polycythemia. Secondary Polycythemia. Whenever the tissues becomehypoxic because of too little oxygen in the breathed air, such ... Polycythemia Vera (Erythremia). In addition to thosepeople who have physiologic polycythemia, others have a pathological ... A common type of secondary polycythemia, called physiologic polycythemia, occurs in natives who live ataltitudes of 14,000 to ...
... is a type of Myeloproliferative Neoplasms. Subtypes of Polycythemia Vera include Polycythaemia Vera ... title Polycythemia Vera type cancerType mainType Myeloproliferative Neoplasms tissue Myeloid oncoTreeId PV parentOncoTreeId MPN ...
Polycythemia vera answers are found in the Diagnosaurus powered by Unbound Medicine. Available for iPhone, iPad, Android, and ... Zeiger, Roni F.. "Polycythemia Vera." Diagnosaurus, 4th ed., McGraw-Hill Education, 2015. Medicine Central, im.unboundmedicine. ... com/medicine/view/Diagnosaurus/114657/all/Polycythemia_vera. Zeiger RFR. Polycythemia vera. Diagnosaurus. McGraw-Hill Education ... https://im.unboundmedicine.com/medicine/view/Diagnosaurus/114657/all/Polycythemia_vera. Zeiger RFR. Polycythemia Vera [Internet ...
Extramedullary haematopoiesis presenting with cardiac tamponade in a patient with polycythaemia vera. ... Extramedullary haematopoiesis presenting with cardiac tamponade in a patient with polycythaemia vera. Together they form a ...
Polycythemia vera. Polycythemia vera (PV) is a type of blood condition that causes the body to produce too many red blood cells ... Polycythemia vera (PV). (n.d.).. https://www.mpnresearchfoundation.org/polycythemia-vera-pv/. ... https://www.lls.org/myeloproliferative-neoplasms/polycythemia-vera/signs-and-symptoms. *. Symptoms of lymphoma. (2021).. https ...
Ruxolitinib (Jakafi®) in the Treatment of Polycythemia Vera. by Joshua , Oct 7, 2021 , Patient Care, PQI ... This PQI will review appropriate patient identification and management of Polycythemia Vera (PV) with the use of ruxolitinib ...
Twice as many babies die each year from Twin-to-Transfusion Syndrome (TTTS) and Twin Anemia Polycythemia Sequence (TAPS) than ... Twin to Twin Transfusion Syndrome & Twin Anemia Polycythemia Sequence-Sharing Isnt Always Caring. ...
Polycythemia Vera Protocol. Take The Symptom Survey Circuplex (9). Ostrophin PMG (6). Spleen PMG (3). Vitanox (2). Bilberry ... Supplements can play a role in alleviating or eliminating the symptoms of Polycythemia Vera. Supplements aid the body in its ... own ability to address Polycythemia Vera. By unleashing the Forbidden Doctor within, our protocols give support to a body ...
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What is Polycythemia Vera? What is its relationship with Myelofibrosis? ... What Is Polycythemia Vera? Polycythemia vera causes your body to produce too many red blood cells. After years of this, your ... Is Polycythemia Vera a Form of Cancer? Polycythemia vera is a form of cancer of the blood. It causes your bone marrow to ... Polycythemia Vera and Myelofibrosis An uncommon condition like polycythemia vera (polly-sigh-THEE-me-ah-VAIR-Ah), often known ...
What Is Polycythemia Vera (PV)?. Polycythemia vera (PV) is a chronic, progressive myeloproliferative neoplasm (MPN) primarily ... The trigger for polycythemia vera (PV) and other myeloproliferative neoplasms (MPNs) isnt known. However, researchers have ... Common diagnostic tests for polycythemia vera include:. Blood Tests. A complete blood count can identify an increase in ... POLYCYTHEMIA VERA (PV). Learn how Kenny continues his cycling passion despite his PV diagnosis. ...
5.4 Polycythemia 5.5 Venous Thromboembolism (VTE) 5.6 Cardiovascular Risk 5.7 Abuse of Testosterone and Monitoring of Serum ... 5.4 Polycythemia Increases in hematocrit, reflective of increases in red blood cell mass, may require discontinuation of ... Blood and Lymphatic System Disorders: polycythemia, thrombocytopenia. Cardiac Disorders: angina pectoris, cardiac arrest, ...
