Blood Platelets
Platelet Aggregation
Core Binding Factor Alpha 2 Subunit
Megakaryocyte Progenitor Cells
Hemorrhagic Disorders
Bernard-Soulier Syndrome
Thrombasthenia
Platelet Adhesiveness
Pedigree
Genes, Dominant
Platelet Membrane Glycoproteins
Platelet Factor 4
Leukemia, Myeloid, Acute
Serotonin
Adenosine Diphosphate
Platelet Transfusion
Platelet Glycoprotein GPIIb-IIIa Complex
Platelet Glycoprotein GPIb-IX Complex
beta-Thromboglobulin
Platelet Activation
Bipolar Disorder
Platelet Activating Factor
Platelet Function Tests
Liver Failure, Acute
Liver Failure
Liver, Artificial
Acetaminophen
Hepatic Encephalopathy
Analgesics, Non-Narcotic
The gene for May-Hegglin anomaly localizes to a <1-Mb region on chromosome 22q12.3-13.1. (1/259)
The May-Hegglin anomaly (MHA) is an autosomal dominant platelet disorder of unknown etiology. It is characterized by thrombocytopenia, giant platelets, and leukocyte inclusion bodies, and affected heterozygotes are predisposed to bleeding episodes. The MHA gene has recently been localized, by means of linkage analysis, to a 13.6-cM region on chromosome 22, and the complete chromosome 22 sequence has been reported. We recently performed a genome scan for the MHA gene in 29 members of a large, multigenerational Italian family, and we now confirm that the MHA locus is on chromosome 22q12. 3-13.1. The maximal two-point LOD score of 4.50 was achieved with the use of marker D22S283, at a recombination fraction of.05. Haplotype analysis narrowed the MHA critical region to 6.6 cM between markers D22S683 and D22S1177. It is of note that the chromosome 22 sequence allowed all markers to be ordered correctly, identified all the candidate genes and predicted genes, and specifically determined the physical size of the MHA region to be 0. 7 Mb. These results significantly narrow the region in which the MHA gene is located, and they represent the first use of chromosome 22 data to positionally clone a disease gene. (+info)Ultrastructural aspects of interactions of platelets with microcrystalline collagen. (2/259)
Whole blood anticoagulated with EDTA was stirred with high concentrations of a microcrystalline bovine dermal collagen preparation in order to study the interactions of blood cells with collagen at the ultrastructural level. Blood from normal subjects and from patients congenitally deficient in Factors VIII or XII or with thrombasthenia or von Willebrands disease was used. In scanning and transmission electron microscopic studies with blood from normal subjects and patients, platelets were seen to adhere to collagen, develop cell surface undulations, form pseudopods, and undergo morphologic changes suggestive of the release reaction. Although thrombasthenic platelets adhered to collagen, pseudopods formed by these cells were remarkably angulated and nodular. Relatively few von Willebrands platelets adhered to collagen, but those platelets that did adhere underwent the usual sequence of morphologic changes. (+info)Low-density lipoprotein activates the small GTPases Rap1 and Ral in human platelets. (3/259)
Physiological concentrations of low-density lipoprotein (LDL) sensitize blood platelets to alpha-thrombin- and collagen-induced secretion, and after prolonged contact trigger secretion independent of other agonists. Here we report that LDL activates the small GTPases Rap1 and Ral but not Ras, as assessed by specific precipitation of the GTP-bound enzymes. In unstirred suspensions, the inhibitor SB203580 blocks Rap1 activation by 60-70%, suggesting activation via p38 mitogen-activated protein kinase and a second, unidentified route. Inhibitors of cyclooxygenase (indomethacin) and the thromboxane A(2) (TxA(2)) receptor (SQ30741) induce complete inhibition, indicating that Rap1 activation is the result of TxA(2) formation. Stirring reveals a second, TxA(2)-independent Rap1 activation, which correlates quantitatively with a slow induction of dense granule secretion. Both pathways are unaffected by inhibitors of ligand binding to integrin alpha(IIb)beta(3). The results suggest that Rap1 and Ral, but not Ras, may take part in signalling routes initiated by LDL that initially enhance the sensitivity of platelets to other agonists and later trigger LDL-dependent secretion. (+info)Improved platelet counting using two-dimensional laser light scatter. (4/259)
Clinical management of platelet disorders depends on accurate platelet counts. We evaluated a new analytic approach for platelet counting based on improved platelet discrimination. Current automated counting methods provide accurate platelet counts for most samples but often are unable to discriminate platelets accurately from nonplatelet particles such as microcytic RBCs, RBC fragments, and cellular debris that may falsely elevate platelet counts. The new approach measures 2 light-scatter angles of platelets and nonplatelet particles as they pass through a laser beam. The volume and refractive index of each platelet and particle are derived from the light-scatter measurements using the Mie scattering theory. Together, these 2 measurements provide improved platelet discrimination compared with 1-dimensional methods. With its improved discrimination, 2-dimensional platelet analysis provides more accurate platelet counts in samples containing interfering particles and may contribute to more effective clinical management of patients with platelet disorders. (+info)Mediterranean macrothrombocytopenia. (5/259)
