Platelet Transfusion
Blood Transfusion
Blood Platelets
Plateletpheresis
Erythrocyte Transfusion
Platelet Aggregation
Blood Component Transfusion
Antigens, Human Platelet
Thrombocytopenia, Neonatal Alloimmune
Isoantibodies
Blood Transfusion, Intrauterine
Blood Transfusion, Autologous
Blood Grouping and Crossmatching
Platelet Adhesiveness
Blood Preservation
Exchange Transfusion, Whole Blood
Platelet Membrane Glycoproteins
Hematology
Blood Component Removal
Blood Group Incompatibility
Anemia, Aplastic
Platelet Factor 4
Thrombopoietin
Fetofetal Transfusion
Anemia, Refractory
Hemostasis
Bleeding Time
Thrombasthenia
Leukemia
Platelet Function Tests
HLA Antigens
Platelet Glycoprotein GPIIb-IIIa Complex
Platelet Activating Factor
Thrombopoiesis
Interleukin-11
Leukapheresis
Pancytopenia
Hematopoietic Stem Cell Transplantation
ABO Blood-Group System
Platelet Glycoprotein GPIb-IX Complex
Thrombelastography
Purpura, Thrombocytopenic, Idiopathic
Granulocyte Colony-Stimulating Factor
Treatment Outcome
Retrospective Studies
Histocompatibility Testing
Bone Marrow Transplantation
Leukocyte Transfusion
Transplantation, Autologous
Leukemia, Myeloid
Adenosine Diphosphate
Isoantigens
Cyclophosphamide
Myelodysplastic Syndromes
Disseminated Intravascular Coagulation
Prospective Studies
Immunization
Fibrinogen
Antineoplastic Combined Chemotherapy Protocols
Leukocyte Count
Transplantation, Homologous
Lymphoma, Non-Hodgkin
P-Selectin
Antigens, CD34
Hemoglobins
Anemia, Neonatal
Leukemia, Myeloid, Acute
Etoposide
Erythroblastosis, Fetal
Hematopoietic Stem Cell Mobilization
Antibodies
Graft Survival
Leukocytes
Postoperative Hemorrhage
Hematopoiesis
von Willebrand Factor
Hepatic Veno-Occlusive Disease
Autologous transplantation of chemotherapy-purged PBSC collections from high-risk leukemia patients: a pilot study. (1/463)
We have recently demonstrated that the combination of the alkylating agent nitrogen mustard (NM) and etoposide (VP-16) is capable of eliminating, ex vivo, leukemic cells contaminating PBSC collections and this is associated with a significant recovery of primitive and committed hematopoietic progenitor cells. Based on these data a pilot study on autologous transplantation of NM/VP-16 purged PBSC for high-risk leukemic patients was recently initiated. Twelve patients (seven females and five males) with a median age of 46 years (range 18-57) have been treated. Two patients had acute myeloblastic leukemia (AML) resistant to conventional induction treatment, four patients had secondary AML in I complete remission (CR), one patient was in II CR after failing a previous autologous BM transplantation, while two additional AML individuals were in I CR achieved after three or more cycles of induction treatment. Two patients with high-risk acute lymphoblastic leukemia (ALL) in I CR and one patient with mantle cell lymphoma and leukemic dissemination were also included. Eight patients showed karyotypic abnormalities associated with a poor clinical outcome. The mobilizing regimens included cytosine arabinoside and mitoxantrone with (n = 6) or without fludarabine (n = 3) followed by subcutaneous administration of G-CSF (5 microg/kg/day until the completion of PBSC collection) and G-CSF alone (n = 3) (15 microg/kg/day). A median of two aphereses (range 1-3) allowed the collection of 7.2 x 10(8) TNC/kg (range 3.4-11.5), 5 x 10(6) CD34+ cells/kg (range 2.1-15.3) and 9.2 x 10(4) CFU-GM/kg (0.3-236). PBSC were treated with a constant dose of 20 microg of VP-16/ml and a median individual-adjusted dose (survival < or = 5% of steady-state BM CFU-GM) of NM of 0.7 microg/ml (range 0.25-1.25). Eleven patients were reinfused after busulfan (16 mg/kg) and Cy (120 mg/kg) conditioning with a median residual dose of 0.3 x 10(4) CFU-GM/kg (0-11.5). The median time to neutrophil engraftment (>0.5 x 10(9)/l) for evaluable patients was 25 days (range 12-59); the median time to platelet transfusion independence (>20 and >50 x 10(9)/l) was 40 days (18-95) and 69 days (29-235), respectively. Hospital discharge occurred at a median of 25 days (18-58) after stem cell reinfusion. Four individuals are alive in CR (n = 3) or with residual nodal disease (n = 1 lymphoma patient) with a follow-up of 32, 26, 3 and 14 months, respectively. Seven patients died due to disease progression or relapse (n = 5) or extrahematological transplant toxicity (n = 2). Our data suggest that pharmacological purging of leukapheresis collections of leukemic patients at high-risk of relapse is feasible and ex vivo treated cells reconstitute autologous hematopoiesis. (+info)A restrictive platelet transfusion policy allowing long-term support of outpatients with severe aplastic anemia. (2/463)
The threshold for prophylactic platelet transfusions in patients with hypoplastic thrombopenia generally recommended in the standard literature is 20,000 platelets/microL. A more restrictive transfusion policy may be indicated in patients with chronic severe aplastic anemia (SAA) in need of long-term platelet support. We evaluated the feasibility and safety of a policy with low thresholds for prophylactic transfusions (+info)Changes in endogenous TPO levels during mobilization chemotherapy are predictive of CD34+ megakaryocyte progenitor yield and identify patients at risk of delayed platelet engraftment post-PBPC transplant. (3/463)
Patients with delayed platelet recovery post-PBPC transplant (PBPCT) are a high-risk group for thrombocytopenic bleeding and platelet transfusion dependence. Total CD34+ cell dosage has been proposed as the most important factor influencing the rate of platelet recovery. To achieve the shortest time to platelet engraftment, a minimum leukapheresis target of 10x10(6) CD34+ cells/kg was established for 30 patients. Of the 29 evaluable patients, 62% had rapid (group I: time to platelets >20x10(9)/l < or =10 days and 50x10(9)/l < or =14 days) platelet recoveries while 38% had delayed (group II: 20x10(9)/l >10 days and 50x10(9)/l >14 days) recoveries. Groups I and II were compared for: (1) pretreatment variables; (2) mobilizing capability of CD34+ cells and subsets including megakaryocyte (Mk) progenitors; (3) infused dose of these cells at transplant; (4) changes in endogenous levels of Mpl ligand (or TPO) during mobilization and myeloablative chemotherapy. Group II patients received significantly more platelet transfusions (6 vs. 2.1, P = 0.002) post-PBPCT, had a higher proportion of patients with a prior history of BM disease (64% vs. 6%, P = 0.001), and showed a reduced ability to mobilize differentiated (CD34+/38+, CD34+/DR+) and Mk progenitors (CD34+/42a+, CD34+/61+). Only the number of Mk progenitors reinfused at transplant was significantly different between the groups (group II vs. group I: CD34+/42a+ = 1.02 vs. 2.56x10(6)/kg, P = 0.013; CD34+/61+ = 1.12 vs. 2.70x10(6)/kg, P = 0.015). The ability to mobilize Mk progenitors correlated with percentage changes in endogenous levels of TPO from baseline to platelet nadir during mobilization chemotherapy (CD34+/42a+: r = 0.684, P = 0.007; CD34+/61+: r = 0.684, P = 0.007), with group II patients experiencing lower percentage changes. An inverse trend but no correlation was observed between serial TPO levels and platelet counts. TPO levels remained elevated in group II patients throughout a prolonged period of thrombocytopenia (median days to 50x10(9)/l = 25 vs. 11 for group I), indicating that delayed engraftment was not due to a deficiency of TPO but to a lack of Mk progenitor target cells. Our results show that the number of reinfused Mk progenitors is a better predictor of platelet engraftment than total CD34+ cell dosage. Small changes in endogenous TPO levels during mobilization predict for low Mk progenitor yields. (+info)Subsets of CD34+ hematopoietic progenitors and platelet recovery after high dose chemotherapy and peripheral blood stem cell transplantation. (4/463)
