Leukostasis
Blood-Retinal Barrier
Diabetic Retinopathy
Acridine Orange
Cellophane
Sulfinpyrazone
Capillary Permeability
Intercellular Adhesion Molecule-1
Diabetes Mellitus, Experimental
Use of genetically manipulated strains of Clostridium perfringens reveals that both alpha-toxin and theta-toxin are required for vascular leukostasis to occur in experimental gas gangrene. (1/48)
A hallmark of gas gangrene (clostridial myonecrosis) pathology is a paucity of leukocytes infiltrating the necrotic tissue. The cause of this paucity most likely relates to the observation of leukocyte aggregates at the border of the area of tissue necrosis, often within the microvasculature itself. Infecting mice with genetically manipulated strains of Clostridium perfringens type A (deficient in either alpha-toxin or theta-toxin production) resulted in significantly reduced leukocyte aggregation when alpha-toxin was absent and complete abrogation of leukocyte aggregation when theta-toxin was absent. Thus, both alpha-toxin and theta-toxin are necessary for the characteristic vascular leukostasis observed in clostridial myonecrosis. (+info)Prevention of leukostasis and vascular leakage in streptozotocin-induced diabetic retinopathy via intercellular adhesion molecule-1 inhibition. (2/48)
Diabetic retinopathy is a leading cause of adult vision loss and blindness. Much of the retinal damage that characterizes the disease results from retinal vascular leakage and nonperfusion. This study shows that diabetic retinal vascular leakage and nonperfusion are temporally and spatially associated with retinal leukocyte stasis (leukostasis) in the rat model of streptozotocin-induced diabetes. Retinal leukostasis increases within days of developing diabetes and correlates with the increased expression of retinal intercellular adhesion molecule-1 (ICAM-1). ICAM-1 blockade with a mAb prevents diabetic retinal leukostasis and vascular leakage by 48.5% and 85.6%, respectively. These data identify the causal role of leukocytes in the pathogenesis of diabetic retinopathy and establish the potential utility of ICAM-1 inhibition as a therapeutic strategy for the prevention of diabetic retinopathy. (+info)Tumor necrosis factor induces tumor necrosis via tumor necrosis factor receptor type 1-expressing endothelial cells of the tumor vasculature. (3/48)
Activation of endothelial cells, fibrin deposition, and coagulation within the tumor vasculature has been shown in vivo to correlate with the occurrence of tumor necrosis factor (TNF)-induced tumor necrosis in mice. In the present study we investigated which target cells mediate the TNF-induced necrosis in fibrosarcomas grown in wild type (wt), TNF receptor type 1-deficient (TNFRp55-/-), and TNF receptor type 2-deficient (TNFRp75-/-) mice. TNF administration resulted in tumor necrosis exclusively in wt and TNFRp75-/-, but not in TNFRp55-/- mice, indicating a dependence of TNF-mediated tumor necrosis on the expression of TNF receptor type 1. However, using wt and TNFRp55-/- fibrosarcomas in wt mice, we found that TNF-mediated tumor necrosis was completely independent of TNF receptor type 1 expression in tumor cells. Thus we could exclude any direct tumoricidal effect of TNF in this model. Soluble TNF induced leukostasis in wt and TNFRp75-/- mice but not in TNFRp55-/- mice. TNF-induced leukostasis in TNFRp55-/- mice was restored by adoptive bone marrow transplantation of wt hematopoietic cells, but TNF failed to induce tumor necrosis in these chimeric mice. Because TNF administration resulted in both activation and focal damage of tumor endothelium, TNF receptor type 1-expressing cells of the tumor vasculature, likely to be endothelial cells, appear to be target cells for mediating TNF-induced tumor necrosis. (+info)Vascular endothelial growth factor (VEGF)-induced retinal vascular permeability is mediated by intercellular adhesion molecule-1 (ICAM-1). (4/48)
Two prominent vascular endothelial growth factor (VEGF)-induced retinal effects are vascular permeability and capillary nonperfusion. The mechanisms by which these effects occur are not completely known. Using a rat model, we show that intravitreous injections of VEGF precipitate an extensive retinal leukocyte stasis (leukostasis) that coincides with enhanced vascular permeability and capillary nonperfusion. The leukostasis is accompanied by the up-regulation of intercellular adhesion molecule-1 expression in the retina. The inhibition of intercellular adhesion molecule-1 bioactivity with a neutralizing antibody prevents the permeability and leukostasis increases by 79% and 54%, respectively. These data are the first to demonstrate that a nonendothelial cell type contributes to VEGF-induced vascular permeability. Additionally, they identify a potential mechanism for VEGF-induced retinal capillary nonperfusion. (+info)Endothelial cell activation by myeloblasts: molecular mechanisms of leukostasis and leukemic cell dissemination. (5/48)