Platelet count, platelet size, and circulating platelet biomass concentration estimates made with an erythrocyte-calibrated electronic sizing system on EDTA-anticoagulated blood samples gave population medians and 95% ranges for 145 asymptomatic Mediterranean and 200 healthy Northern European subjects. The Mediterraneans had lower platelet counts [161,000 (89,000-290,000)/mul compared with 219,000 (148,000-323,000)/mul] and higher arithmetic mean volumes [17.8 (10.8-29.2) cu mum compared with 12.4 (9.9-15.6) cu mum], while the individual lognormal platelet size distribution profiles were comparable [geomatric standard deviations of 1.78 (1.60-1.98) against 1.70 (1.54-1.88)]; and the platelet biomass concentrations, given by count per microliter times mean volume times 10- minus 7 and expressed as a volumetric percentage of whole blood, were almost identical [0.286% (0.216%-0.379%) against 0.272% (0.201%-0.367%)]. Mediterranean macrothrombocytopenia is, therefore, considered a benign morphologic variant that requires differentiation from thrombocytopenias in which the circulating platelet biomass concentration is decreased. (+info)A pregnancy complicated with Fechtner syndrome: a case report. (6/259)
A 21-year-old woman was diagnosed with Fechtner syndrome at 15 weeks gestation. She had a familial history of this disorder; her mother, two siblings and maternal grandmother were also affected. She presented with neither bleeding from the genital tract nor symptoms suggestive of placental abruption. Labor progressed uneventfully and resulted in the birth of a healthy female infant weighing 3436 g at 41 weeks of gestation. The puerperium was uneventful for both mother and infant. (+info)Autosomal-dominant giant platelet syndromes: a hint of the same genetic defect as in Fechtner syndrome owing to a similar genetic linkage to chromosome 22q11-13. (7/259)
Families with 3 different syndromes characterized by autosomal dominant inheritance of low platelet count and giant platelets were studied. Fechtner syndrome is an autosomal-dominant variant of Alport syndrome manifested by nephritis, sensorineural hearing loss, and cataract formation in addition to macrothrombocytopenia and polymorphonuclear inclusion bodies. Sebastian platelet syndrome is an autosomal-dominant macrothrombocytopenia combined with neutrophil inclusions that differ from those found in May-Hegglin syndrome or Chediak-Higashi syndrome or the Dohle bodies described in patients with sepsis. These inclusions are, however, similar to those described in Fechtner syndrome. Other features of Alport syndrome, though, including deafness, cataracts, and nephritis, are absent in Sebastian platelet syndrome. Epstein syndrome is characterized by macrothrombocytopenia without neutrophil inclusions, in addition to the classical Alport manifestations-deafness, cataracts, and nephritis-and it is also inherited in an autosomal-dominant mode. We mapped the disease-causing gene to the long arm of chromosome 22 in an Italian family with Fechtner syndrome, 2 German families with the Sebastian platelet syndrome, and an American family with the Epstein syndrome. Four markers on chromosome 22q yielded an LOD score greater than 2.76. A maximal 2-point LOD score of 3.41 was obtained with the marker D22S683 at a recombination fraction of 0.00. Recombination analysis placed the disease-causing gene in a 3.37-Mb interval between the markers D22S284 and D22S693. The disease-causing gene interval in these 3 syndromes is similar to the interval described recently in an Israeli family with a slightly different Fechtner syndrome than the one described here. Recombination analysis of these 3 syndromes refines the interval containing the disease-causing gene from 5.5 Mb to 3.37 Mb. The clinical likeness and the similar interval containing the disease-causing gene suggest that the 3 different syndromes may arise from a similar genetic defect. (+info)Platelets from a patient heterozygous for the defect of P2CYC receptors for ADP have a secretion defect despite normal thromboxane A2 production and normal granule stores: further evidence that some cases of platelet 'primary secretion defect' are heterozygous for a defect of P2CYC receptors. (8/259)
Two unrelated patients with a congenital bleeding diathesis associated with a severe defect of the platelet ADP receptor coupled to adenylate cyclase (P2(CYC)) have been described so far. In one of them, platelet secretion was shown to be abnormal. We recently showed that platelets with the primary secretion defect (PSD; characterized by abnormal secretion but normal granule stores, thromboxane A(2) production, and ADP-induced primary wave of aggregation) have a moderate defect of P2(CYC). Therefore, the interaction of ADP with the full complement of its receptors seems to be essential for normal platelet secretion, and PSD patients may be heterozygotes for the congenital severe defect of P2(CYC). In this study, we describe 2 new related patients with a severe defect of P2(CYC) and the son of one of them, who is to be considered an obligate heterozygote for the defect. The 2 patients with the severe defect had lifelong histories of abnormal bleeding, prolonged bleeding times, abnormalities of platelet aggregation and secretion, lack of inhibition of adenylate cyclase by ADP, and a deficiency of platelet-binding sites for [(33)P]2 MeS-ADP (240 and 225 sites per platelet; normal range, 530 to 1102). The son of one of them had a mildly prolonged bleeding time and abnormalities of platelet aggregation and secretion similar to those found in patients with PSD. In addition, his platelets showed a moderate defect of binding sites for [(33)P]2 MeS-ADP (430 sites per platelet) and of adenylate cyclase inhibition by ADP. This study of a family with the platelet disorder characterized by a defect of the platelet P2(CYC) receptor supports our hypothesis that the full complement of the platelet ADP receptors is essential for normal platelet secretion and that some patients with the common, ill-defined diagnosis of PSD are actually heterozygous for the defect. (+info)Some common types of blood platelet disorders include:
1. Thrombocytopenia: This is a condition in which there are too few platelets in the blood. It can be caused by a variety of factors, including autoimmune disorders, bone marrow disorders, and certain medications.