BACKGROUND AND OBJECTIVE: Randomized clinical trials have shown that peripheral blood stem cell transplantations (PBSCT) with appropriate doses of CD34+ cells are associated with rapid, complete and sustained recovery of marrow functions. Nevertheless, in a minority af patients delayed platelet recovery may occur and it remains to be established whether analysis of transplanted CD34+ cell subsets may demonstrate correlation with this phenomenon. We studied a series of 80 consecutive transplanted patients with the aim of evaluating the effect of CD34+ stem cell numbers and, in a subgroup of 32 patients, the effect of the lineage specific subset numbers on time to platelet engraftment (i.e. time to platelet counts higher than 20x10(9)/L for two consecutive days without the need for platelet transfusions). DESIGN AND METHODS: Different clinical and paraclinical factors were examined in a multivariate analysis for effect on platelet engraftment in 80 patients. RESULTS: The number of CD34+ cells/kg infused was the most important factor predicting the time to platelet engraftment. Patients receiving more than 10x10(6) CD34+ cells/kg had prompt platelet engraftment. The majority of the patients (78%) received fewer than 10x10(3) CD34+ cells/kg and 17/62 (27%) of these patients experienced delayed platelet engraftment. In 32 patients receiving fewer than 10x10(6) CD34+ cells/kg we focused on the content of different lineage specific CD34+ subsets in the PBSC products. The most significant correlation was recognized for CD34+/CD61+ megakaryocytic cell number and platelet engraftment. An inverse correlation between the CD34+/CD38Eth subset and platelet engraftment was found, indicating that a high number of CD34+/CD38Eth in the PBSC product might increase the risk for delayed engraftment. These results were further confirmed by the observation that patients who experienced platelet engraftment after day 20 had significantly more CD34+/CD38Eth cells/kg infused than patients with fast engraftment. INTERPRETATION AND CONCLUSIONS: The number of total CD34+ cells/kg infused was the most important factor predicting time to platelet engraftment. CD34+ subset analysis in a subgroup of patients suggests that a high number of uncommitted progenitors may be associated with slower platelet recovery than transplantation with a higher fraction of more committed peripheral blood stem cells. (+info)Serious hazards of transfusion (SHOT) initiative: analysis of the first two annual reports. (5/463)
OBJECTIVE: To receive and collate reports of death or major complications of transfusion of blood or components. DESIGN: Haematologists were invited confidentially to report deaths and major complications after blood transfusion during October 1996 to September 1998. SETTING: Hospitals in United Kingdom and Ireland. SUBJECTS: Patients who died or experienced serious complications, as defined below, associated with transfusion of red cells, platelets, fresh frozen plasma, or cryoprecipitate. MAIN OUTCOME MEASURES: Death, "wrong" blood transfused to patient, acute and delayed transfusion reactions, transfusion related acute lung injury, transfusion associated graft versus host disease, post-transfusion purpura, and infection transmitted by transfusion. Circumstances relating to these cases and relative frequency of complications. RESULTS: Over 24 months, 366 cases were reported, of which 191 (52%) were "wrong blood to patient" episodes. Analysis of these revealed multiple errors of identification, often beginning when blood was collected from the blood bank. There were 22 deaths from all causes, including three from ABO incompatibility. There were 12 infections: four bacterial (one fatal), seven viral, and one fatal case of malaria. During the second 12 months, 164/424 hospitals (39%) submitted a "nil to report" return. CONCLUSIONS: Transfusion is now extremely safe, but vigilance is needed to ensure correct identification of blood and patient. Staff education should include awareness of ABO incompatibility and bacterial contamination as causes of life threatening reactions to blood. (+info)Correlation of cytokine elaboration with mononuclear cell adhesion to platelet storage bag plastic polymers: a pilot study. (6/463)
The basis for many febrile nonhemolytic transfusion reactions associated with platelet transfusion therapy is cytokine elaboration and accumulation in the storage bag, which correlate with the leukocyte content and the length of platelet storage. We propose that a possible additional variable in the elaboration and accumulation of cytokines is the differential adhesion of mononuclear cells to the plastic substrate of the platelet storage bag. We hypothesize that mononuclear cell adhesion-induced cytokine release is greater in random-donor platelet bags composed of the polyolefin polymer compared to the single-donor apheresis platelet bags composed of the polyvinyl chloride polymer with the tri-(2-ethylhexyl) trimellitate (TEHTM) plasticizer. For four blood donors, we demonstrate preferential mononuclear cell adhesion, in vitro, to discs of polyolefin polymer versus discs of polyvinyl chloride polymer with the TEHTM plasticizer. Scanning electron microscopy corroborates this. In addition, proinflammatory cytokine (interleukin 1beta [IL-1beta] and tumor necrosis factor alpha [TNF-alpha]) levels are greater in culture wells containing discs of polyolefin polymer than in those containing discs of polyvinyl chloride polymer with the TEHTM plasticizer, and even more so in storage bags containing polyolefin polymer versus polyvinyl chloride polymer with the TEHTM plasticizer (IL-1beta, TNF-alpha, IL-6, and IL-8). This study suggests, for the first time, that differential plastic substrate mononuclear cell adhesion may contribute to cytokine release during platelet storage. This may represent an additional variable in the pathophysiology of febrile nonhemolytic transfusion reactions in patients receiving stored platelet units. (+info)Immunoglobulin therapy for severe thrombocytopenia complicating falciparum malaria. (7/463)
A 12-year-old Saudi boy with falciparum malaria developed profound thrombocytopenia with associated significant bleeding. Immunoglobulin was used to treat this case. (+info)Sickle cell disease and aortic valve replacement: use of cardiopulmonary bypass, partial exchange transfusion, platelet sequestration, and continuous hemofiltration. (8/463)
Sickle cell disease in patients undergoing open heart procedures presents a multitude of challenges to the medical staff. With improved techniques of cardiopulmonary bypass, surgery, and anesthesia for treating patients with sickle cell disease, perfusionists will likely encounter patients with this genetic disorder on a more frequent basis. A 40-year-old black woman was admitted to our institution with recurrent Staphylococcus epidermidis and sepsis. She underwent transesophageal echocardiography and cardiac catheterization and was subsequently diagnosed with severe aortic insufficiency. The aortic valve was replaced. Herein, we report our experience in the preoperative, perioperative, and postoperative management of this patient. We present a concise update on the current literature and techniques used by others in similar cases, and we provide a brief section on future considerations to assist fellow practitioners in recognizing this disease and meeting the accompanying challenges. (+info)There are several possible causes of thrombocytopenia, including:
1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.
Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.
In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.
The exact cause of NAIT is not fully understood, but it is thought to be due to a combination of genetic and environmental factors. The condition is more common in certain ethnic groups, such as African Americans and Hispanics, and in mothers who have a history of previous pregnancy complications or blood type incompatibility with their baby.
The symptoms of NAIT can vary from mild to severe and may include:
* Easy bruising or bleeding
* Petechiae (small red or purple spots on the skin)
* Nosebleeds
* Gingivitis (inflammation of the gums)
* Bleeding in the digestive tract
If NAIT is suspected, the baby's platelet count will be checked and the mother's blood will be tested for antibodies against the baby's platelets. Treatment may involve intravenous immunoglobulin (IVIG) to reduce the mother's antibody production or a blood transfusion to increase the baby's platelet count. In severe cases, phototherapy may be used to help break down the antibodies and prevent bleeding.