The Agency for Toxic Substances and Disease Registry (ATSDR) will update community members on the polycythemia vera (PV) ... to update area residents on recent efforts regarding polycythemia vera (PV). ...
Polycythemia can be caused by a bone marrow disorder caused polycythemia vera or from other causes outside the bone marrow ... However, some patients have hemoglobin that is too high called polycythemia. ... called secondary polycythemia. Distinguishing between the two became much easier about ten years ... Polycythemia can be caused by a bone marrow disorder caused polycythemia vera or from other causes outside the bone marrow ...
Find information about polycythemia vera (PV) and Jakafi® (ruxolitinib), the first FDA-approved prescription medicine for ... POLYCYTHEMIA VERA. Discover Your Path to Possible. When it comes to moving your polycythemia vera (PV) treatment journey ... The most common side effects of Jakafi include: for certain types of myelofibrosis (MF) and polycythemia vera (PV) - low ... Jakafi is a prescription medicine used to treat adults with polycythemia vera who have already taken a medicine called ...
Are you an adult with polycythemia vera or thrombocytosis? This study aims to find a new treatment or cure for polycythemia ... To participate in this study, you must have polycythemia vera with elevated hemoglobin (higher than 18 in men and 16 in women) ...
Polycythemia vera. Somatic mutations in the TET2 gene are associated with polycythemia vera, a disorder characterized by ... Mutations in this gene have been found in approximately 16 percent of people with polycythemia vera. It is unclear what role ... TET2 mutations and their clinical correlates in polycythemia vera, essential thrombocythemia and myelofibrosis. Leukemia. 2009 ...
  • In some of these families, the risk of developing polycythemia vera appears to have an autosomal dominant pattern of inheritance . (medlineplus.gov)
  • Autosomal dominant inheritance means that one copy of an altered gene in each cell is sufficient to increase the risk of developing polycythemia vera, although the cause of this condition in familial cases is unknown. (medlineplus.gov)
  • Some people with polycythemia vera experience headaches, dizziness, ringing in the ears (tinnitus), impaired vision, or itchy skin. (medlineplus.gov)
  • Although mutations in the TET2 gene have been found in approximately 16 percent of people with polycythemia vera, it is unclear what role these mutations play in the development of the condition. (medlineplus.gov)
  • The arterial pressure is also normal in most people with polycythemia, although in about one third of them, the arterial pressure is elevated. (brainkart.com)
  • Chronic pulmonary disease (e.g., emphysema , which is abnormal distension of the lungs with air) and extreme obesity (which may severely impair pulmonary ventilation) result in absolute polycythemia (Pickwickian syndrome). (medicinenet.com)
  • Absolute polycythemia, however, is when the exact cause is known and is called erythrocytosis. (medicinenet.com)
  • On the other hand, the absolute polycythemia is characterized by absolute increase in the red blood cell mass circulating, as an outcome of a certain increase in the production of bone marrow. (meowlovers.com)
  • Relative and transient polycythemia go away when the underlying condition that has caused it is treated. (medicinenet.com)
  • The transient polycythemia is due to splenic contraction that injects concentrated red blood cells through the circulation in a brief reaction to epinephrine -a hormone that reacts to anger, fear, and stress. (meowlovers.com)
  • Secondary polycythemia is a rare disease that involves the overproduction of red blood cells. (statpearls.com)
  • This activity illustrates the evaluation and management of secondary polycythemia and highlights the role of the interprofessional team in improving care for patients with this condition. (statpearls.com)
  • Identify the pathophysiology of secondary polycythemia. (statpearls.com)
  • Describe the appropriate evaluation of secondary polycythemia. (statpearls.com)
  • Outline management options available for secondary polycythemia. (statpearls.com)
  • Summarize the importance of collaboration and communication amongst the interprofessional team to enhance care coordination for patients with secondary polycythemia. (statpearls.com)