2. Bernard-Soulier syndrome: This is a rare inherited disorder that affects the function of platelets and causes easy bruising and prolonged bleeding.
3. Glanzmann's thrombasthenia: This is a rare inherited disorder that affects the platelets' ability to clot properly, leading to excessive bleeding.
4. Platelet dysfunction: This can be caused by a variety of factors, including certain medications, infections, and autoimmune disorders. It can lead to excessive bleeding or prolonged bleeding after injury or surgery.
5. Congenital amegakaryocytic thrombocytopenia: This is a rare inherited disorder that affects the development of platelets in the bone marrow, leading to a lack of platelets in the blood.
6. Grey platelet syndrome: This is a rare inherited disorder that affects the structure of platelets, making them more prone to rupture and lead to easy bruising and prolonged bleeding.
7. Platelet-type von Willebrand disease: This is a mild bleeding disorder caused by a deficiency of von Willebrand factor, a protein that helps platelets stick together to form clots.
8. acquired platelet dysfunction: This can be caused by various conditions such as infections, medications, and autoimmune disorders.
These disorders can be diagnosed through blood tests, including a complete blood count (CBC) and a platelet function test. Treatment options vary depending on the specific disorder and may include medication, surgery, or lifestyle changes.
There are several types of hemorrhagic disorders, including:
1. Hemophilia: A genetic disorder that affects the blood's ability to clot and stop bleeding. People with hemophilia may experience spontaneous bleeding or bleeding after injury or surgery.
2. von Willebrand disease: A mild bleeding disorder caused by a deficiency of a protein called von Willebrand factor, which is important for blood clotting.
3. Platelet disorders: Disorders that affect the platelets, such as thrombocytopenia (low platelet count) or thrombocytosis (high platelet count).
4. Bleeding and clotting disorders caused by medications or drugs.
5. Hemorrhagic stroke: A type of stroke that is caused by bleeding in the brain.
6. Gastrointestinal bleeding: Bleeding in the digestive tract, which can be caused by a variety of factors such as ulcers, inflammation, or tumors.
7. Pulmonary hemorrhage: Bleeding in the lungs, which can be caused by a variety of factors such as pneumonia, injury, or tumors.
8. Retinal hemorrhage: Bleeding in the blood vessels of the retina, which can be caused by high blood pressure, diabetes, or other eye disorders.
Symptoms of hemorrhagic disorders can vary depending on the specific condition and the location of the bleeding. Common symptoms include bruising, petechiae (small red spots on the skin), nosebleeds, gum bleeding, and heavy menstrual periods. Treatment for hemorrhagic disorders depends on the underlying cause and may include medications, blood transfusions, or surgery.
The syndrome is caused by mutations in the ITGA2B gene, which encodes a protein called integrin alpha-IIb. This protein is essential for platelet adhesion and aggregation, which are important steps in the formation of blood clots. Individuals with BSS may experience mild to severe bleeding, including spontaneous bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding after injury or surgery.
The symptoms of BSS can vary in severity and may include:
1. Mild to moderate bleeding episodes, which may be spontaneous or triggered by trauma or surgery.
2. Prolonged bleeding after injury or surgery.
3. Easy bruising, especially in the extremities (hands and feet).
4. Petechiae (small red or purple spots on the skin).
5. Nosebleeds.
6. Gingival bleeding (bleeding from the gums).
7. Post-injury bleeding.
8. Prolonged bleeding after dental extractions or other medical procedures.
9. Bleeding into the joints (hemarthrosis).
BSS is diagnosed based on a combination of clinical findings, laboratory tests, and genetic analysis. Treatment for BSS typically involves platelet transfusions and/or medications to improve platelet function. In severe cases, liver or bone marrow transplantation may be considered.
The prognosis for BSS varies depending on the severity of the disorder and the presence of other medical conditions. In general, individuals with mild forms of the syndrome may experience few complications and can lead relatively normal lives. However, those with more severe forms of the disorder may have a higher risk of bleeding complications and may require more frequent platelet transfusions or other treatments to manage their condition.
Genetic counseling is important for individuals with BSS, as the disorder can be inherited in an autosomal dominant manner. This means that a single copy of the mutated gene can cause the condition, and each child of an affected parent has a 50% chance of inheriting the mutation. Family members may wish to consider genetic testing to determine their risk of developing BSS.
Overall, BSS is a rare but potentially serious bleeding disorder that requires careful management and monitoring to prevent complications. With appropriate treatment and support, individuals with BSS can lead fulfilling lives and manage their condition effectively.
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 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.
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.
Bipolar Disorder Types:
There are several types of bipolar disorder, including:
1. Bipolar I Disorder: One or more manic episodes with or without depressive episodes.
2. Bipolar II Disorder: At least one major depressive episode and one hypomanic episode (a less severe form of mania).
3. Cyclothymic Disorder: Periods of hypomania and depression that last at least 2 years.
4. Other Specified Bipolar and Related Disorders: Symptoms that do not meet the criteria for any of the above types.
5. Unspecified Bipolar and Related Disorders: Symptoms that do not meet the criteria for any of the above types, but there is still a noticeable impact on daily life.