Prevention of NAIT is challenging, but it is important for pregnant women to be aware of their risk factors and seek medical attention if they experience any symptoms of the condition. Proper monitoring and prompt treatment can help reduce the risk of complications and improve outcomes for affected babies.
Example sentence: The patient had a hemorrhage after the car accident and needed immediate medical attention.
Blood group incompatibility can occur in various ways, including:
1. ABO incompatibility: This is the most common type of blood group incompatibility and occurs when the patient's blood type (A or B) is different from the donor's blood type.
2. Rh incompatibility: This occurs when the patient's Rh factor is different from the donor's Rh factor.
3. Other antigens: In addition to ABO and Rh, there are other antigens on red blood cells that can cause incompatibility, such as Kell, Duffy, and Xg.
Blood group incompatibility can be diagnosed through blood typing and cross-matching tests. These tests determine the patient's and donor's blood types and identify any incompatible antigens that may cause an immune response.
Treatment of blood group incompatibility usually involves finding a compatible donor or using specialized medications to reduce the risk of a negative reaction. In some cases, plasmapheresis, also known as plasma exchange, may be used to remove the incompatible antibodies from the patient's blood.
Prevention of blood group incompatibility is important, and this can be achieved by ensuring that patients receive only compatible blood products during transfusions. Blood banks maintain a database of donor blood types and perform thorough testing before releasing blood for transfusion to ensure compatibility. Additionally, healthcare providers should carefully review the patient's medical history and current medications to identify any potential allergies or sensitivities that may affect blood compatibility.
Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, and increased risk of bleeding or infection. Treatment options for aplastic anemia typically involve blood transfusions and immunosuppressive drugs to stimulate the bone marrow to produce new blood cells. In severe cases, a bone marrow transplant may be necessary.
Overall, aplastic anemia is a rare and serious condition that requires careful management by a healthcare provider to prevent complications and improve quality of life.
During fetofetal transfusion, blood flows from one fetus to another through the placenta, which is a vital organ that provides oxygen and nutrients to the developing fetuses and removes waste products. The transfer of blood can occur through various channels, including the placental vasculature, umbilical cord, or other fetal-maternal interfaces.
There are different types of fetofetal transfusion, depending on the direction of blood flow:
1. Fetofetal transfusion in utero (in the womb): This is the most common type, where blood flows from one fetus to another within the womb.
2. Fetofetal transfusion through the placenta: In this type, blood flows from one fetus to the other through the placenta, which acts as a filter and regulates the exchange of nutrients and waste products between the mother's bloodstream and the fetuses'.
3. Fetofetal transfusion through the umbilical cord: This type occurs when the umbilical cord becomes tangled or compressed, causing blood to flow from one fetus to another.
The causes of fetofetal transfusion are not yet fully understood, but it is believed to be more common in multiple gestations (twins, triplets, etc.) and in cases where there is a placental abnormality or other complications during pregnancy.
Fetofetal transfusion can have both positive and negative effects on the development and health of the fetuses. On one hand, it can provide beneficial effects, such as:
1. Increased blood volume and oxygen supply: The transferred blood can help increase the blood volume and oxygen supply to the recipient fetus, which may be beneficial for its development and growth.
2. Improved nutrient supply: The transferred blood can also provide an increased supply of nutrients to the recipient fetus, which may improve its overall health and development.
However, fetofetal transfusion can also have negative effects, such as:
1. Anemia in the donor fetus: The loss of blood from the donor fetus can lead to anemia, which can negatively affect its growth and development.
2. Increased risk of complications: Fetofetal transfusion can increase the risk of complications during pregnancy, such as preterm labor, preeclampsia, and placental abruption.
3. Adverse effects on fetal development: The transferred blood can also contain substances that are not beneficial for the recipient fetus, which can lead to adverse effects on its development and growth.
Fetofetal transfusion is usually detected during routine ultrasound examinations, where it may appear as an abnormal flow of blood between the fetuses or as a collection of blood in the placenta or umbilical cord. If diagnosed early, fetofetal transfusion can be monitored and managed with regular ultrasound examinations and close maternal monitoring. In some cases, the condition may resolve on its own without any complications.
In severe cases, however, fetofetal transfusion may require medical intervention, such as:
1. Blood sampling: Blood samples may be taken from the donor fetus to determine the extent of the transfer and to monitor the health of both fetuses.
2. Corticosteroid therapy: Corticosteroids may be administered to the mother to promote fetal maturity and reduce the risk of complications.
3. Planned delivery: In some cases, planned delivery may be necessary to avoid any potential risks to the fetuses.
It is important for pregnant women who have a multiple pregnancy to be aware of the risk of fetofetal transfusion and to seek regular prenatal care to monitor the health of both fetuses. Early detection and management can help reduce the risk of complications and improve outcomes for both fetuses.
There are several subtypes of refractory anemia, including:
1. Refractory anemia with excess blasts (RAEB): This type of anemia is characterized by a high number of immature red blood cells in the bone marrow.
2. Refractory anemia with ringed sideroblasts (RARS): This type of anemia is characterized by the presence of abnormal red blood cells that have a "ring-like" appearance under a microscope.
3. Refractory anemia with multilineage dysplasia (RARMD): This type of anemia is characterized by abnormal cell development in the bone marrow, including immature red blood cells, white blood cells, and platelets.
Refractory anemia can be caused by a variety of factors, including genetic mutations, exposure to certain chemicals or toxins, and certain medical conditions such as chronic kidney disease or rheumatoid arthritis. Treatment for refractory anemia typically involves blood transfusions and supportive care, such as folic acid supplements and antibiotics to prevent infection. In some cases, bone marrow transplantation may be recommended.
In general, surgical blood loss is considered excessive if it exceeds 10-20% of the patient's total blood volume. This can be determined by measuring the patient's hemoglobin levels before and after the procedure. A significant decrease in hemoglobin levels post-procedure may indicate excessive blood loss.
There are several factors that can contribute to surgical blood loss, including:
1. Injury to blood vessels or organs during the surgical procedure
2. Poor surgical technique
3. Use of scalpels or other sharp instruments that can cause bleeding
4. Failure to control bleeding with proper hemostatic techniques
5. Pre-existing medical conditions that increase the risk of bleeding, such as hemophilia or von Willebrand disease.
Excessive surgical blood loss can lead to a number of complications, including:
1. Anemia and low blood counts
2. Hypovolemic shock (a life-threatening condition caused by excessive fluid and blood loss)
3. Infection or sepsis
4. Poor wound healing
5. Reoperation or surgical intervention to control bleeding.
To prevent or minimize surgical blood loss, surgeons may use a variety of techniques, such as:
1. Applying topical hemostatic agents to the surgical site before starting the procedure
2. Using energy-based devices (such as lasers or ultrasonic devices) to seal blood vessels and control bleeding
3. Employing advanced surgical techniques that minimize tissue trauma and reduce the risk of bleeding
4. Monitoring the patient's hemoglobin levels throughout the procedure and taking appropriate action if bleeding becomes excessive.
The term "thrombasthenia" comes from the Greek words "thrombos," meaning clot, and "basis," meaning foundation. It was first used by the British physician Sir William Osler in the late 19th century to describe a group of rare bleeding disorders characterized by abnormal platelet function.
There are three main types of thrombasthenia:
1. Bernard-Soulier syndrome: This is the most common type of thrombasthenia and is caused by a defect in the gene that codes for the protein known as platelet membrane glycoprotein (PMG) IIb. People with this condition have large, fragile platelets that are prone to bleeding.
2. Glanzmann's thrombasthenia: This is a rare type of thrombasthenia caused by a defect in the gene that codes for the protein known as platelet membrane glycoprotein (PMG) IIIa. People with this condition have small, irregular platelets that are unable to form proper blood clots.
3. Gray platelet syndrome: This is a rare type of thrombasthenia caused by a defect in the gene that codes for the protein known as alpha-granule membrane protein (AGM). People with this condition have small, gray-colored platelets that are prone to bleeding.
