platelet

[xuè xi ǎ o b ǎ n]

Visible components in blood

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Platelets mature from bone marrow Megakaryocyte Cytoplasm Splitting and falling off small pieces Cytoplasm 。 Although megakaryocytes in bone marrow Hematopoietic cells The smallest number in the Total number of bone marrow nucleated cells 0.05%, but the platelets it produces are extremely important for the hemostatic function of the body. In case of blood loss due to vascular trauma, the functional activities of platelets in the process of physiological hemostasis can be roughly divided into two stages: the first stage is mainly that after the trauma, platelets quickly adhere to the trauma and form a cluster to form a soft hemostatic embolus; The second section is mainly to promote blood coagulation and form a solid hemostatic embolus.^[1]

Chinese name: platelet
Foreign name: platelet
Essence: One part of mammalian blood
Quantity: (100~300) × 10 ^ 9/L

Features: Plasma membrane, without nuclear structure^[2]
Discovery time: 1882
Discoverer: Italian physician J.B. Bizozero
physiological function: Helps stop bleeding and form thrombus

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Activated platelets

Until 1882, Italian physician J B. Bizozero found them in Vascular injury The name of platelet was proposed for the first time because it played an important role in the process of hemostasis. low grade vertebrate Cyclostomata yes spindle The cells act as coagulants, Fishes Start with specific Thrombocyte 。 There are thrombocytes in the blood of amphibians, reptiles and birds nucleus Its function is similar to that of platelets. invertebrate There is no specific thrombocyte, such as Molluscs The deformable cells of T cell have both defensive and wound healing functions. Crustacea only one kind blood corpuscle It also has the function of coagulation.

Platelets are disc shaped, with diameters ranging from 1~4 μ m to 7~8 μ m, and individual differences are great (5~12 cubic μ m). Platelets can move and deform, so they appear to be polymorphic when observed by general methods. Platelets have a complex structure. In short, from outside to inside, there are three layers, namely adventitia , unit membrane and under membrane Microfilament The periphery of the structure is the first floor; The second layer is Gelatinous layer The structure of microfilaments and microtubules parallel to the surrounding area was observed under the electron microscope; The third layer is the micro organ layer, with mitochondria, compact bodies and residual nuclei Isostructure 。

Activated platelet color electron microscope

Platelet normal value: (100 to 300) × 10 ^ 9/L.

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platelet count The concept of Counting unit The normal value of platelet count is 125~320 × 10 ^ 9/L. Thrombocytopenia is caused by Bleeding time Prolongation, severe injury or in the state of stress may lead to bleeding. When the platelet count is<50 × 10 ^ 9/L, slight injury may cause Skin mucosa Purpura , bleeding may occur after operation; When the platelet count is less than 20 × 10 ^ 9/L spontaneity Bleeding. It is generally believed that when the platelet count is less than 20 × 10 ^ 9/L, prophylactic platelet transfusion is required. If the platelet count is>50 × 10 ^ 9/L and the platelet function is normal, no obvious bleeding will occur during the operation.

1． Thrombocytosis : When the platelet count is greater than 400 × 10 ^ 9/L, it is thrombocytosis, Primary Thrombocytosis is common in Myeloproliferative disease , such as Chronic myeloid leukemia , authenticity red blood cell Hypertrophy, Primary thrombocytosis Etc; Thrombocytosis Common in emergencies chronic inflammation ， iron-deficiency anemia and cancer In patients, such increase generally does not exceed 500 × 10 ^ 9/L. After treatment, the condition improves, and the number of platelets will soon fall to the normal level. splenectomy After that, the platelet will rise significantly, often higher than 600 × 10 ^ 9/L, and then slowly decline to the normal range.

2． Thrombocytopenia ： When the platelet count is less than 100 × 10 ^ 9/L, it means thrombocytopenia, which is common in Thrombopoiesis Obstacles, such as Aplastic anemia ， acute leukemia ， Acute radiation sickness Etc; Increased platelet destruction, such as Primary thrombocytopenic purpura ， Hypersplenism ， Gaucher disease Etc., excessive consumption such as Diffuse intravascular coagulation , familial thrombocytopenia such as Giant platelet syndrome Etc.