Bipolar Disorder Causes:
The exact cause of bipolar disorder is unknown, but it is believed to involve a combination of genetic, environmental, and neurobiological factors. Some potential causes include:
1. Genetics: Individuals with a family history of bipolar disorder are more likely to develop the condition.
2. Brain structure and function: Imbalances in neurotransmitters and abnormalities in brain structure have been found in individuals with bipolar disorder.
3. Hormonal imbalances: Imbalances in hormones such as serotonin, dopamine, and cortisol have been linked to bipolar disorder.
4. Life events: Traumatic events or significant changes in life circumstances can trigger episodes of mania or depression.
5. Medical conditions: Certain medical conditions, such as multiple sclerosis or stroke, can increase the risk of developing bipolar disorder.
Bipolar Disorder Symptoms:
The symptoms of bipolar disorder can vary depending on the individual and the specific type of episode they are experiencing. Some common symptoms include:
1. Manic episodes: Increased energy, reduced need for sleep, impulsivity, and grandiosity.
2. Depressive episodes: Feelings of sadness, hopelessness, and loss of interest in activities.
3. Mixed episodes: A combination of manic and depressive symptoms.
4. Hypomanic episodes: Less severe than full-blown mania, but still disrupt daily life.
5. Rapid cycling: Experiencing four or more episodes within a year.
6. Melancholic features: Feeling sad, hopeless, and worthless.
7. Atypical features: Experiencing mania without elevated mood or grandiosity.
8. Mood instability: Rapid changes in mood throughout the day.
9. Anxiety symptoms: Restlessness, feeling on edge, and difficulty concentrating.
10. Sleep disturbances: Difficulty falling or staying asleep, or oversleeping.
11. Substance abuse: Using drugs or alcohol to cope with symptoms.
12. Suicidal thoughts or behaviors: Having thoughts of harming oneself or taking actions that could lead to death.
It's important to note that not everyone with bipolar disorder will experience all of these symptoms, and some people may experience additional symptoms not listed here. Additionally, the severity and frequency of symptoms can vary widely between individuals.
Causes:
1. Viral hepatitis (hepatitis A, B, or C)
2. Overdose of medications or supplements
3. Toxic substances (e.g., alcohol, drugs, or chemicals)
4. Sepsis or other infections that spread to the liver
5. Certain autoimmune disorders (e.g., hemochromatosis, Wilson's disease)
6. Cancer that has metastasized to the liver
7. Blood vessel blockage or clotting in the liver
8. Lack of blood flow to the liver
Symptoms:
1. Jaundice (yellowing of skin and eyes)
2. Nausea and vomiting
3. Abdominal swelling and discomfort
4. Fatigue, weakness, and loss of appetite
5. Confusion or altered mental state
6. Seizures or coma
7. Pale or clay-colored stools
8. Dark urine
Diagnosis:
1. Physical examination and medical history
2. Laboratory tests (e.g., liver function tests, blood tests, imaging studies)
3. Biopsy of the liver tissue (to rule out other liver diseases)
Treatment:
1. Supportive care (fluids, nutrition, and medication to manage symptoms)
2. Addressing underlying causes (e.g., stopping alcohol or drug use, treating infections)
3. Transjugular intrahepatic portosystemic shunt (TIPS), a procedure that creates a new pathway for blood to flow through the liver
4. Liver transplantation (in severe cases where other treatments have failed)
Prognosis:
The prognosis for acute liver failure depends on the underlying cause of the condition and the severity of the liver damage. In general, the earlier the diagnosis and treatment, the better the outcome. However, acute liver failure can be a life-threatening condition, and the mortality rate is high, especially in cases where there is severe liver damage or no available donor liver for transplantation.
There are several causes of liver failure, including:
1. Alcohol-related liver disease: Prolonged and excessive alcohol consumption can damage liver cells, leading to inflammation, scarring, and eventually liver failure.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver, leading to liver failure.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, leading to inflammation and scarring.
4. Drug-induced liver injury: Certain medications can cause liver damage and failure, especially when taken in high doses or for extended periods.
5. Genetic disorders: Certain inherited conditions, such as hemochromatosis and Wilson's disease, can cause liver damage and failure.
6. Acute liver failure: This is a sudden and severe loss of liver function, often caused by medication overdose or other toxins.
7. Chronic liver failure: A gradual decline in liver function over time, often caused by cirrhosis or NAFLD.
Symptoms of liver failure can include:
1. Jaundice (yellowing of the skin and eyes)
2. Fatigue
3. Loss of appetite
4. Nausea and vomiting
5. Abdominal pain
6. Confusion and altered mental state
7. Easy bruising and bleeding
Diagnosis of liver failure is typically made through a combination of physical examination, medical history, and laboratory tests, such as blood tests to check for liver enzymes and bilirubin levels. Imaging tests, such as ultrasound and CT scans, may also be used to evaluate the liver.
Treatment of liver failure depends on the underlying cause and severity of the condition. In some cases, a liver transplant may be necessary. Other treatments may include medications to manage symptoms, such as nausea and pain, and supportive care to maintain nutrition and hydration. In severe cases, hospitalization may be required to monitor and treat complications.
Prevention of liver failure is important, and this can be achieved by:
1. Avoiding alcohol or drinking in moderation
2. Maintaining a healthy weight and diet
3. Managing underlying medical conditions, such as diabetes and high blood pressure
4. Avoiding exposure to toxins, such as certain medications and environmental chemicals
5. Getting vaccinated against hepatitis A and B
6. Practicing safe sex to prevent the spread of hepatitis B and C.
This condition is most commonly seen in people with advanced liver disease, such as cirrhosis or liver cancer. It can also be caused by other conditions that affect the liver, such as hepatitis or portal hypertension.