Thrombasthenia can be diagnosed through blood tests that evaluate platelet function and genetic testing to identify the specific defect responsible for the disorder. Treatment typically involves avoiding medications that can exacerbate bleeding, using platelet transfusions to increase platelet numbers, and in some cases, undergoing surgery to repair or remove affected blood vessels.
There are several different types of leukemia, including:
1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.
Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.
Symptoms of pancytopenia may include fatigue, weakness, shortness of breath, and increased risk of bleeding or infection. Treatment depends on the underlying cause, but may include blood transfusions, antibiotics, or immunosuppressive medications. In severe cases, pancytopenia can lead to anemia, infections, or bleeding complications that can be life-threatening.
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The main symptoms of PTI include:
* Purple spots or bruises (purpura) on the skin, which may be caused by minor trauma or injury.
* Thrombocytopenia (low platelet count), typically less than 50,000 platelets/mm3.
* Mild anemia and reticulocytosis (increased immature red blood cells).
* Elevated levels of autoantibodies against platelet membrane glycoproteins (GP) and other platelet proteins.
* No evidence of other causes of thrombocytopenia, such as bone marrow disorders or infections.
The exact cause of PTI is unknown, but it is believed to involve an immune-mediated response triggered by a genetic predisposition. Treatment options for PTI include corticosteroids, intravenous immunoglobulin (IVIG), and splenectomy in severe cases. The prognosis for PTI is generally good, with most patients experiencing resolution of symptoms and normalization of platelet counts within a few months to a year after treatment. However, some individuals may experience recurrent episodes of thrombocytopenia and purpura throughout their lives.
Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:
1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.
The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
There are several subtypes of MDS, each with distinct clinical features and prognosis. The most common subtype is refractory anemia with excess blasts (RAEB), followed by chronic myelomonocytic leukemia (CMMoL) and acute myeloid leukemia (AML).
The exact cause of MDS is not fully understood, but it is believed to result from a combination of genetic mutations and environmental factors. Risk factors for developing MDS include exposure to certain chemicals or radiation, age over 60, and a history of previous cancer treatment.
Symptoms of MDS can vary depending on the specific subtype and severity of the disorder, but may include fatigue, weakness, shortness of breath, infection, bleeding, and easy bruising. Diagnosis is typically made through a combination of physical examination, medical history, blood tests, and bone marrow biopsy.
Treatment for MDS depends on the specific subtype and severity of the disorder, as well as the patient's overall health and preferences. Options may include supportive care, such as blood transfusions and antibiotics, or more intensive therapies like chemotherapy, bone marrow transplantation, or gene therapy.
Overall, myelodysplastic syndromes are a complex and heterogeneous group of disorders that can have a significant impact on quality of life and survival. Ongoing research is focused on improving diagnostic accuracy, developing more effective treatments, and exploring novel therapeutic approaches to improve outcomes for patients with MDS.
In DIC, the body's normal blood coagulation mechanisms become overactive and begin to form clots throughout the circulatory system, including in small blood vessels and organs. This can cause a range of symptoms, including bleeding, fever, and organ failure.
DIC is often seen in sepsis, which is a severe infection that has spread throughout the body. It can also be caused by other conditions such as trauma, cancer, and autoimmune disorders.
Treatment of DIC typically involves addressing the underlying cause, such as treating an infection or injury, as well as supporting the body's natural clotting mechanisms and preventing further bleeding. In severe cases, hospitalization and intensive care may be necessary to monitor and treat the condition.
In summary, Disseminated Intravascular Coagulation (DIC) is a serious medical condition that can cause widespread clotting and damage to the body's organs and tissues. It is often seen in sepsis and other severe conditions, and treatment typically involves addressing the underlying cause and supporting the body's natural clotting mechanisms.
1. Leukemia: A type of cancer that affects the blood and bone marrow, characterized by an overproduction of immature white blood cells.
2. Lymphoma: A type of cancer that affects the immune system, often involving the lymph nodes and other lymphoid tissues.
3. Multiple myeloma: A type of cancer that affects the plasma cells in the bone marrow, leading to an overproduction of abnormal plasma cells.
4. Myelodysplastic syndrome (MDS): A group of disorders characterized by the impaired development of blood cells in the bone marrow.
5. Osteopetrosis: A rare genetic disorder that causes an overgrowth of bone, leading to a thickened bone marrow.
6. Bone marrow failure: A condition where the bone marrow is unable to produce enough blood cells, leading to anemia, infection, and other complications.
7. Myelofibrosis: A condition characterized by the scarring of the bone marrow, which can lead to an overproduction of blood cells and an increased risk of bleeding and infection.
8. Polycythemia vera: A rare blood disorder that causes an overproduction of red blood cells, leading to an increased risk of blood clots and other complications.
9. Essential thrombocythemia: A rare blood disorder that causes an overproduction of platelets, leading to an increased risk of blood clots and other complications.
10. Myeloproliferative neoplasms (MPNs): A group of rare blood disorders that are characterized by the overproduction of blood cells and an increased risk of bleeding and infection.
These are just a few examples of bone marrow diseases. There are many other conditions that can affect the bone marrow, and each one can have a significant impact on a person's quality of life. If you suspect that you or someone you know may have a bone marrow disease, it is important to seek medical attention as soon as possible. A healthcare professional can perform tests and provide a proper diagnosis and treatment plan.
There are several subtypes of NHL, including:
1. B-cell lymphomas (such as diffuse large B-cell lymphoma and follicular lymphoma)
2. T-cell lymphomas (such as peripheral T-cell lymphoma and mycosis fungoides)
3. Natural killer cell lymphomas (such as nasal NK/T-cell lymphoma)
4. Histiocyte-rich B-cell lymphoma
5. Primary mediastinal B-cell lymphoma
6. Mantle cell lymphoma
7. Waldenström macroglobulinemia
8. Lymphoplasmacytoid lymphoma
9. Myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN) related lymphoma
These subtypes can be further divided into other categories based on the specific characteristics of the cancer cells.
Symptoms of NHL can vary depending on the location and size of the tumor, but may include:
* Swollen lymph nodes in the neck, underarm, or groin
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
* Abdominal pain
* Swollen spleen
Treatment for NHL typically involves a combination of chemotherapy, radiation therapy, and in some cases, targeted therapy or immunotherapy. The specific treatment plan will depend on the subtype of NHL, the stage of the cancer, and other individual factors.
Overall, NHL is a complex and diverse group of cancers that require specialized care from a team of medical professionals, including hematologists, oncologists, radiation therapists, and other support staff. With advances in technology and treatment options, many people with NHL can achieve long-term remission or a cure.
There are many different types of anemia, each with its own set of causes and symptoms. Some common types of anemia include:
1. Iron-deficiency anemia: This is the most common type of anemia and is caused by a lack of iron in the diet or a problem with the body's ability to absorb iron. Iron is essential for making hemoglobin.
2. Vitamin deficiency anemia: This type of anemia is caused by a lack of vitamins, such as vitamin B12 or folate, that are necessary for red blood cell production.
3. Anemia of chronic disease: This type of anemia is seen in people with chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer.
4. Sickle cell anemia: This is a genetic disorder that affects the structure of hemoglobin and causes red blood cells to be shaped like crescents or sickles.
5. Thalassemia: This is a genetic disorder that affects the production of hemoglobin and can cause anemia, fatigue, and other health problems.
The symptoms of anemia can vary depending on the type and severity of the condition. Common symptoms include fatigue, weakness, pale skin, shortness of breath, and dizziness or lightheadedness. Anemia can be diagnosed with a blood test that measures the number and size of red blood cells, as well as the levels of hemoglobin and other nutrients.
Treatment for anemia depends on the underlying cause of the condition. In some cases, dietary changes or supplements may be sufficient to treat anemia. For example, people with iron-deficiency anemia may need to increase their intake of iron-rich foods or take iron supplements. In other cases, medical treatment may be necessary to address underlying conditions such as kidney disease or cancer.