  • An elevated erythropoietin (EPO) level, usually as a secondary response to chronic hypoxemia, leads to secondary polycythemia. (statpearls.com)
  • Secondary polycythemia is due to an increased level of EPO or other transcription factors that, in turn, lead to an increase in the production of RBC mass. (statpearls.com)
  • Polycythemia vera: This neoplastic disorder is the result of increased erythroid progenitor cells as well as increased sensitivity to erythropoietin secondary to a mutation called JAK mutation. (statpearls.com)
  • [1] Secondary polycythemia can also be classified as congenital or acquired depending upon when the individual developed the defect. (statpearls.com)
  • This condition is called secondary polycythemia, and the red cell count commonly rises to 6 to 7 million/mm 3 , about 30 per cent above normal. (brainkart.com)
  • A common type of secondary polycythemia, called physiologic polycythemia, occurs in natives who live ataltitudes of 14,000 to 17,000 feet, where the atmos-pheric oxygen is very low. (brainkart.com)
  • Polycythemia can be caused by a bone marrow disorder caused polycythemia vera or from other causes outside the bone marrow called secondary polycythemia. (gboncology.com)
  • Secondary polycythemia can be caused by conditions that cause low oxygen levels in the blood. (gboncology.com)
  • The best treatment for secondary polycythemia is treating the underlying condition such as smoking cessation or the treatment of the sleep apnea. (gboncology.com)
  • If none of the aforementioned secondary conditions is present, it's possible that the cause of the condition is polycythemia vera. (meowlovers.com)
  • Secondary erythrocytosis such as those related with renal tumors should be taken into consideration during the diagnosis of polycythemia vera. (biomedcentral.com)
  • Recent studies have demonstrated neutrophil overexpression of the polycythemia rubra vera-1 (PRV-1) gene in polycythemia vera (PV) but not in secondary or spurious polycythemia (SP). (uthscsa.edu)
  • Polycythemia (also called polyglobulia) is a disease in which the hematocrit level (volume of red blood cells) and hemoglobin concentration are raised in the peripheral blood. (medicinenet.com)
  • Polycythemia is considered when hematocrit levels are over 48% in women and 52% in men. (medicinenet.com)
  • Absolute or true erythrocytosis differentiates from relative polycythemia, where the hematocrit is increased, but the red cell mass lies within the normal range. (statpearls.com)
  • In addition to thosepeople who have physiologic polycythemia, others have a pathological condition known as polycythemiavera, in which the red blood cell count may be 7 to 8million/mm 3 and the hematocrit may be 60 to 70 per cent instead of the normal 40 to 45 per cent. (brainkart.com)
  • In polycythemia vera, not only does the hematocrit increase, but the total blood volume also increases, on some occasions to almost twice normal. (brainkart.com)
  • [ 49 ] It most often occurs in patients with an underlying thrombotic diathesis, including in those who are pregnant or who have a tumor, a chronic inflammatory disease, a clotting disorder, an infection, or a myeloproliferative disorder , such as polycythemia vera or paroxysmal nocturnal hemoglobinuria . (medscape.com)
  • What are the signs and symptoms of polycythemia? (medicinenet.com)
  • Symptoms of polycythemia occur gradually over time. (medicinenet.com)
  • Many of the signs and symptoms of polycythemia vera are related to a shortage of oxygen in body tissues. (medlineplus.gov)
  • Supplements can play a role in alleviating or eliminating the symptoms of Polycythemia Vera. (forbiddendoctor.com)
  • Click here if you would like to watch an overview video of the diagnosis, presenting symptoms, disease course, and treatment options of polycythemia vera for patients, their caregivers, and their loved ones created by Dr. Ruben A. Mesa and Dr. Robyn M. Scherber of UT Health San Antonio, MD Anderson Cancer Center. (mpnfoundation.org)
  • In this article we will discuss some more interesting facts about polycythemia in cats including the cause, symptoms, prognosis and treatment. (meowlovers.com)
  • Due to the fact that the red blood cells influence all the systems of the body of a cat, the symptoms of polycythemia may become seemingly noticeable and somewhat unrelated symptoms. (meowlovers.com)