Leukostasis and tissue infiltration by leukemic cells are poorly understood life-threatening complications of acute leukemia. This study has tested the hypothesis that adhesion receptors and cytokines secreted by blast cells play central roles in these reactions. Immunophenotypic studies showed that acute myeloid leukemia (AML) cells (n = 78) of the M0 to M5 subtypes of the French-American-British Cooperative Group expressed various amounts of adhesion receptors, including CD11a, b, c/CD18, CD49d, e, f/CD29, CD54, sCD15, and L-selectin. The presence of functional adhesion receptors was evaluated using a nonstatic adhesion assay. The number of blast cells attached to unactivated endothelium increased by 7 to 31 times after a 6-hour exposure of endothelium to tumor necrosis factor (TNF)-alpha. Inhibition studies showed that multiple adhesion receptors--including L-selectin, E-selectin, VCAM-1, and CD11/CD18--were involved in blast cell adhesion to TNF-alpha-activated endothelium. Leukemic cells were then cocultured at 37 degrees C on unactivated endothelial cell monolayers for time periods up to 24 hours. A time-dependent increase in the number of blasts attached to the endothelium and a concomitant induction of ICAM-1, VCAM-1, and E-selectin were observed. Additional experiments revealed that endothelial cell activation by leukemic myeloblasts was caused by cytokine secretion by blast cells, in particular TNF-alpha and IL-1 beta, and direct contacts between adhesion receptors expressed by blast cells and endothelial cells. Thus, leukemic cells have the ability to generate conditions that promote their own adhesion to vascular endothelium, a property that may have important implications for the pathophysiology of leukostasis and tissue infiltration by leukemic blast cells. (Blood. 2001;97:2121-2129) (+info)Characterization of retinal leukostasis and hemodynamics in insulin resistance and diabetes: role of oxidants and protein kinase-C activation. (6/48)
Increases in leukostasis/monocyte adhesion to the capillary endothelium (leukostasis) and decreases in retinal blood flow may be causally associated and are implicated in the pathogenesis of diabetic retinopathy. In this study, we demonstrate that increases in leukostasis are observed in insulin-resistant states without diabetes, whereas decreases in retinal blood flow require diabetes and hyperglycemia. Microimpaction studies using beads mimicking retinal capillary obstruction by leukocytes did not affect retinal blood flow. In diabetic rats, treatment with the antioxidant alpha-lipoic acid normalized the amount of leukostasis but not retinal blood flow. In contrast, treatment with D-alpha-tocopherol and protein kinase-C beta-isoform inhibition (LY333531) prevented the increases in leukostasis and decreases in retinal blood flow in diabetic rats. Serum hydroxyperoxide, a marker of oxidative stress, was increased in diabetic rats, but normalized by treatment with antioxidants alpha-lipoic acid and D-alpha-tocopherol and, surprisingly, PKC beta-isoform inhibition. These findings suggest that leukostasis is associated with endothelial dysfunction, insulin resistance, and oxidative stress but is not related to retinal blood flow and is not sufficient to cause diabetic-like retinopathy. Moreover, treatment with PKC beta inhibition is effective to normalize diabetes or hyperglycemia-induced PKC beta-isoform activation and oxidative stress. (+info)VEGF164 is proinflammatory in the diabetic retina. (7/48)
PURPOSE: The objectives of this study were to characterize the differential potency of two major VEGF isoforms, VEGF(120) and VEGF(164), for inducing leukocyte stasis (leukostasis) within the retinal vasculature and blood-retinal barrier (BRB) breakdown and to determine whether endogenous VEGF(164) mediates retinal leukostasis and BRB breakdown in early and established diabetes. METHODS: Retinal leukostasis and BRB breakdown were simultaneously quantified by combining concanavalin A lectin (ConA) perfusion labeling with a fluorophotometric dextran leakage assay. CD45 immunohistochemistry was performed to confirm that ConA-stained cells within the vasculature were leukocytes. Retinal leukostasis and BRB breakdown were compared in nondiabetic rats receiving intravitreous injections of VEGF(120) or VEGF(164). Retinal intercellular adhesion