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Generation process

platelet

From bone marrow Hematopoietic tissue In Megakaryocyte Generate. multi-function Hematopoietic stem cells After directional differentiation in hematopoietic tissue, primitive megakaryocytes are formed, and then mature megakaryocytes are formed. Mature megakaryocytes form many sunken , in Cytoplasm The adjacent sunken cell membranes fuse with each other in the deep part of the sunken, separating part of the cytoplasm of megakaryocytes from the mother. Finally, these components separated from the cytoplasm of megakaryocytes surrounded by cell membranes separated from megakaryocytes and passed through the Blood sinus They enter the blood circulation and become platelets. The newly generated platelets first pass through the spleen, where about 1/3 are stored. The stored platelets can be freely exchanged with the platelets entering the circulating blood to maintain the normal amount in the blood. Number of platelets produced by each megakaryocyte Cubic millimeter About 200~8000. It is generally believed that the formation of platelets is affected by Thrombopoietin Regulation, but its detailed process and mechanism are still unclear. Platelet life About 7-14 days, about 1/10 of the total renewal amount every day. Most of the aged platelets are cleared in the spleen.

morphological structure

Platelet description: Cell debris , small in size, irregular in shape, often distributed in groups red blood cell between.

Red blood cells, platelets and macrophages

In circulating blood Normal state Platelets with a shape of slightly concave, oval or disc on both sides are called circulating platelets. The average diameter of human platelets is about 2-4 microns, the thickness is 0.5-1.5 microns, and the average volume is 7 cubic microns. Although platelets have no nuclei^[2] , but there are Organelle In addition, there are scattered particles inside. Once platelets are mixed with wound surface or glass Vascular intima Surface contact, that is, rapid expansion, the particles concentrate towards the center, and stretch out several Pseudopodia The platelets become dendritic platelets, most of the particles are released immediately, and the platelets fuse to form sticky deformed platelets. If the stimulating factors of dendritic platelets are eliminated in time, they can also become circulating platelets, while sticky and deformed platelets are irreversible changes. Platelets have complex structure and composition. Platelet membrane is attached or inlaid with protein double Molecular layer Of Lipid membrane , the membrane contains a variety of glycoprotein It is known that glycoprotein Ib is related to adhesion, and glycoprotein IIb/IIIa is related to Aggregation Related, glycoprotein V is the receptor of thrombin. Platelet membrane is attached with Plasma protein 、 Coagulation factor AND AND Fibrinolysis system The plasma layer (the outer coating of platelets) related to molecular composition. platelet Cytoplasm There are two types of piping systems in: open piping systems connected to surfaces and dense piping systems. The former is platelet membrane Invagination The pipeline system is formed in the cytoplasm. The membrane of the pipeline is continuous with the platelet membrane Internal surface It also has the same outer coating as the platelet membrane. Through this pipeline system, plasma can enter into the platelet, thus expanding the contact area Because of the developed pipeline system connected to the surface, platelets form a structure similar to sponge; The latter is the compact pipe system, which is thin and short, and is not connected with the outside world Endoplasmic reticulum 。 There are more than ten layers of microtubules arranged in a ring parallel under the platelet membrane around the platelet, and there are dense microfilaments near the platelet membrane（ Actin ）And Myosin , and the maintenance of platelet morphology and Deformation movement of There are two kinds of particles scattered in the platelet: α Particles and dense particles. α The particulate content is medium electron density Some particles have cores with high electron density in the center. α The particles contain Fibrinogen , platelet factor 4 Cathepsin A 、 cathepsin D、 acid hydrolase Etc. The electronic density of the content of dense particles is extremely high, containing 5-hydroxy Tryptamine 、ADP、ATP、 calcium ion , adrenaline, anti Blood Fibrin Enzymes inorganpyrophosphate Etc. In addition, mitochondria Glycogen Particles, etc.

Function

The main function of platelets is to coagulate and stop bleeding, and repair damaged blood vessels. The surface sugar coating of platelets can adsorb plasma protein and coagulation factor III. Platelet particles contain substances related to coagulation. When the blood vessel is damaged or ruptured, the platelet is stimulated and changes from a static phase to a functional phase, which immediately deforms, Surface viscosity Increase and agglomerate into clusters; At the same time, under the action of surface factor III prothrombin To thrombin, which catalyzes fibrin Formed into filamentous fibrin, it forms clots with blood cells to stop bleeding. platelet Particulate matter And further promote hemostasis and coagulation. Platelets also protect vascular endothelium, participate in endothelial repair, and prevent atherosclerosis Role of. The number of platelets in the blood is less than 100000/ μ L (100 × 10 ^ 9/L) is thrombocytopenia, less than 50000/ μ L (50 × 10 ^ 9/L) is at risk of bleeding.