Symptoms of hepatic encephalopathy can include confusion, disorientation, slurred speech, memory loss, and difficulty with coordination and balance. In severe cases, it can lead to coma or even death.
Diagnosis of hepatic encephalopathy is typically made through a combination of physical examination, medical history, and diagnostic tests such as blood tests and imaging studies. Treatment options include medications to reduce the production of ammonia in the gut, antibiotics to treat any underlying infections, and transjugular intrahepatic portosystemic shunt (TIPS) to improve liver function. In severe cases, a liver transplant may be necessary.
Overall, hepatic encephalopathy is a serious condition that can have significant impact on quality of life and survival in people with advanced liver disease. Early detection and prompt treatment are essential to prevent complications and improve outcomes.
The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:
"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."
The ICDCR definition includes several key features of DILI, including:
1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).
The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.
Lymphocyte
Quebec platelet disorder
FCGR2A
Giant platelet disorder
Mean platelet volume
Uterine atony
MYH9
Blood
May-Hegglin anomaly
Scott syndrome
Hermansky-Pudlak syndrome
Noonan syndrome
List of diseases (B)
Eltrombopag
Josh Phegley
MMRV vaccine
Quebec (disambiguation)
MHA
Heavy menstrual bleeding
GP1BB
Blood vessel disorder
Hematologic disease
Post-transplant lymphoproliferative disorder
Harris platelet syndrome
Fostamatinib
Hemolytic-uremic syndrome
Multimerin 1
Platelet
Multiple electrode aggregometry
Anorexia nervosa
Proto-oncogene tyrosine-protein kinase Src
Strømme syndrome
Rocky Mountain spotted fever
THPO
Nephron
Thromboxane-A synthase
Lyme disease
Doxepin
Singapore Cord Blood Bank
Factor XIII
Interleukin 3
Waldenström macroglobulinemia
Acid sphingomyelinase
Hemolysis
Allogeneic processed thymus tissue
Seasonal effects on suicide rates
Primary effusion lymphoma
Childhood immunizations in the United States
Platelet storage pool deficiency
Cervical artery dissection
Pearson syndrome
Diamond-Blackfan anemia
Vaccine hesitancy
Iranian Blood Transfusion Organization
Multiple organ dysfunction syndrome
Sex differences in human physiology
Ken Strauss
Glutamate-rich protein 3
Diffuse proliferative nephritis
Lipid signaling
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Thrombocytopenia15
- Immune thrombocytopenia (ITP) is an organ-specific autoimmune disease, which is characterized by decreased platelet count and skin and mucosal bleeding. (clinicaltrials.gov)
- Thrombocytopenia caused by hypersplenism, platelet destruction, or surgery/hemodilution. (medlineplus.gov)
- Thrombocytopenia is a common feature of hemorrhagic fevers and vascular permeability disorders ( 8 ), but the decrease in platelet counts in acute LF is not low enough to cause spontaneous hemorrhage. (cdc.gov)
- ABSTRACT: Thrombocytopenia is a common hematological disorder characterized by abnormally low number of platelets in circulating blood from multiple causes. (scirp.org)
- Immune disorders such as idiopathic thrombocytopenic purpura (ITP) or immune thrombocytopenia . (clevelandclinic.org)
- Patients with a bleeding disorder called immune thrombocytopenia (ITP) are at risk for blood loss if they need to have surgery. (blood.ca)
- Thrombocytopenia is any disorder in which there are not enough platelets. (vaccineinjuryhelpcenter.com)
- A common clinical finding in benzene hematotoxicity is cytopenia, which is a decrease in various cellular elements of the circulating blood manifested as anemia, leukopenia, or thrombocytopenia in humans and in animals. (cdc.gov)
- thrombocytopenia, platelet disorder, dengue fever. (bvsalud.org)
- Thrombocytopenia is a hematologic disorder that is characterized by a markedly decreased number of circulating blood platelets. (bvsalud.org)
- In March 2021, fol owing reports of rare blood coagulation disorders in a few individuals who had received the AZ vaccine in Europe, the WHO's Global Advisory Committee on Vaccine Safety (GACVS) and European Medicines Agency (EMA) reviewed al available information and data on thromboembolic events (blood clots) and thrombocytopenia (low platelets) after vaccination. (who.int)
- Thrombocytopenia (platelet count less than 150,000/µl) is commonly encountered in routine hematological investigations. (who.int)
- Aim: Calculate the prevalence of various conditions causing thrombocytopenia, in cases referred for bone marrow examination, and Understand the various megakaryocytic alterations in hematological disorders presenting with thrombocytopenia due to different mechanisms. (who.int)
- All cases of thrombocytopenia (platelet count less than 1,50,000/µl) diagnosed on hematology analyzer and later confirmed by peripheral blood film examination, referred for bone marrow examination for various reasons were included in this study. (who.int)
- Conclusion: Further studies on the evaluation of megakaryocytic alteration and their contribution to thrombocytopenia can provide growing knowledge to the pathogenesis of numerous hematopoietic disorders that may identify broader clinical applications of the newer strategies to regulate platelet count and functioning. (who.int)
Coagulation Disorders1
- The inherited deficiency of factor VII (FVII), the crucial enzyme triggering blood coagulation, 1 is the most common of the rare coagulation disorders transmitted in an autosomal recessive manner. (haematologica.org)
Bone marrow5
- The fundamental mechanisms involved are: ineffective production of platelets by the bone marrow, accerlated destruction of platelets or platelet splenic sequestration. (scirp.org)