molecule (ICAM)-1 and VEGF protein levels were studied by Western blot and ELISA, respectively. An anti-VEGF(164(165)) aptamer (EYE001) was administered by intravitreous injection to 2-week and 3-month diabetic rats, and the effect on retinal leukostasis and BRB breakdown was quantified. RESULTS: Compared with VEGF(120), VEGF(164) more potently increased retinal ICAM-1 levels (2.2-fold), leukostasis (1.9-fold), and BRB breakdown (2.1-fold, P < 0.01 for all), despite negligible differences in vitreoretinal VEGF levels at the time of evaluation (P > 0.05). Retinal leukostasis and leakage increased with the duration of diabetes (P < 0.01) and correlated closely (P < 0.01, r = 0.889). The isoform-specific blockade of endogenous VEGF(164) with EYE001 resulted in a significant suppression of retinal leukostasis and BRB breakdown in both early (72.4% and 82.6%, respectively) and established (48.5% and 55.0%, respectively) diabetes (P < 0.01). CONCLUSIONS: On an equimolar basis, VEGF(164) is at least twice as potent as VEGF(120) at inducing ICAM-1-mediated retinal leukostasis and BRB breakdown in vivo. The inhibition of diabetic retinal leukostasis and BRB breakdown with EYE001 in early and established diabetes indicates that VEGF(164) is an important isoform in the pathogenesis of early diabetic retinopathy. (+info)Case report: mantle cell lymphoma, prolymphocytoid variant, with leukostasis syndrome. (8/48)
A 76-year-old man presented with leukostasis syndrome, including oculodynia, blurred vision, and visual field defects, due to mantle cell lymphoma, prolymphocytoid variant, with marked leukocytosis, 1227 x 10(9)/l. He had splenomegaly but no lymphadenopathy or hepatomegaly. The tumor cells were CD5+, CD19+, CD20+, FMC-7+, and kappa light chain restricted. Immunohistochemistry showed expression of p53 and of cyclin D1. Fluorescent in situ hybridization demonstrated t(11;14) with translocation between CYCLIN D1 and the immunoglobulin heavy-chain genes. The patient received leukapheresis and aggressive chemotherapy, but the leukocyte count remained above 100 x 10(9)/l. The patient's condition rapidly deteriorated with lymphomatous infiltration of his lungs and soft tissues, and he expired 6 months after diagnosis. While it is known that mantle cell lymphoma may have a leukemic phase, the degree of leukocytosis in this case exceeds that previously reported in the literature and resulted in a clinical syndrome of leukostasis. (+info)Leukostasis is not a formal medical diagnosis, but rather a complication that can occur in certain medical conditions. It's often used in the context of leukemia, where there is a rapid accumulation of white blood cells (leukocytes) in the small blood vessels, leading to impaired circulation, particularly in the lungs and brain. This can result in symptoms such as shortness of breath, cough, chest pain, headache, altered mental status, or even stroke. It's a medical emergency that requires immediate treatment, often involving leukopheresis (a procedure to remove white blood cells from the blood) and chemotherapy.
The blood-retinal barrier (BRB) is a specialized physiological barrier in the eye that helps regulate the movement of molecules between the retina and the bloodstream. It is made up of tight junctions between the endothelial cells of retinal blood vessels and between the pigment epithelium cells of the retina, which restrict the paracellular diffusion of solutes.
The BRB plays a crucial role in maintaining the health and function of the retina by preventing harmful substances from entering the retina while allowing essential nutrients and oxygen to reach the retinal tissues. Disruption of the BRB has been implicated in various retinal diseases, including diabetic retinopathy, age-related macular degeneration, and retinal vein occlusion.
Retinal vessels refer to the blood vessels that are located in the retina, which is the light-sensitive tissue that lines the inner surface of the eye. The retina contains two types of blood vessels: arteries and veins.
The central retinal artery supplies oxygenated blood to the inner layers of the retina, while the central retinal vein drains deoxygenated blood from the retina. These vessels can be visualized during a routine eye examination using an ophthalmoscope, which allows healthcare professionals to assess their health and any potential abnormalities.
Retinal vessels are essential for maintaining the health and function of the retina, and any damage or changes to these vessels can affect vision and lead to various eye conditions such as diabetic retinopathy, retinal vein occlusion, and hypertensive retinopathy.