Preventing anemia is important for maintaining good health and preventing complications. To prevent anemia, it is important to eat a balanced diet that includes plenty of iron-rich foods, vitamin C-rich foods, and other essential nutrients. It is also important to avoid certain substances that can interfere with the absorption of nutrients, such as alcohol and caffeine. Additionally, it is important to manage any underlying medical conditions and seek medical attention if symptoms of anemia persist or worsen over time.
In conclusion, anemia is a common blood disorder that can have significant health implications if left untreated. It is important to be aware of the different types of anemia, their causes, and symptoms in order to seek medical attention if necessary. With proper diagnosis and treatment, many cases of anemia can be successfully managed and prevented.
A condition where newborn babies have a lower than normal number of red blood cells or low levels of hemoglobin in their blood. The condition can be caused by various factors such as premature birth, low birth weight, infections, and genetic disorders. Symptoms may include jaundice, fatigue, and difficulty breathing. Treatment options may vary depending on the underlying cause but may include blood transfusions and iron supplements.
Example usage: "Neonatal anemia is a common condition in newborn babies that can be caused by various factors such as premature birth or low birth weight."
AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.
There are several subtypes of AML, including:
1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.
The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:
* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures
AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.
Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:
1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.
It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.
The condition is caused by sensitization of the mother's immune system to the Rh factor, which can occur when the mother's blood comes into contact with the fetus's blood during pregnancy or childbirth. The antibodies produced by the mother's immune system can attack the red blood cells of the fetus, leading to hemolytic anemia and potentially causing stillbirth or death in the newborn.
Erythroblastosis fetalis is diagnosed through blood tests that measure the levels of antibodies against the Rh factor. Treatment typically involves the administration of Rh immune globulin, which can help to prevent the mother's immune system from producing more antibodies against the Rh factor and reduce the risk of complications for the fetus. In severe cases, a blood transfusion may be necessary to increase the newborn's red blood cell count.
Erythroblastosis fetalis is a serious condition that requires close monitoring and proper medical management to prevent complications and ensure the best possible outcome for both the mother and the baby.
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.
Symptoms of neutropenia may include recurring infections, fever, fatigue, weight loss, and swollen lymph nodes. The diagnosis is typically made through a blood test that measures the number of neutrophils in the blood.
Treatment options for neutropenia depend on the underlying cause but may include antibiotics, supportive care to manage symptoms, and in severe cases, bone marrow transplantation or granulocyte-colony stimulating factor (G-CSF) therapy to increase neutrophil production.
1. Injury to blood vessels during surgery
2. Poor suturing or stapling techniques
3. Bleeding disorders or use of anticoagulant medications
4. Infection or hematoma (a collection of blood outside the blood vessels)
5. Delayed recovery of blood clotting function
Postoperative hemorrhage can range from mild to severe and life-threatening. Mild bleeding may present as oozing or trickling of blood from the surgical site, while severe bleeding can lead to hypovolemic shock, organ failure, and even death.
To diagnose postoperative hemorrhage, a physical examination and medical history are usually sufficient. Imaging studies such as ultrasound, computed tomography (CT) or magnetic resonance imaging (MRI) may be ordered to evaluate the extent of bleeding and identify any underlying causes.
Treatment of postoperative hemorrhage depends on the severity and location of the bleeding. Mild bleeding may be managed with dressings, compression bandages, and elevation of the affected limb. Severe bleeding may require interventions such as:
1. Surgical exploration to locate and control the source of bleeding
2. Transfusion of blood products or fresh frozen plasma to restore clotting function
3. Use of vasopressors to raise blood pressure and perfuse vital organs
4. Hemostatic agents such as clotting factors, fibrin sealants, or hemostatic powder to promote clot formation
5. In some cases, surgical intervention may be required to repair damaged blood vessels or organs.
Prevention of postoperative hemorrhage is crucial in reducing the risk of complications and improving patient outcomes. Preventive measures include:
1. Proper preoperative evaluation and preparation, including assessment of bleeding risk factors
2. Use of appropriate anesthesia and surgical techniques to minimize tissue trauma
3. Conservative use of hemostatic agents and blood products during surgery
4. Closure of all bleeding sites before completion of the procedure
5. Monitoring of vital signs, including pulse rate and blood pressure, during and after surgery
6. Preoperative and postoperative management of underlying conditions such as hypertension, diabetes, and coagulopathies.
Early recognition and prompt intervention are critical in effectively managing postoperative hemorrhage. In cases of severe bleeding, timely and appropriate interventions can reduce the risk of complications and improve patient outcomes.
VOD is most commonly seen in patients who have undergone hematopoietic stem cell transplantation (HSCT) or solid organ transplantation, as well as those with certain inherited genetic disorders. It is caused by a combination of factors, including immune system dysfunction, infection, and exposure to certain drugs or toxins.
Symptoms of VOD can include nausea, vomiting, abdominal pain, fatigue, and jaundice (yellowing of the skin and eyes). In severe cases, VOD can lead to liver failure, sepsis, and death.
Treatment for VOD typically involves supportive care, such as fluids and medications to manage symptoms, as well as therapies aimed at addressing any underlying causes of the condition. In severe cases, a liver transplant may be necessary. Prognosis for VOD varies depending on the severity of the condition and the presence of any underlying medical conditions.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
Platelet transfusion
Platelet transfusion refractoriness
Plateletpheresis
Jacobsen syndrome
Blood donation
CD36
Mark Elliott Brecher
Thrombotic thrombocytopenic purpura
Embolic and thrombotic events after COVID-19 vaccination
Blood bank
Induced stem cells
Devaanshi Mehta
Allergic transfusion reaction
Hodgkin lymphoma
Complete blood count
Giant platelet disorder
Platelet swirling
Acute lymphoblastic leukemia
Transfusion-associated circulatory overload
South African National Blood Service
Neutrophil extracellular traps
X-linked thrombocytopenia
Fludarabine
Blood transfusion
Akhil Maheshwari
Whole blood
Multiple myeloma
Chemotherapy
Blood product
Non-Hodgkin lymphoma
Strømme syndrome
Rocky Mountain spotted fever
Joe Dolan
Lyme disease
CD151
Edmund Klein
Lassa fever
Hemolysis
Platelet storage pool deficiency
Diamond-Blackfan anemia
Iranian Blood Transfusion Organization
Mirror syndrome
Giulio Bizzozero
Psoralen
Immunohaematology
Cerebral venous sinus thrombosis
Plasma frozen within 24 hours
Necrotizing enterocolitis
Chronic lymphocytic leukemia
Megakaryocyte
Lower gastrointestinal bleeding
Apheresis
Hematemesis
William Holmes Crosby Jr.
Bleeding diathesis
Welsh Blood Service
Multiple electrode aggregometry
Granulocyte
Collaborative study to enlarge the first WHO repository of platelet transfusion-relevant bacterial reference strains: Expert...
Randomized trial of platelet-transfusion thresholds in neonates<...
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Prophylactic platelet transfusion prior to central venous catheter placement in patients with thrombocytopenia: study protocol...
CDC Media Relations: MMWR News Synopsis for February 25, 2005
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ABO on platelets goes beyond transfusion | Blood | American Society of Hematology
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White cells and platelets in blood transfusion :
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Spinal Cord Hemorrhage: Background, Pathophysiology, Epidemiology
Neonatal alloimmune thrombocytopenia (NAIT): An overview
Bleeding disorders: MedlinePlus Medical Encyclopedia
Emerging Infectious Diseases - CDC
Publications by Neil Blumberg, M.D. - University of Rochester Medical Center
DailyMed - TEPADINA- thiotepa injection, powder, for solution
Scientific Publications by FDA Staff
Diagnosis and Management of Squamous Cell Carcinoma of Unknown Primary in the Head and Neck Guidelines Pocket Guide - Guideline...