  • The symptoms of polycythemia in cats may progress in a gradual manner and it might be hard to notice for several months. (meowlovers.com)
  • Hyperviscosity is the cause of clinical symptoms in infants presumed to be symptomatic from polycythemia. (mhmedical.com)
  • Half of these patients are symptomatic, although it is not at all certain whether their symptoms are caused by polycythemia. (mhmedical.com)
  • Polycythemia vera (PV) as a primary condition is a type of clonal disorder of bone marrow stem cells which is often caused by a mutation in exon 12 of the janus kinase 2 ( JAK2 ) tyrosine kinase gene [ 4 , 5 ]. (biomedcentral.com)
  • Polycythemia vera is a disease process resulting in excess production of blood cells and platelets in the bone marrow which actuates ischemic events in both the large and small vessels in the body. (fortunepublish.com)
  • Regarded as an irregular increase in the number of red blood cells in the circulatory system, the polycythemia is a fairly serious blood condition. (meowlovers.com)
  • Some diseases such as chronic myeloid leukemia (CML), chronic neutrophilic leukemia (CNL), and chronic eosinophilic leukemia (CEL) express primarily a myeloid phenotype, while in others such as polycythemia vera (PV), primary myelofibrosis (PMF), and essential thrombocytosis (ET), erythroid or megakaryocytic hyperplasia predominates. (mhmedical.com)
  • Philadelphia-negative myeloproliferative neoplasms (MPN) are frequent and chronic myeloid malignancies including Polycythemia Vera (PV), essential thrombocythemia (ET), Primary Myelofibrosis (PMF) and Prefibrotic myelofibrosis (PreMF). (clinicaltrials.gov)
  • Mutations in the JAK2 and TET2 genes are associated with polycythemia vera. (medlineplus.gov)
  • Changes in expression levels of erythrocyte and immune-related genes are associated with high altitude polycythemia. (bvsalud.org)
  • Jakafi is a prescription medicine used to treat adults with polycythemia vera who have already taken a medicine called hydroxyurea (HU) and it did not work well enough or they could not tolerate it. (jakafi.com)
  • The Agency for Toxic Substances and Disease Registry (ATSDR) will update community members on the polycythemia vera (PV) research projects in the tri-county area of Schuylkill, Luzerne, and Carbon Counties, PA on September 20, 2012 in Tamaqua, PA. (cdc.gov)
  • The federal Agency for Toxic Substances and Disease Registry (ATSDR) will hold a public meeting in the Tamaqua Area Auditorium at Tamaqua High School, 500 Penn St, Tamaqua, PA, on Saturday, October 24, 2009 from 10:00 to 11:30 a.m. to update area residents on recent efforts regarding polycythemia vera (PV). (cdc.gov)
  • If you leave this without any diagnosis and treatment, polycythemia may lead to austere coronary signs, even heart failure. (meowlovers.com)
  • Treatment of polycythemia vera is removal of the extra blood in a process called phlebotomy. (gboncology.com)
  • Congenital heart disorders, enzymatic or hemoglobin abnormality, excessive use of coal tar derivatives, and tumors can also cause polycythemia. (medicinenet.com)
  • Twice as many babies die each year from Twin-to-Transfusion Syndrome (TTTS) and Twin Anemia Polycythemia Sequence (TAPS) than from Sudden Infant Death Syndrome (SIDS). (arizona.edu)
  • The trigger for polycythemia vera (PV) and other myeloproliferative neoplasms (MPNs) isn't known. (mpnfoundation.org)
  • Polycythemia vera typically develops in adulthood, around age 60, although in rare cases it occurs in children and young adults. (medlineplus.gov)
  • Polycythemia occurs in 2-4% of the general newborn population. (mhmedical.com)
  • Hyperviscosity without polycythemia occurs in 1% of normal (nonpolycythemic) newborns. (mhmedical.com)
  • Actually, the cardiac output in polycythemia is not far from normal, because these two factors more or less neutralize each other. (brainkart.com)
  • In most cases, polycythemia is not innate (passed down through generations), yet it is genetic in a few cases. (medicinenet.com)
  • Changes in the TET2 gene are also found in polycythemia cells. (medicinenet.com)
  • Typically, all individuals diagnosed with polycythemia have a mutated JAK2 gene. (medicinenet.com)
  • JAK2 gene mutations seem to be particularly important for the development of polycythemia vera, as nearly all affected individuals have a mutation in this gene. (medlineplus.gov)