Function

platelet aggregation

Platelets are small pieces of bone marrow megakaryocytoplasmic shed off, so there is no nucleus, and there is a complete cell membrane on the surface. Platelets are small in size, with a diameter of 2-4 microns, in the shape of a double convex disc, which is vulnerable to mechanical and chemical stimulation. At this time, they protrude into irregular shapes. Under the electron microscope, the membrane surface of platelets is coated with sugar, which can absorb plasma proteins and coagulation factors. Platelets are bleeding Coagulation process Play an important role in.

Platelets are the smallest cells in the blood. Platelets in electron microscope The lower part is like an olive shaped disc, and there are also shuttle shaped or irregular shapes. platelet Is long 1.5~4 μ m, 0.5~2 μ m wide. In normal human blood platelet count It is (100~300) × 10 ^ 9/liter, and 1/3 of the platelets are stored in the spleen at ordinary times. The main function of platelets is to coagulate and stop bleeding, and repair damaged blood vessels. The average life span of platelets is 7-14 days. When human body is injured and bleeding, platelets will rush to close the wound in groups within a few seconds to stop bleeding. Platelets and other clotting substances in the blood, such as calcium ions and thrombin, gather on the broken blood vessel wall to form thrombus and block the broken wound and blood vessel. Platelets can also release adrenaline, causing vasoconstriction , promote hemostasis.

platelet

Platelets were considered as nonfunctional cell fragments in blood for a long time. It was not until 1882 that Italian doctor Bizozero found that they played an important role in the hemostasis process after vascular injury that he first proposed the name of platelets. It is found that platelets are small pieces of cytoplasm shed from megakaryocytes in bone marrow. Each megakaryocyte can produce 300~4000 platelets.

It is formed by invading bone marrow Hematopoietic function Low disease will affect the quality and quantity of platelets. When the number of platelets decreases, it is easy to have bleeding. After the platelet comes out, it will burst and release the clotting substances it contains—— lectin 。 When lectin encounters Agglutinogen Will be combined into Coagulant 。 The clotting element combines with the fibrinogen in the plasma to form fibrin, which quickly coagulates into long and thin fibers. These fibers crisscross again, forming a "fiber wall" to block the wound, and scabs gradually formed in a few days.

Physiological function

Physiological function of platelet^[3]

Thrombosis and lysis When blood vessels are damaged, platelets are stimulated by the activation factors at the damaged site to form platelet clots, which play a primary hemostatic role. Then platelets undergo complex changes to produce thrombin, which makes fibrin It turns into fibrin, and the interwoven fibrin binds the platelet clot and blood cells into blood clot, that is, thrombus (see coagulation factor). At the same time, the protuberances of platelets extend into the fibrin network. With the contraction of platelet microfilaments (actin) and myosin, the blood clot shrinks and the thrombus becomes more solid, which can more effectively stop bleeding. This is a secondary hemostatic effect. With the formation of thrombus, thromboxane A2 is released from platelets; Dense particles and α Particles release ADP 5-hydroxytryptamine , platelet factor 4 β thrombus Globulin 、 Thrombin sensitive protein 、 Cell growth factor 、 Blood coagulation factor V, VII, XII and vascular permeability factors Active substances These active substances can enhance the hemostatic effect by activating surrounding platelets, promoting vasoconstriction, promoting fibrin formation and other ways. Substance can strengthen inflammation and immune reaction 。 Blood coagulation After, you can see clot There are some yellow transparent liquids around. This kind of liquid is not only different from plasma in color, but also has no fibrinogen, which is called serum.

When thrombus is formed at the injured part of the blood vessel, it is necessary to prevent the infinite increase of the thrombus after the blood loss stops, so as to avoid the resulting blockage of the blood vessel. At this time, 5-hydroxytryptamine, etc. produced by platelets vascular endothelial cell Works to release Fibrinolytic enzyme Proactivator, which can promote the formation of fibrinolytic enzyme, and then Fibrinolysis 。 Platelets themselves have Fibrinolysin Activator and plasminogen produce fibrinolytic enzyme to participate in the fibrinolysis of thrombus.