Diabetic retinopathy is a diabetes complication that affects the eyes. It's caused by damage to the blood vessels of the light-sensitive tissue at the back of the eye (retina).
At first, diabetic retinopathy may cause no symptoms or only mild vision problems. Eventually, it can cause blindness. The condition usually affects both eyes.
There are two main stages of diabetic retinopathy:
1. Early diabetic retinopathy. This is when the blood vessels in the eye start to leak fluid or bleed. You might not notice any changes in your vision at this stage, but it's still important to get treatment because it can prevent the condition from getting worse.
2. Advanced diabetic retinopathy. This is when new, abnormal blood vessels grow on the surface of the retina. These vessels can leak fluid and cause severe vision problems, including blindness.
Diabetic retinopathy can be treated with laser surgery, injections of medication into the eye, or a vitrectomy (a surgical procedure to remove the gel-like substance that fills the center of the eye). It's important to get regular eye exams to detect diabetic retinopathy early and get treatment before it causes serious vision problems.
Leukocytosis is a condition characterized by an increased number of leukocytes (white blood cells) in the peripheral blood. A normal white blood cell count ranges from 4,500 to 11,000 cells per microliter of blood in adults. Leukocytosis is typically considered present when the white blood cell count exceeds 11,000 cells/µL. However, the definition might vary slightly depending on the laboratory and clinical context.
Leukocytosis can be a response to various underlying conditions, including bacterial or viral infections, inflammation, tissue damage, leukemia, and other hematological disorders. It is essential to investigate the cause of leukocytosis through further diagnostic tests, such as blood smears, differential counts, and additional laboratory and imaging studies, to guide appropriate treatment.
Acridine Orange is a fluorescent dye commonly used in various scientific applications, particularly in the field of cytology and microbiology. Its chemical formula is C17H19N3O.
In medical terms, Acridine Orange is often used as a supravital stain to differentiate between live and dead cells or to identify bacteria, fungi, and other microorganisms in samples. It can also be used to detect abnormalities in DNA and RNA, making it useful in the identification of certain types of cancerous cells.
When exposed to ultraviolet light, Acridine Orange exhibits a green fluorescence when bound to double-stranded DNA and a red or orange-red fluorescence when bound to single-stranded RNA. This property makes it a valuable tool in the study of cell division, gene expression, and other biological processes that involve nucleic acids.
However, it is important to note that Acridine Orange can be toxic to living cells in high concentrations or with prolonged exposure, so it must be used carefully and in accordance with established safety protocols.
"Cellophane" is not a medical term. It is a type of thin, transparent sheet material made from regenerated cellulose, which is often used for packaging or wrapping purposes in various industries including food and medical. However, it does not have a specific medical definition.
Sulfinpyrazone is a medication that belongs to the class of drugs known as uricosurics. It works by increasing the amount of uric acid that is removed from the body through urine, which helps to lower the levels of uric acid in the blood. This makes it useful for the treatment of conditions such as gout and kidney stones that are caused by high levels of uric acid.
In addition to its uricosuric effects, sulfinpyrazone also has antiplatelet properties, which means that it can help to prevent blood clots from forming. This makes it useful for the prevention of heart attacks and strokes in people who are at risk.
Sulfinpyrazone is available by prescription and is typically taken by mouth in the form of tablets. It may be used alone or in combination with other medications, depending on the individual patient's needs and medical condition. As with any medication, sulfinpyrazone should be used under the supervision of a healthcare provider, and patients should follow their provider's instructions carefully to ensure safe and effective use.
Capillary permeability refers to the ability of substances to pass through the walls of capillaries, which are the smallest blood vessels in the body. These tiny vessels connect the arterioles and venules, allowing for the exchange of nutrients, waste products, and gases between the blood and the surrounding tissues.
The capillary wall is composed of a single layer of endothelial cells that are held together by tight junctions. The permeability of these walls varies depending on the size and charge of the molecules attempting to pass through. Small, uncharged molecules such as water, oxygen, and carbon dioxide can easily diffuse through the capillary wall, while larger or charged molecules such as proteins and large ions have more difficulty passing through.
Increased capillary permeability can occur in response to inflammation, infection, or injury, allowing larger molecules and immune cells to enter the surrounding tissues. This can lead to swelling (edema) and tissue damage if not controlled. Decreased capillary permeability, on the other hand, can lead to impaired nutrient exchange and tissue hypoxia.