  • Written by Neal Dave, PharmD, Texas Oncology Download Here Description: This PQI will review appropriate patient identification and management of Polycythemia Vera (PV) with the use of ruxolitinib therapy. (ncoda.org)
  • Patients with polycythemia may have other blood disorders as well. (medicinenet.com)
  • However, some patients have hemoglobin that is too high called polycythemia. (gboncology.com)
  • Polycythemia is considered when hemoglobin levels are over 16.5 grams/dL in women and 18.5 grams/dL in men. (medicinenet.com)
  • Other complications of polycythemia vera include an enlarged spleen (splenomegaly), stomach ulcers, gout (a form of arthritis caused by a buildup of uric acid in the joints), heart disease, and cancer of blood-forming cells (leukemia). (medlineplus.gov)
  • In these families, people seem to inherit an increased risk of polycythemia vera, not the disease itself. (medlineplus.gov)
  • Polycythemia vera (PV) is a rare blood disease. (hoacny.com)
  • We present an unusual case of a female with polycythemia vera who was diagnosed with ischemic gangrene in her extremities as a result of diabetic ketoacidosis, despite having only mildly elevated blood counts from her underlying disease. (fortunepublish.com)
  • Because of a history of polycythemia vera, the patient had been treated for the condition for 9 years. (biomedcentral.com)
  • A 71-year-old man with polycythemia vera who was in the same ward as the index case-patient for 6 days acquired infection with H7N9 and pH1N1 viruses. (cdc.gov)
  • In rare cases, neonatal polycythemia may occur due to the transfusion of placental blood to the baby or chronic oxygen insufficiency of the fetus (intrauterine hypoxia ) due to placental inadequacy. (medicinenet.com)
  • Further, she cause of this main form of polycythemia in cats isn't understood well, even up to this moment. (meowlovers.com)
  • Polycythemia is the result of increased demand for oxygen in the body. (medicinenet.com)
  • Polycythemia vera is a condition characterized by an increased number of red blood cells in the bloodstream. (medlineplus.gov)
  • Polycythemia, derived from poly (many) and cythemia (cells in the blood), is a condition defined as an abnormal increase in the red blood cell (RBC) mass. (statpearls.com)
  • The second one, the cause of the condition seen by the vet might be addressed, or in an instance of polycythemia vera, preventive treatment might be recommended. (meowlovers.com)
  • Relative polycythemia may be the result of abnormally high fluid intake or excessive loss of body fluid, for example, severe vomiting , diarrhea , or non-stop sweating . (medicinenet.com)
  • The relative polycythemia may develop when a reduction in the plasma volume, commonly due to dehydration, may produce a fair increase in the red blood cells circulating. (meowlovers.com)
  • The treatment for polycythemia in cats may progress in two stages. (meowlovers.com)
  • As a chronic mountain sickness (CMS) with the highest incidence and the greatest harm, the pathogenesis of high altitude polycythemia (HAPC) is still not fully understood. (bvsalud.org)
  • What are treatment options for polycythemia? (medicinenet.com)
  • We will review the various treatment options currently available for polycythemia vera. (fortunepublish.com)
  • In rare instances, polycythemia vera has been found to run in families. (medlineplus.gov)
  • A high concentration of red blood cells indicates polycythemia. (medicinenet.com)
  • Polycythemia vera (PV) is a chronic, progressive myeloproliferative neoplasm (MPN) primarily characterized by an elevation of the red blood cells. (mpnfoundation.org)
  • In medical terms, the overproduction of red blood cells in cats is known as polycythemia. (meowlovers.com)
  • The first one, red blood cells may be removed directly from the bloodstream of the cat to treat the acute polycythemia. (meowlovers.com)
  • Supplements aid the body in its own ability to address Polycythemia Vera. (forbiddendoctor.com)
  • Also, the urine sample is commonly used in order to ascertain whether the polycythemia has started to affect the other organ systems or in ruling out some other diagnoses. (meowlovers.com)
  • Clinical and hematological presentation of children and adolescents with polycythemia vera. (medlineplus.gov)
  • Medicine Central , im.unboundmedicine.com/medicine/view/Diagnosaurus/114657/all/Polycythemia_vera. (unboundmedicine.com)