- This disorder is characterized by reduction of all cellular elements in the peripheral blood and in bone marrow, leading to fibrosis, an irreversible replacement of bone marrow. (cdc.gov)
- A reduction in platelet number or function can occur through a variety of mechanisms, including autoimmune destruction, spleen sequestration, bone marrow infiltration by tumor cells, infection (e.g. dengue fever), and adverse drug reaction. (bvsalud.org)
- Records regarding the clinical indication for the procedure, peripheral blood smear reports, blood counts and significant findings on bone-marrow aspiration smears were retrieved. (who.int)
- The role of bone-marrow aspiration in the diagnosis of hematological and non- hematological disorders was reviewed in the study. (who.int)
Counts6
- Blood disorders, such as low platelet counts or anemia. (everythingnaturalpa.com)
- A person with thrombocytopenic purpura has low platelet counts. (clevelandclinic.org)
- Spontaneous clinical hemorrhages are usually not observed until platelet counts fall below 30x10 3 /mm 3 . (bvsalud.org)
- Deep red to black hemorrhagic bullae may occur with very low platelet counts 3 . (bvsalud.org)
- Blood erythrocyte counts returned to normal by 7 months. (cdc.gov)
- No significant changes occurred in leukocyte or platelet counts. (cdc.gov)
Thrombosis1
- If MPN patients are also considered to be cancer patients in many countries, the pathophysiology of thrombosis is quite specific (hyperviscosity, platelet abnormalities, clonality, specific cytokines…) and they are exposed to a lower risk of digestive hemorrhages. (clinicaltrials.gov)
Abnormalities2
- Disorders caused by abnormalities in platelet count or function. (bvsalud.org)
- Inherited bleeding disorders are heterogeneous in aetiology and bleeds[9,10] with clotting factor concentrate (CFC) replacement therapy, clinical presentation and may arise from platelet, blood vessel or administered by intravenous infusion and therefore requiring specific clotting factor structural or functional abnormalities. (who.int)
Antibodies5
- This blood test shows if you have antibodies against platelets in your blood. (medlineplus.gov)
- Sometimes the body may produce antibodies that affect its own platelets. (medlineplus.gov)
- In the case of anti-platelet antibodies, your body creates antibodies that attack or coat your own platelets. (medlineplus.gov)
- This means that you do not have anti-platelet antibodies in your blood. (medlineplus.gov)
- Abnormal results show that you have anti-platelet antibodies. (medlineplus.gov)
Transfusions1
- Educational and preventive measures, few hemostatic drugs, platelet transfusions, thrombopoietin receptor agonists, and in life-threatening IPDs, allogeneic hematopoietic stem cell transplantation are therapeutic possibilities. (fwgbd.org)
Clot3
- Platelets are particles in the blood that help the blood clot. (medlineplus.gov)
- Platelets help your blood clot and prevent severe bleeding. (clevelandclinic.org)
- Because their blood doesn't clot as it should, ITP patients are commonly treated before surgery with intravenous immune globulin (IVIg), which helps their blood clot by increasing the number of platelets. (blood.ca)
Vessel2
- Platelet and blood vessel disorders. (medlineplus.gov)
- Poor blood vessel health (weak, fragile or inflamed blood vessels). (clevelandclinic.org)
Destruction1
- ITP is a kind of disease with increased platelet destruction and impaired platelet production caused by autoimmunity. (clinicaltrials.gov)
Dysfunction2
- The impaired homeostasis and platelet dysfunction implicate alterations in the protein C pathway, which might contribute to the loss of endothelial barrier function in fatal infections. (cdc.gov)
- Consequently, disorders accompanied by insufficiencies of platelet number or platelet dysfunction may contribute to pathologic bleeding states 1 . (bvsalud.org)
Anemia3
- A female showed a clinical spectrum of decreasing platelet count along with anemia due to oral ingestion of hair dye. (scirp.org)
- Checks for anemia, infections and other blood disorders. (wyominghealthfairs.com)
- Benzene also causes a life-threatening disorder called aplastic anemia in humans and animals. (cdc.gov)
Antibody2
- An autoimmune disorder screening, ANA is a type of auto-antibody that attacks proteins inside your cells. (wyominghealthfairs.com)
- The IgM antibody response to sheep red blood cells (SRBC) was significantly increased at 0.75% - but not at the higher concentrations - in the spleen and serum. (cdc.gov)
Hematological disorder1
- Based on the clinical examination, hematological disorder due to dengue fever was chiefly considered, while differential diagnoses included oral squamous cell carcinoma of tongue and buccal mucosa and other infections like influenza, measles, rubella and bacterial sepsis. (bvsalud.org)
Count6
- Inherited platelet disorders (IPDs), affecting either platelet count or platelet functions, comprise a heterogenous group of about sixty rare diseases caused by molecular anomalies in many culprit genes. (fwgbd.org)
- The molecular diagnostic rate was determined by the clinical phenotype , with an overall rate of 49.2% for all thrombotic, coagulation, platelet count , and function disorder patients and a rate of 3.2% for patients with unexplained bleeding disorders characterized by normal hemostasis test results. (bvsalud.org)
- This test is often ordered because you have a bleeding problem or a low platelet count. (medlineplus.gov)
- A complete blood count of red and white blood cells, platelet levels, hemoglobin and hematocrit. (wyominghealthfairs.com)
- A platelet count of 150-450x10 3 / mm 3 is considered normal 2 . (bvsalud.org)