Overall, the permeability of capillaries is a critical factor in maintaining the health and function of tissues throughout the body.
Intercellular Adhesion Molecule-1 (ICAM-1), also known as CD54, is a transmembrane glycoprotein expressed on the surface of various cell types including endothelial cells, fibroblasts, and immune cells. ICAM-1 plays a crucial role in the inflammatory response and the immune system by mediating the adhesion of leukocytes (white blood cells) to the endothelium, allowing them to migrate into surrounding tissues during an immune response or inflammation.
ICAM-1 contains five immunoglobulin-like domains in its extracellular region and binds to several integrins present on leukocytes, such as LFA-1 (lymphocyte function-associated antigen 1) and Mac-1 (macrophage-1 antigen). This interaction facilitates the firm adhesion of leukocytes to the endothelium, which is a critical step in the extravasation process.
In addition to its role in inflammation and immunity, ICAM-1 has been implicated in several pathological conditions, including atherosclerosis, cancer, and autoimmune diseases. Increased expression of ICAM-1 on endothelial cells is associated with the recruitment of immune cells to sites of injury or infection, making it an important target for therapeutic interventions in various inflammatory disorders.
I couldn't find a medical definition specifically for "Diabetes Mellitus, Experimental." However, I can provide you with information about experimental diabetes research and its relevance to understanding the disease.
Experimental diabetes models are used in biomedical research to study the pathophysiology of diabetes mellitus and to test potential therapies or treatments. These models can be broadly categorized into two types: chemically-induced and genetically modified.
1. Chemically-induced diabetes models: These involve administering chemicals, such as alloxan or streptozotocin, to animals (commonly mice or rats) to destroy their pancreatic β-cells, which produce insulin. This results in hyperglycemia and symptoms similar to those seen in type 1 diabetes in humans.
2. Genetically modified diabetes models: These involve altering the genes of animals (commonly mice) to create a diabetes phenotype. Examples include non-obese diabetic (NOD) mice, which develop an autoimmune form of diabetes similar to human type 1 diabetes, and various strains of obese mice with insulin resistance, such as ob/ob or db/db mice, which model aspects of type 2 diabetes.
These experimental models help researchers better understand the mechanisms behind diabetes development and progression, identify new therapeutic targets, and test potential treatments before moving on to human clinical trials. However, it's essential to recognize that these models may not fully replicate all aspects of human diabetes, so findings from animal studies should be interpreted with caution.
Leukocytes, also known as white blood cells (WBCs), are a crucial component of the human immune system. They are responsible for protecting the body against infections and foreign substances. Leukocytes are produced in the bone marrow and circulate throughout the body in the bloodstream and lymphatic system.
There are several types of leukocytes, including:
1. Neutrophils - These are the most abundant type of leukocyte and are primarily responsible for fighting bacterial infections. They contain enzymes that can destroy bacteria.
2. Lymphocytes - These are responsible for producing antibodies and destroying virus-infected cells, as well as cancer cells. There are two main types of lymphocytes: B-lymphocytes and T-lymphocytes.
3. Monocytes - These are the largest type of leukocyte and help to break down and remove dead or damaged tissues, as well as microorganisms.
4. Eosinophils - These play a role in fighting parasitic infections and are also involved in allergic reactions and inflammation.
5. Basophils - These release histamine and other chemicals that cause inflammation in response to allergens or irritants.
An abnormal increase or decrease in the number of leukocytes can indicate an underlying medical condition, such as an infection, inflammation, or a blood disorder.