Safety and Efficacy Study of Loncastuximab Tesirine + Ibrutinib in Diffuse Large B-Cell or Mantle Cell Lymphoma - Full Text...
Pericarditis & Pericardiectomy pt. 5
Vibrio Infections Treatment & Management: Medical Care, Surgical Care, Consultations
Current version of study NCT03298399 on ClinicalTrials.gov
Should Endurance Athletes Donate Blood? | TrainingPeaks
Should Endurance Athletes be Donating Blood? - Trail Runner Magazine
When Cancer Was Conquerable
Selinexor (Xpovio™) | OncoLink
Purpura: Blood Spots, Thrombocytopenic, Symptoms & Causes
Thrombocytopenia17
- BACKGROUND: Platelet transfusions are commonly used to prevent bleeding in preterm infants with thrombocytopenia. (uea.ac.uk)
- Data are lacking to provide guidance regarding thresholds for prophylactic platelet transfusions in preterm neonates with severe thrombocytopenia. (uea.ac.uk)
- METHODS: In this multicenter trial, we randomly assigned infants born at less than 34 weeks of gestation in whom severe thrombocytopenia developed to receive a platelet transfusion at platelet-count thresholds of 50,000 per cubic millimeter (high-threshold group) or 25,000 per cubic millimeter (low-threshold group). (uea.ac.uk)
- CONCLUSIONS: Among preterm infants with severe thrombocytopenia, those randomly assigned to receive platelet transfusions at a platelet-count threshold of 50,000 per cubic millimeter had a significantly higher rate of death or major bleeding within 28 days after randomization than those who received platelet transfusions at a platelet-count threshold of 25,000 per cubic millimeter. (uea.ac.uk)
- Immune thrombocytopenia (ITP) is a type of platelet disorder . (nih.gov)
- Severe thrombocytopenia should be corrected by prophylactic platelet transfusion prior to central venous catheter (CVC) insertion, according to national and international guidelines. (biomedcentral.com)
- This is the first prospective, randomised controlled trial powered to test the hypothesis of whether omitting forgoing platelet transfusion prior to central venous cannulation leads to an equal occurrence of clinical relevant bleeding complications in critically ill and haematologic patients with thrombocytopenia. (biomedcentral.com)
- FRIDAY, May 26, 2023 (HealthDay News) - For patients with severe thrombocytopenia, withholding of prophylactic platelet transfusion before ultrasound-guided placement of a central venous catheter (CVC) results in more CVC-related bleeding events than prophylactic platelet transfusion, according to guidelines published in the May 25 issue of the New England Journal of Medicine . (newsazi.com)
- Floor L.F. van Baarle, M.D., from the University of Amsterdam, and colleagues conducted a multicenter, randomized, noninferiority trial involving patients with severe thrombocytopenia (platelet count, 10,000 to 50,000 per mm 3 ) who were treated on the hematology ward or the intensive care unit. (newsazi.com)
- Alternative agents versus prophylactic platelet transfusion for preventing bleeding in patients with thrombocytopenia due to chronic bone marrow failure: a network meta-analysis and systematic review. (ox.ac.uk)
- The objectives are as follows: To compare the relative efficacy of different treatments for thrombocytopenia (artificial platelet substitutes, platelet-poor plasma, fibrinogen, rFVIIa, rFXIII, thrombopoietin mimetics, antifibrinolytic drugs or platelet transfusions) in patients with chronic bone marrow failure and to derive a hierarchy of potential alternate treatments to platelet transfusions. (ox.ac.uk)
- Learn more about low platelet counts, or thrombocytopenia. (medicalnewstoday.com)
- However, the spectrum of disease ranges from mild to moderate thrombocytopenia , which refers to a low platelet count, to more severe. (medicalnewstoday.com)
- 14. Vincristine-laden platelet transfusion for patients with refractory thrombocytopenia. (nih.gov)
- 18. Clinical effect of buffy-coat vs. apheresis platelet concentrates in patients with severe thrombocytopenia after intensive chemotherapy. (nih.gov)
- Thus, the development of safe, small, molecules to enhance platelet production would be advantageous for the treatment of thrombocytopenia. (nih.gov)
- No cases of thrombocytopenia (low platelets) were diagnosed among almost 490,000 vaccinated adults. (heart.org)
Prophylactic7
- Even though correction is thought to prevent bleeding complications, evidence supporting the routine administration of prophylactic platelets is absent. (biomedcentral.com)
- The objective of the current trial is, therefore, to demonstrate that omitting prophylactic platelet transfusion prior to CVC placement in severely thrombocytopenic patients is non-inferior compared to prophylactic platelet transfusion. (biomedcentral.com)
- Consecutive patients are randomly assigned to either receive 1 unit of platelet concentrate, or receive no prophylactic platelet transfusion prior to CVC insertion. (biomedcentral.com)
- Current national and international guidelines are conflicting, most recent Dutch and UK guidelines support prophylactic platelet transfusion below a platelet count of 50 × 10 9 /L, prior to CVC placement [ 10 , 11 ]. (biomedcentral.com)
- Participants were randomly assigned to receive one unit of prophylactic platelet transfusion or no platelet transfusion before ultrasound-guided CVC placement. (newsazi.com)
- The net savings were $410 per catheter placement for withholding prophylactic platelet transfusion before CVC placement. (newsazi.com)
- 10. Efficacy of prophylactic transfusions using single donor apheresis platelets versus pooled platelet concentrates in AML/MDS patients receiving allogeneic hematopoietic stem cell transplantation. (nih.gov)
Units are contaminated with bacteria1
- an estimated one in 1,000--3,000 platelet units are contaminated with bacteria, resulting in transfusion-associated sepsis in many recipients ( 2 ). (cdc.gov)
Human Platelet3
- In the Trial to Reduce Alloimmunization to Platelets (TRAP) study, 101 of 530 participants became refractory to platelet transfusions without evidence of HLA or human platelet antigen (HPA) antibodies. (nih.gov)
- Platelets have proteins on their surface called human platelet antigens (HPAs). (medicalnewstoday.com)
- MSCs will be expanded ex vivo in human platelet lysate to the specified dose level. (clinicaltrials.gov)
Concentrates10
- Patient A. In October 2004, a man aged 74 years in Ohio with leukemia received a transfusion consisting of a pool of five platelet unit concentrates. (cdc.gov)
- Rapid selection of single-stranded DNA aptamers binding Staphylococcus epidermidis in platelet concentrates. (fda.gov)
- Staphylococcus epidermidis is the most common transfusion-associated pathogen contaminating platelet concentrates. (fda.gov)
- Our data identified an aptamer that may be useful as a ligand to capture, detect or remove S. epidermidis contaminant from platelet concentrates. (fda.gov)
- 1. Comparative clinical studies of platelet concentrates: effects on clinical outcome and the use of healthcare resources. (nih.gov)
- 3. Use of random versus apheresis platelet concentrates. (nih.gov)
- 9. A prospective randomized study of three types of platelet concentrates in patients with haematological malignancy: corrected platelet count increments and frequency of nonhaemolytic febrile transfusion reactions. (nih.gov)
- 12. [Risk Assessment of Single-Donor (Apheresis) Platelet Concentrates and Pooled Whole-Blood-Derived Platelet Concentrates]. (nih.gov)
- 13. [Introduction of platelet additive solution in platelet concentrates: towards a decrease of blood transfusion reactions]. (nih.gov)
- 16. Markers of platelet activation and apoptosis in platelet concentrates collected by apheresis. (nih.gov)
Antibodies6
- You also may have a blood test to check for the antibodies that attack platelets. (nih.gov)
- It occurs when the birthing parent's immune system produces antibodies that attack and destroy the fetuses' platelets. (medicalnewstoday.com)
- The antibodies then cross the placenta and target the fetus's platelets. (medicalnewstoday.com)
- These antibodies are responsible for platelet destruction in the fetus or newborn. (medicalnewstoday.com)
- There is no routine blood test to see if a birthing parent has antibodies to platelets. (medicalnewstoday.com)
- The serologic test can determine if the birthing parent has produced antibodies against any of the platelet antigens from the other parent. (medicalnewstoday.com)