- Hematological examinations revealed platelet level less than 40,000/mm 3 , along with decrease in level of hemoglobin, red blood cells count, packed cell volume and erythrocyte sedimentation rate. (bvsalud.org)
Transfusion10
- The increasing prevalence of chronic disorders is notably driving the market growth, although factors such as risks associated with blood transfusion may impede the market growth. (technavio.com)
- Blood group testing is required for cancer patients as they may require blood transfusion for the treatment. (technavio.com)
- The risks associated with blood transfusion will be a major challenge for the market during the forecast period. (technavio.com)
- Blood transfusion plays a major role in replacing the blood lost during surgeries, injuries, or due to chemotherapy drug effects among cancer patients. (technavio.com)
- Some of the risks and complications associated with blood transfusion include acute immune hemolytic reaction, wherein the immune system attacks the transfused RBCs if the donor blood type is not a good match. (technavio.com)
- But a study published in The Lancet Haematology and led by Dr. Donald Arnold, director of the McMaster Centre for Transfusion Research, shows that an oral medication that stimulates the production of platelets, called eltrombopag, is an effective alternative to IVIg for this patient group. (blood.ca)
- MCTR receives funding support from Canadian Blood Services through the Transfusion Medicine Research Program Support Award. (blood.ca)
- Through discovery, development and applied research, Canadian Blood Services drives world-class innovation in blood transfusion, cellular therapy and transplantation-bringing clarity and insight to an increasingly complex healthcare future. (blood.ca)
- When a person is in dire need of blood, a blood transfusion seems like a simple solution. (blood.ca)
- Patient had suffered from dengue fever six months before, for which she had undergone blood transfusion, as per her previous medical reports. (bvsalud.org)
Spleen2
- Exposure to the high dose (3.0%) also produced a significant increase in spleen weights and number of platelets. (cdc.gov)
- and increased breakdown of platelets in the spleen or liver (called extravascular). (vaccineinjuryhelpcenter.com)
Diseases1
- Hence, the rise in the prevalence of chronic diseases, coupled with the demand for early diagnosis through blood grouping, has significantly led to the growth of the market. (technavio.com)
Patients8
- Diagnostic high-throughput sequencing of 2396 patients with bleeding, thrombotic, and platelet disorders. (bvsalud.org)
- We have sequenced 2396 index patients using the ThromboGenomics HTS panel test of diagnostic-grade genes known to harbor variants associated with rare bleeding , thrombotic, or platelet disorders (BTPDs). (bvsalud.org)
- The preliminary results show that 50% of patients in the treatment ≥ 12 weeks and the initial dose is 400 mg BID group have reached the primary endpoint and maintained platelet response. (clinicaltrials.gov)
- In Sierra Leone during 2015-2018, we assessed LF patients' day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function. (cdc.gov)
- Effect of erucic acid on platelets in patients with adrenoleukodystrophy. (rxlist.com)
- Blood products such as platelets used for treating cancer patients have a short shelf life, which increases their demand. (technavio.com)
- Patients with platelet-mediated disorders often present clinical manifestations of bruising and bleeding. (bvsalud.org)
- Optimal care of patients with inherited bleeding disorders requires that bleeding episodes are treated early, or still better prevented, through extension of patient care beyond hospital-based treatment to home-based therapy. (who.int)
Hemostasis2
- Platelets play a major role in hemostasis as ppwell as in many other physiological and pathological processes. (fwgbd.org)
- Platelets or thrombocytes are a critical component of vascular 'plugs' that form during hemostasis to limit blood loss secondary to vascular damage. (bvsalud.org)
Hematology1
- In 2016, the European Hematology Association (EHA) published the EHA Roadmap for European Hematology Research1 aiming to highlight achievements in the diagnostics and treatment of blood disorders, and to better inform European policy makers and other stakeholders about the urgent clinical and scientific needs and priorities in the field of hematology. (univr.it)
Purpura10
- Mucocutaneous bleeding diathesis (epistaxis, gum bleeding, purpura, menorrhagia), but also multisystemic disorders and/or malignancy comprise the clinical spectrum of IPDs. (fwgbd.org)
- Purpura causes red, purple or brown blood spots on your skin. (clevelandclinic.org)
- Purpura may resemble a bruise or look like a spot of blood under your skin. (clevelandclinic.org)
- Purpura can also be caused by drug interactions, vitamin deficiencies or congenital disorders. (clevelandclinic.org)
- Purpura is commonly referred to as a blood spot under your skin. (clevelandclinic.org)
- The two main types of purpura are related to blood platelet levels . (clevelandclinic.org)
- A person with nonthrombocytopenic purpura has platelet levels in a normal range. (clevelandclinic.org)
- The cause of purpura isn't related to your platelet level. (clevelandclinic.org)
- This type of purpura happens when our blood vessels become weak. (clevelandclinic.org)
- Regardless of the cause, platelet disorders typically manifest with petechiae, purpura, and bleeding of the mucous membranes 3 . (bvsalud.org)
Deficiency2
- decreased red blood cells and deficiency in oxygen and body tissues hypoxia. (slideshare.net)