Hemostasis and coagulation

When blood vessels are injured and bleeding, there are many mechanisms for hemostasis and coagulation effects, but most of them are related to the role of platelets, which can be summarized as follows:

1. Contraction of blood vessels to help stop bleeding temporarily

Giant platelet

The hemostatic effect of platelets is achieved by releasing vasoconstrictive substances, aggregating platelets to block damaged blood vessels and promoting blood coagulation. Platelets can release serotonin, catecholamine Isoangiotensin can make the injured blood vessel tightly closed to varying degrees, and at the same time blood flow Reduce and prevent blood loss.

2. It forms a hemostatic plug to block the rupture of blood vessels

Platelets are easy to adhere and deposit in the exposed Collagen fiber Upper, gather into a group to form a hemostatic suppository; The thrombus is directly blocked at the vascular fissure, which can not only play the role of blocking, but also maintain the integrity of the vascular wall.

3. Coagulation of platelets

Release the substances that promote blood coagulation, and accelerate the formation of clots at the rupture of blood vessels.

Platelet coagulation process

Platelet Coagulation: Platelet 3 Factor Provides Phospholipids Surface adsorption Most coagulation factors increase coagulation reaction rate 。

The damaged blood vessel or tissue is producing some factors, which can start endogenous and Exogenous The hemagglutination system, under the combined effect of different factors released by platelets, completed a series of enzymatic biochemical chain reactions within a few minutes, and finally led to the transformation of soluble fibrinogen into insoluble fibrin in plasma. The molecular weight of fibrinogen is about 340000, and several are observed under electron microscope Peptide chain Spirally coiled Four level structure On the whole, it looks like a ball. Fibrin is slender and interwoven Networking Therefore, blood cells are netted to form jelly like blood clots.

4. Release anti fibrinolytic factor, inhibit Fibrinolytic system Activities for

Fibrin in plasma is easy to degrade under the action of fibrinolysis system. Because platelets contain anti fibrinolytic factors and inhibit the activity of fibrinolytic system, the formed blood clots will not collapse.

5. Nutrition and support capillary endothelium

6. Promote blood circulation

Platelets are the smallest blood cells in the blood. The blood count of normal people is 100 × 10 ^ 9/L - 300 × 10 ^ 9/L, accounting for 0.3% of the blood volume. Women can reduce 50% - 75% in the menstrual period, and children's content is slightly lower. About 2/3 platelets are in peripheral blood circulation, 1/3 platelets are in spleen, and between them Mutual exchange 。

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Microscopic platelets

The rapid flow of blood in blood vessels can sometimes damage Vascular wall , platelets can be transferred from flowing state to attached endothelial cells Surface cell membrane Disappear, cytoplasm They fuse with each other to repair endothelial cells.

The mechanism of platelet adhesion, release and aggregation There are many different receptors on the surface of platelets Ligand binding Is activated. When vascular endothelial cell When damaged, endothelium The type I and type III collagen in the lower tissue are exposed, and there is a 9-peptide structure Active site 。 From this active site, through VWF factor and receptor on platelet membrane glycoprotein 1b connection, realizing the adhesion of platelets to the injured part. After platelet activation, annular Of microtubule Concave inward. Platelets have radial protuberances, which are consistent with their long axis Microfilament Microtubules. The particles are concentrated towards the center of the platelet and close to the pipeline system connected to the surface. Platelets changed from circulating type to dendritic type. stay optical microscope lower Blood smear Platelets seen above, such as those divided into central granular area and peripheral Transparent area Is the characteristic of this stage.

Adhered platelets begin to release their Contents With the change of platelet morphology Lipid bilayer Of phospholipid Intramolecular Arachidonic acid Free, and then formed by the action of enzymes on the platelet membrane Thromboxane A2 Etc. Platelet granule Inclusion The release of is not simultaneous. ADP 5-hydroxytryptamine The reaction of. α The release time of particles varies with their contents; Containing platelet factor 4 β thrombus Globulin Isocomponent α Particles are released first, including acid hydrolase Of particles (equivalent to lysosome ）Post release. Release is a process of energy demand. Supramembranous Calcium pump Pump Ca2+into platelets to activate ATPase Finally, it causes the contraction of platelets and the release of particles in platelets.