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Pulmonary leukostasis5
- Reversal of hemodialysis granulocytopenia and pulmonary leukostasis. (umn.edu)
- The C5a(desarg) so produced can induce reversible granylocyte aggregation in vitro and in vivo, and we hypothesized that the pulmonary leukostasis responsible for the granulocytopenia results from embolization of aggregates formed under the influence of C5a(desarg) produced in the dialyzer. (umn.edu)
- Dive into the research topics of 'Reversal of hemodialysis granulocytopenia and pulmonary leukostasis. (umn.edu)
- Major complications associated with therapeutic leukapheresis procedures include pulmonary leukostasis, acute renal failure, and sometimes even death. (marketsandmarkets.com)
- They are caused by pulmonary leukostasis secondary to complement activation by the dialysis membrane. (revistanefrologia.com)
Acute myeloid2
- Leukostasis (also called symptomatic hyperleukocytosis) is a medical emergency most commonly seen in patients with acute myeloid leukemia. (wikipedia.org)
- Leukostasis is associated with people who have bone and blood disorders and is very common among people with acute myeloid leukemia or chronic myeloid leukemia. (wikipedia.org)
Hyperleukocytosis3
- Symptomatic Hyperleukocytosis (Leukostasis) is defined by a tremendously high blast cell count along with symptoms of decreased tissue perfusion. (wikipedia.org)
- The mechanism in which hyperleukocytosis or leukostasis manifests and disrupts homeostasis is greatly associated with leukemia's but multiple other factors may cause leukocytosis. (wikipedia.org)
- Hyperleukocytosis can result in leukostasis leading to end organ dysfunction, spontaneous tumor lysis syndrome (TLS) and disseminated intravascular coagulopathy (DIC). (oncicu.com)
Retinal3
- Diabetes related retinal changes, including leukostasis, acellular capilliaries, and microglial activation were assessed at different stages of disease. (qub.ac.uk)
- Although blood glucose levels and Hbac-1 were comparable between LysMCre-SOCS3fl/fl and WT mice after STZ injection, the LysMCreSOCS3 fl/fl diabetic mice developed severe retinal vasculopathy, including increased leukostasis and microglial activation at one month and enhanced acellular capillary formation at 6 months after diabetes induction. (qub.ac.uk)
- Additional VEGF functions under study include retinal leukostasis and neuroprotection. (retinavitreousjournal.com)
100,0001
- Symptoms of leukostasis start when blood levels of leukocytes reach over 100 x 10^9 / L (100,000 / microL). (wikipedia.org)
Blast2
- Increased blood viscosity due to large leukemic blast populations which are less deformable than mature leukocytes may lead to leukostasis. (wikipedia.org)
- The accumulation of less malleable blast products in the bloodstream accumulate within the microcirculation causing an accumulation of blockages leading to leukostasis. (wikipedia.org)
Secondary1
- It can present with a variety of symptoms secondary to leukostasis, a syndrome caused by the sludging of circulating leukemic blasts in the microvasculature. (symptoma.com)
Diagnosis1
- Leukostasis is a pathologic diagnosis that inhibits efficient flow to the microvasculature of the body. (wikipedia.org)
Hemodialysis1
- These studies suggest that C5a(desarg) is indeed generated by the dialyzer throughout hemodialysis and that the transience of the leukostasis and granulocytopenia is due to selective down-regulation of cellular responses to C5a(desarg) - a phenomenon that hitherto has been described only in vitro and that may be important in limiting the deleterious effects of adherent granulocytes on the endothelium in patients with intravascular complement activation. (umn.edu)
Organs1
- When a patient has symptomatic leukocytosis, specifically caused by a form of leukemia, it is common to find leukostasis in all their organs. (wikipedia.org)
Medical emergency3
- Continued and untreated leukostasis presents respiratory and neurological distress simultaneously and is a medical emergency, with untreated patient mortality rates reaching a minimum of 20 and a maximum of 40 percent. (wikipedia.org)
- This may cause a rare medical emergency called leukostasis. (medicalnewstoday.com)
- Leukostasis is rare but is a medical emergency that needs to be treated urgently. (news-medical.net)
Result2
- The pathophysiology of leukostasis is not well understood, but inadequate delivery of oxygen to the body's cells is the result. (wikipedia.org)
- White blood cell levels in hematopoietic cells, such as persistent leukaemias, may be high enough to result in leukostasis. (giikorea.co.kr)
Normal1
- Los individuos heterocigotos son sanos y tienen una función normal de los granulocitos en tanto que los homocigotos presentan ocasionalmente anomalías esqueléticas, retraso del desarrollo y convulsiones. (bvsalud.org)
Acute6