- Crohn's disease is a chronic inflammatory bowel disease that causes inflammation of the lining of the intestines This inflammation can come and go throughout a person's life While it has been said that Crohn's disease is an autoimmune disorder there is no evidence to support the claim that it is an immune system deficiency. (usa-good.com)
Inflammation2
- Inflammation of your blood vessels ( vasculitis ). (clevelandclinic.org)
- An elevated CRP is a marker of inflammation and can help to evaluate risk of cardiovascular disease, inflammatory disorders or infections. (wyominghealthfairs.com)
Clots1
- Your blood over clots because proteins that control blood clotting are overactive. (clevelandclinic.org)
Placental blood flow2
- impaired placental blood flow, which then presentation after 20 weeks gestation with induces the release of a critical placental sustained and elevated blood pressure (BP) substance into the maternal circulation. (who.int)
- Pre-eclampsia occurs in 2 phases: abnormal implantation of the placenta leads to impaired placental blood flow, which then induces the release of a critical placental substance into the maternal circulation. (who.int)
Abnormal1
- 70%. Severe cases exhibit abnormal coagulation, endothelial barrier disruption, and dysfunctional platelet aggregation but the underlying mechanisms remain poorly understood. (cdc.gov)
Genes1
- PID/IEI disorders can be caused by defects inside the genes that control the immune gadget, and may be inherited. (usa-good.com)
Infections2
- Primary immunodeficiency disorders - additionally referred to as number one immune issues or primary immunodeficiency - weaken the immune gadget, allowing infections and other health troubles to arise more easily. (usa-good.com)
- disorders Primary immunodeficiency disorders are a family of genetic disorders that prevent the immune system from functioning correctly The immune system is a complex system made up of many different cells tissues and organs It works hard to protect people against everyday germs that can make you sick When a person has an immunodeficiency disorder the immune system cannot fight off germs bacteria or infections like it should. (usa-good.com)
20191
- Blood;134(23): 2082-2091, 2019 12 05. (bvsalud.org)
Reduction1
- Benzene- associated cytopenias vary and may involve a reduction in one (unicellular cytopenias) to all three (pancytopenia) cellular elements of the blood. (cdc.gov)
Liver1
- Evaluation of the Patient With a Liver Disorder History and physical examination often suggest a cause of potential liver disorders and narrow the scope of testing for hepatic and biliary disorders. (merckmanuals.com)
Hemoglobin1
- Shows size of red blood cells and hemoglobin concentration. (wyominghealthfairs.com)
Infection2
Function1
- Drugs or medications that affect platelet function or clotting. (clevelandclinic.org)
Hemorrhagic1
- In this report, we describe a patient who presented isolated oral features of hemorrhagic bullae with bleeding, indicative of a bleeding disorder. (bvsalud.org)
Production1
- Accordingly, production of about 10 11 platelet per day as well as appropriate survival and functions are life essential events. (fwgbd.org)
Chronic3
- Chronic lymphocytic leukemia (CLL) is a type of blood cancer. (medicalnewstoday.com)
- One of the key factors driving growth in the market is the increasing prevalence of chronic disorders. (technavio.com)
- The most characteristic systemic effect resulting from intermediate and chronic benzene exposure is arrested development of blood cells. (cdc.gov)
Donor2
Nutrient1
- Detects B12 and folate nutrient levels necessary for normal red blood cell (RBC) and white blood cell (WBC) formation and repair of tissues and cells. (wyominghealthfairs.com)
Treatment3
- When you have a complete response, the treatment lowered cancer cells to a level that blood tests couldn't detect. (medicalnewstoday.com)
- Dr. Arnold explains that in Canada, IVIg is provided to hospitals by Canadian Blood Services, but it is an expensive treatment option. (blood.ca)
- Blood plasma-derived IVIg holds promise as a treatment for Alzheimer's disease. (blood.ca)
Moderate1
- When the needle is inserted to draw blood, some people feel moderate pain. (medlineplus.gov)
Laboratory2
- Do not miss the laboratory blood tests that your doctor may ask you to have done. (who.int)
- This testing is obtained through one vial of blood sent to the laboratory to identify individuals, who have been exposed to the virus. (wyominghealthfairs.com)
Normal1
- As a result, you will have a lower than normal number of platelets in your body. (medlineplus.gov)
Disease2
- It is also imperative for doctors and surgeons to identify the biochemical composition of blood group antigens of the patient to establish a relationship between the blood type biochemistry and the risk of disease to identify druggable targets. (technavio.com)
- Primary immunodeficiency is also known as primary immunodeficiency disease or disorder (or PIDD). (usa-good.com)
Donors1
- The questionnaire is used by most U.S. blood centers to screen potential blood donors. (cdc.gov)
Levels4
- Our research report extensively covers external factors influencing the parent market growth potential in the coming years, which will determine the levels of growth of the blood-grouping reagents market during the forecast period. (technavio.com)
- A screening that reflects average blood sugar levels for the past two to three months. (wyominghealthfairs.com)
- Early biomarkers of exposure to relatively low levels of benzene include depressed numbers of one or more of the circulating blood cell types. (cdc.gov)
- There was no reopening after the ductal closure during the hospital stay or in the follow-up visits in either group and no excessive increases in the blood urea nitrogen or serum creatinine levels were observed. (who.int)