Apheresis2
- Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis. (rochester.edu)
- 8. The use of PEG-rhuMGDF in platelet apheresis. (nih.gov)
METHODS4
- It is imperative to first validate the involvement of recipient platelets by standardizing the animal models, methods, reagents, and readouts for lung injury and taking the animal housing environment into consideration. (lu.se)
- Methods to reduce or eliminate contaminating bacteria from platelet units are critical for improving the safety of blood transfusions. (fda.gov)
- 6. A critical comparison of platelet preparation methods. (nih.gov)
- Biomolecular Consequences of Platelet Pathogen Inactivation Methods. (rodekruis.be)
Immune5
- Platelets are versatile cells which are capable of eliciting nonhemostatic immune functions, especially under inflammatory conditions. (lu.se)
- In ITP, however, your immune system attacks and destroys your body's platelets by mistake. (nih.gov)
- Typically, NAIT occurs when the immune cells in the birth parent's bloodstream identify the platelets from the baby as foreign and begin attacking them. (medicalnewstoday.com)
- Immune platelet refractoriness responsive to treatment with IVIg or eculizumab, or other immunosuppressive therapy within the 3 preceding months. (nih.gov)
- This trial is being conducted as a step toward testing the long-term hypothesis that freshly cultured, autologous mesenchymal stromal cells (MSCs) grown in platelet lysate-containing medium will modulate recipient T-cell immune responses and promote engraftment in haploidentical hematopoietic cell transplant (HCT) recipients. (clinicaltrials.gov)
20191
- Transfusion Medicine Reviews, 2019 Jan;33(1):29-34. (rodekruis.be)
Bone marrow4
- Platelets are tiny blood cells that are made in the bone marrow. (nih.gov)
- 15d-PGJ(2) also promotes platelet formation from culture-derived mouse and human megakaryocytes and accelerates platelet recovery after in vivo radiation-induced bone marrow injury. (nih.gov)
- The platelets arise from the fragmentation of the cytoplasm of megakaryocytes in the bone marrow and circulate in blood as disc-shaped anucleate particles for 7-10 days. (medscape.com)
- Allogeneic haematopoietic stem cell transplantation (HSCT) involves by Oelofse and Truter[5] found that haematological malignancies the transfusion of donor haematopoietic stem and progenitor were not uncommon in Eastern Cape Province, and the incidence cel s (HSPC) procured from bone marrow, peripheral blood or was comparable to some European populations. (who.int)
Thrombocytopenic3
- 7. Background, rationale, and design of a clinical trial to assess the effects of platelet dose on bleeding risk in thrombocytopenic patients. (nih.gov)
- Collectively, these data support the concept that megakaryocyte redox status plays an important role in platelet generation and that small electrophilic molecules may have clinical efficacy for improving platelet numbers in thrombocytopenic patients. (nih.gov)
- A person with thrombocytopenic purpura has low platelet counts. (clevelandclinic.org)
Severe2
- Low platelet counts can cause severe bleeding. (nih.gov)
- Platelets help your blood clot and prevent severe bleeding. (clevelandclinic.org)
Bacteria1
- Before transfusion, the pooled platelet unit had been tested for bacterial contamination with a reagent strip test (Multistix ® , Bayer Diagnostics, Tarrytown, New York) to determine the pH level, a means for detecting the presence of bacteria. (cdc.gov)
Lysate1
- Evaluation of the procoagulant properties of a newly developed platelet modified lysate product. (rochester.edu)
Donor1
- Genotyping confirmed HEV in a transfused platelet pool and the donor. (cdc.gov)
Counts1
- Some people get very low platelet counts during a disease or treatment. (nih.gov)
Aggregation1
- The platelet GP IIb/IIIa complex mediates platelet-to-platelet interactions (platelet aggregation). (medscape.com)
Disorders2
- Bleeding disorders can also result from a problem with the number or function of platelets. (medlineplus.gov)
- Platelet disorders lead to defects in primary hemostasis and produce signs and symptoms different from coagulation factor deficiencies (disorders of secondary hemostasis). (medscape.com)
Refractoriness2
Alloimmunization1
- Platelet transfusion is the most commonly used therapy but has limitations of alloimmunization, availability, and expense. (nih.gov)
Coagulation factors3
- Problems can occur when platelets are low in number or do not work properly or when certain coagulation factors are low or missing. (medlineplus.gov)
- The hemostatic system consists of platelets, coagulation factors, and the endothelial cells lining the blood vessels. (medscape.com)
- Under physiological circumstances, the resistance of the endothelial cell lining to interactions with platelets and coagulation factors prevents thrombosis. (medscape.com)
Pathogen1
- 20. A prospective observational cohort safety study of 5106 platelet transfusions with components prepared with photochemical pathogen inactivation treatment. (nih.gov)
Abstract1
- ABSTRACT We assessed the practicality of using the transfusion Basic Information Sheet (BIS) for data collection, to determine the overall adequacy of physician documentation of blood product transfusion, and to make an audit of the appropriateness of blood product transfusion. (who.int)
Proteins3
- Normal blood clotting involves blood particles, called platelets, and as many as 20 different plasma proteins that layer over the platelets. (medlineplus.gov)
- Platelet activation allows binding of these proteins, which bridges adjacent platelets. (medscape.com)
- The alpha granules contain hemostatic proteins such as fibrinogen, vWf, and growth factors (eg, platelet-derived growth factor and transforming growth factors). (medscape.com)
Patient's1
- isolates from the patient's blood and the platelet bag were indistinguishable by pulsed-field gel electrophoresis (PFGE). (cdc.gov)
Haematological1
- 5. The value of crossmatch tests and panel tests as a screening tool to predict the outcome of platelet transfusion in a non-selected haematological population of patients. (nih.gov)
Willebrand3
- In this issue of Blood , Dunne et al report that platelets from type O subjects bound poorly to von Willebrand factor (VWF) of mixed ABOs under arterial shear stress, as compared with those from non-O subjects. (ashpublications.org)
- Von Willebrand disease and hemorrhagic abnormalities of platelet and vascular function. (medlineplus.gov)
- Platelets play a primary role in this process, interacting with subendothelium-bound von Willebrand factor (vWf) via the membrane glycoprotein (GP) Ib complex. (medscape.com)
Treatments1
- Is there a risk of transfusion‐transmissible infections after percutaneous needle treatments in blood donors? (rodekruis.be)
Fibrinogen1
- On resting platelets, GP IIb/IIIa is unable to bind fibrinogen or vWf. (medscape.com)
Efficacy1
- 17. Therapeutic efficacy of pooled buffy-coat platelet components prepared and stored with a platelet additive solution. (nih.gov)
Bacterial7
- To reduce this risk, AABB (formerly the American Association of Blood Banks) adopted a new standard on March 1, 2004, that requires member blood banks and transfusion services to implement measures to detect and limit bacterial contamination in all platelet components ( 3 ). (cdc.gov)
- This report summarizes two fatal cases of transfusion-associated sepsis in platelet recipients in 2004 and describes results of a 2004 survey of infectious-disease consultants regarding their knowledge of transfusion-associated bacterial infections and the new AABB standard. (cdc.gov)
- Health-care providers should be aware of the new standard and the need for bacterial testing of platelets to improve transfusion safety. (cdc.gov)
- However, health-care providers also should be able to diagnose transfusion-associated infections, because even when testing complies with the new standard, false negatives can occur and fatal bacterial sepsis can result. (cdc.gov)
- Before transfusion, platelets from the unit bag were tested for bacterial contamination with liquid culture media (BacT/Alert ® , BioMerieux Inc., Durham, North Carolina) by using 4 mL in a standard aerobic blood culture bottle and were found to be negative after 5 days' incubation. (cdc.gov)