- Leukostasis is associated with people who have bone and blood disorders and is very common among people with acute myeloid leukemia or chronic myeloid leukemia. (wikipedia.org)
- Early deaths due to hemorrhage and leukostasis in childhood acute myelogenous leukemia. (nih.gov)
- Leukostasis is generally a risk of acute myeloid leukemia, however it can happen in chronic leukemia too. (shyamhemoncclinic.com)
- 18. Leukapheresis Does Not Improve Early Survival Outcome of Acute Myeloid Leukemia with Leukostasis Patients - A Dual-Center Retrospective Cohort Study. (nih.gov)
- Catastrophic basilar artery leukostasis in the setting of acute myeloid leukemia. (yalemedicine.org)
- Hematologic emergency leukostasis hyperviscosity syndrome thrombotic thrombocytopenic purpura acute hemolytic transfusion reaction cord compression 4. (web.app)
Retinal microvascular1
- Intravitreal injection of Ele can significantly reduce retinal microvascular leakage, leukostasis, and expression of ICAM-1, TNF-α in diabetic rats and inhibits oxygen-induced retinal neovascularization and VEGFR2 phosphorylation in OIR mice. (bvsalud.org)
Symptomatic3
- When a patient has symptomatic leukocytosis, specifically caused by a form of leukemia, it is common to find leukostasis in all their organs. (wikipedia.org)
- 17. Comparing leukapheresis protocols for an AML patient with symptomatic leukostasis. (nih.gov)
- No molecular marker was significantly associated with presence or absence of leukostasis symptoms due to small sample size, though there was a trend for increased NPM1-mutated and NPM1 + FLT3-mutated AML in asymptomatic patients and a greater proportion of symptomatic patients who were negative for all assessed molecular alterations. (bvsalud.org)
Priapism1
- Priapism may be due to leukostasis associated with greatly exaggerated blood leukocyte count as low flow (ischemic) or high flow (non ischemic) type. (ajphs.com)
Symptoms3
- Symptoms of leukostasis start when blood levels of leukocytes reach over 100 x 10^9 / L (100,000 / microL). (wikipedia.org)
- 20. How we approach a patient with symptoms of leukostasis requiring emergent leukocytapheresis. (nih.gov)
- To clarify the role of leukapheresis in the setting of hyperleukocytotic AML, we aimed to find associations between AML morphologic subtypes and molecular alterations on presence or absence of leukostasis symptoms (and hence therapeutic vs prophylactic leukapheresis) and clinical outcomes in the cohort of 41 patients at our single center who underwent leukapheresis for hyperleukocytotic AML. (bvsalud.org)
Transfusion1
- 12. Exchange Transfusion and Leukapheresis in Pediatric Patients with AML With High Risk of Early Death by Bleeding and Leukostasis. (nih.gov)
Leukemic1
- Increased blood viscosity due to large leukemic blast populations which are less deformable than mature leukocytes may lead to leukostasis. (wikipedia.org)
Leukocytes1
- Leukostasis of both monocytes and neutrophils increased with diabetes in the retina, however, transmigration of these cells into the neural retina was not observed, suggesting leukocytes kill endothelial cells from within the vasculature. (arvojournals.org)
Mechanism1
- Since the early reports by Schmidt-Schönbein, leukostasis has evolved as a mechanism by which activated bone marrow-derived cells may damage retinal capillary endothelial cells. (medscape.com)
Blood1
- Upon injection into syngeneic recipients, APL luc cells rapidly migrated to the BM followed by egress to the spleen then to the peripheral blood with death due to leukostasis by day 15. (wustl.edu)
Diseases1
- Similar to other diseases, there is no absolute number above which leukostasis happens. (shyamhemoncclinic.com)
Reduce2
- Once admitted, treatment for LEUKOSTASIS includes intravenous hydration, medicines to reduce wbc count quickly (such as hydroxyrea, ara-c), and if available APHERESIS , other supportive care. (shyamhemoncclinic.com)
- Whereas VEGF inhibitors act to reduce excess vascular permeability by acting only on VEGF, corticosteroids act on several pathways involved in the pathogenesis of DME to reduce the action of inflammatory cytokines and VEGF, reduce leukostasis, and improve other physiologic and structural changes, such as tight junction integrity. (docksci.com)
Data1
- Our data showed that puerarin attenuated IL-1β-mediated leukostasis and cell apoptosis in TR-iBRB2 cells. (molvis.org)
Term1
- LEUKOSTASIS is the term used for effects of very high WBC. (shyamhemoncclinic.com)
Death1
- Damage to the microvasculature of the body is the primary cause of death by leukostasis. (wikipedia.org)
Expression1
- Discussion Mino diminished IR induced neuroinflammation, together with the expression of inflammatory genes and leukostasis, and prevented IR induced permeability and tight junc tion disorganization. (peptide-solubility.com)
Cell1
- Leukostasis is diagnosed when white cell plugs are seen in the microvasculature. (wikipedia.org)