- To assess clinician experience with transfusion-associated bacterial infections and knowledge of the new AABB standard, the Infectious Diseases Society of America (ISDA) conducted a survey of infectious-disease consultants in the United States. (cdc.gov)
- A total of 143 (36%) respondents reported they were aware that bacterial contamination of platelets is one of the most common infectious risks of transfusion therapy. (cdc.gov)
Recipients2
- The occurrence of the acquired immunodeficiency syndrome (AIDS) in intravenous (IV) drug users, blood transfusion recipients, and persons with hemophilia indicates that parenteral transmission of human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV) occurs via infectious blood or blood products (1). (cdc.gov)
- Currently available practices have nearly eliminated these risks for transfusion recipients and persons with hemophilia (2,3). (cdc.gov)
Reactions4
- 2. Universal leukodepletion of blood components results in a significant reduction of febrile non-hemolytic but not allergic transfusion reactions. (nih.gov)
- 11. Effects of prestorage vs poststorage leukoreduction on the rate of febrile nonhemolytic transfusion reactions to platelets. (nih.gov)
- 15. Analysis of transfusion reactions associated with prestorage-pooled platelet components. (nih.gov)
- This initial interaction (platelet adhesion) sets the stage for other adhesive reactions that allow the platelets to interact with other agonists in the vicinity of vessel injury, such as adenosine 5'-diphosphate (ADP), subendothelial collagen, and thrombin. (medscape.com)
Megakaryocytes1
- 15-deoxy-delta12,14-PGJ2 enhances platelet production from megakaryocytes. (nih.gov)
Subendothelial1
- Second, platelet-VWF interaction is the first step that tethers platelets to the subendothelial matrix exposed at the site of vessel injury to initiate hemostasis. (ashpublications.org)
Count15
- In ITP, your blood does not clot as it should, because you have a low platelet count. (nih.gov)
- When you have a low platelet count, you may have trouble stopping bleeding. (nih.gov)
- This test measures your platelet count and the number of other blood cells in your blood. (nih.gov)
- Most people who have chronic ITP can stop treatment at some point and maintain a safe platelet count. (nih.gov)
- Treatment depends on your platelet count and whether you have any symptoms. (nih.gov)
- In mild cases, you may not need any treatment, and your provider will monitor your condition to make sure that your platelet count does not become too low. (nih.gov)
- If your ITP was caused by an infection, treating the infection may help increase your platelet count and lower your risk of bleeding problems. (nih.gov)
- The PACER trial is an investigator-initiated, national, multicentre, single-blinded, randomised controlled, non-inferior, two-arm trial in haematologic and/or intensive care patients with a platelet count of between 10 and 50 × 10 9 /L and an indication for CVC placement. (biomedcentral.com)
- Platelets are responsible for blood clotting, and when their count becomes too low, it can lead to bleeding in the baby's brain or other organs. (medicalnewstoday.com)
- Its symptoms can depend on how low the platelet count drops. (medicalnewstoday.com)
- Having a low platelet count can be harmful to the infant. (medicalnewstoday.com)
- Therefore, many people do not know they are at risk of having a pregnancy involving this condition until they give birth to a baby with a low platelet count and petechiae. (medicalnewstoday.com)
- This test can help determine whether the platelet count is within typical ranges. (medicalnewstoday.com)
- Platelets help your blood clot, so when the count is low you are at a higher risk of bleeding. (oncolink.org)
- If the platelet count becomes too low, you may receive a transfusion of platelets. (oncolink.org)
Infection3
- We describe HEV infection in a previously healthy man in France who received massive transfusions of blood, plas- ma, and platelets after a traumatic skiing accident. (cdc.gov)
- reported recent travel to HEV endemic areas or intake of This case describes HEV infection acquired by an uncooked or poorly cooked pork or game meat in the 3 immunocompetent patient through transfusion of a con- months before the accident. (cdc.gov)
- It is not known whether any of the individual platelet donors or the patient with leukemia had HTLV-III infection. (cdc.gov)
Patients3
- Preoperative anemia management program reduces blood transfusion in elective cardiac surgical patients, improving outcomes and decreasing hospital length of stay. (rochester.edu)
- The transfusion process and clinical indications for transfusions administered to adult hospitalized patients in 3 tertiary care teaching hospitals in Qazvin were prospectively reviewed. (who.int)
- Le processus de transfusion et les indications cliniques de transfusions sanguines administrées aux patients adultes hospitalisés dans trois hôpitaux universitaires de soins tertiaires à Qazvin ont été étudiés prospectivement. (who.int)
Recipient2
- however, it has been hypothesized that recipient platelets and transfused platelets both play a pathogenic role in TRALI. (lu.se)
- next generation transfusion practices to improve recipient safety. (rochester.edu)
Membrane3
- There are 2 possible locations of ABO epitopes on platelets: the mucin-rich region of GPIbα and membrane glycolipids. (ashpublications.org)
- 7 The alternative to being GPIb anchored, ABO could also be attached to glycolipids on platelet membrane and thus regulate GPIb-VWF interaction by orienting the GPIb-IX-V complex differently. (ashpublications.org)
- In addition, when platelets are activated, negatively charged phospholipids move from the inner to the outer leaflet of the membrane bilayer. (medscape.com)
Donors1
- As part of his job, he processed platelets pooled from individual donors for transfusion. (cdc.gov)
Hemoglobin2
- Endurance athletes have long known that blood transfusions may enhance exercise performance by increasing hemoglobin concentration and allowing for improved oxygen delivery to the cells. (trainingpeaks.com)
- Post-transfusion hemoglobin values and patient blood management. (rodekruis.be)
Interaction2
- Platelets contain 2 receptors that bind VWF: the glycoprotein Ib (GPIb)-IX-V complex and the integrin αIIbβ3, but this ABO effect is likely on the GPIb-VWF interaction, which is regulated by fluid shear stress and exhibits "catch bond" characteristics. (ashpublications.org)
- The 2 potential locations of ABO on platelets could also lead to different mechanisms of regulating GPIb-VWF interaction in flowing blood. (ashpublications.org)
Mechanisms2
- These studies will also need to be validated, and moreover, the platelet-derived lipid-mediated mechanisms leading to TRALI will need to be investigated. (lu.se)
- Once activated, platelets have two major mechanisms to recruit additional platelets to the growing hemostatic plug. (medscape.com)
Effectiveness2
- To obtain data to improve the effectiveness of platelet transfusions in people with PTR and decrease the risk of bleeding in some people. (nih.gov)
- BIS-based information along with data collection can be used to provide feedback regarding the effectiveness of and compliance with local and national transfusion guidelines. (who.int)
Exposure2
- Next to the burden of transfusion exposure, blood products are expensive and scarce. (biomedcentral.com)
- Other modes of transmission for dengue virus are less common but include vertical transmission from a mother to a baby, blood transfusion or organ transplantation, needle stick, mucocutaneous exposure, or hospital or laboratory accidents, breast milk, and rarely, sexual transmission. (cdc.gov)
Demonstrate1
- First, this is the first study to demonstrate that the platelet ABO regulates how GPIb interacts with VWF under hydrodynamic conditions that mimic blood flow. (ashpublications.org)
Outcome1
- The noninferiority of withholding transfusion was not shown for the primary outcome of grade 2 to 4 bleeding," the authors write. (newsazi.com)
Study3
- To study the effects of transfusing platelets more slowly than the standard rate. (nih.gov)
- The treating provider may change the platelet transfusion threshold based on the clinical circumstance, patient population, and/or concurrent primary protocol considerations - similar to the PLADO study. (nih.gov)
- NBS Platelet Study Group. (nih.gov)