The adhesion between platelets is called aggregation. ADP、 adrenaline 、 thrombin And collagen are aggregation agents of platelets. The aggregation process caused by different polymerizers is different. If ADP is added, it can directly cause platelet aggregation ADP released by aggregated platelets can cause new platelet aggregation again. Thus, two concentrated waves can appear. Collagen itself cannot directly cause platelet aggregation, but only after inducing platelet to release ADP. The mechanism of aggregation was known as arachidonic acid pathway, dense granule pathway and platelet by 2017 Activation factor Pathway, many factors such as Ca2+and Fibrinogen It is related to platelet aggregation. In activated platelets, arachidonic acid in platelet membrane is free, and finally thromboxane A2 (TXA2) is formed under the action of different enzymes. Thromboxane A2 is the strongest aggregation agent known so far, while endothelial cells release prostaglandin I2 (PGI2) can be activated by Adenylate cyclase send Cyclic adenylate （ cAMP ）The level increases, inhibiting platelet aggregation.

mammal There are species differences in platelets. For example, in rabbit platelet dense particles, in addition to 5-hydroxytryptamine histamine Human platelets have no reaction to aggregation agent ADP, thrombin, etc. Rabbit Rat 、 mice , pigs, sheep and horses did not respond to epinephrine. In 5-hydroxytryptamine content inhibitor Of Reactivity And other aspects Species difference 。

With the development of biology and medicine, cell adhesion becomes Cell Biology One of the important topics in. The study of platelet adhesion and aggregation is expected to make new progress in this subject, and platelets are also ideal Neuropharmacology Model of. Platelet contraction and relaxation skeletal muscle There are similarities in the activities of.

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Thrombocytopenia

Disease Profile

Platelet disease It's due to a decrease in the number of platelets（ Thrombocytopenia ）Or hypofunction (platelet dysfunction) resulting in poor formation of hemostatic suppository and bleeding. The number of platelets is lower than the normal range of 140000~400000/ μ l。 Thrombocytopenia may result from insufficient platelet production, spleen's retention of platelets, increased platelet destruction or utilization, and dilution (Table 133-1). No matter what causes severe thrombocytopenia, it can cause typical bleeding: multiple ecchymosis, most commonly in the lower leg; Or small scattered ecchymosis appeared at the site of minor trauma; Mucosal hemorrhage（ Epistaxis , gastrointestinal and urogenital tract and Vaginal bleeding ）； And massive bleeding after surgery. Massive gastrointestinal bleeding and bleeding in the central nervous system can be life-threatening. However, thrombocytopenia does not show tissue hemorrhage (such as deep visceral hematoma or joint hematocele) as secondary to coagulation diseases.

It may also be caused by heredity. Male onset, female carry. （ WAS syndrome ）

It may also be Gaucher disease (Gaucher's disease, GD). Gaucher disease is a kind of lipid Metabolic disorder A familial autosomal recessive disorder that causes abnormal glucose Cerebroside stay macrophage Internal accumulation. The clinical manifestations are Hepatosplenomegaly ， Epistaxis , ecchymosis, anemia ， Osteodynia ， bone density Lower, Growth retardation And other symptoms.

And leukemia difference

Thrombocytopenia Purpura The typical symptom of the disease is bleeding. In the early stage of the disease, the skin will appear pinprick like red spots, which will later develop into lumps Thrombocytopenic purpura Purpura is of different sizes, small as a soybean grain, and large as a palm.

appear Thrombocytopenic purpura The part of the skin on the body surface is generally loose, such as the neck, around the eyes, lower limbs, etc., accompanied by swelling and pain, and in serious cases Oral mucosa Purple spots appear on the part. The number of normal platelets in the blood is 300000/cubic mm, which can be reduced to 40000~50000 in case of illness. When the number of platelets drops to 20000, patients may have Gastrointestinal bleeding 、 intracranial hemorrhage 、 hematuria Etc., endangering life.

Thrombocytopenic purpura leukemia Some symptoms of thrombocytopenic purpura are similar. Some patients think that thrombocytopenic purpura is a kind of leukemia, Psychological pressure It's very big. In fact, it's totally unnecessary. Experts believe that Purpura Because simple thrombocytopenia Coagulation function Abnormality occurs, while thrombocytopenia and abnormal coagulation function are only one of the symptoms of leukemia white blood cell 、 red blood cell They are totally different.

Coagulation function test

Platelets are moving Venous thrombosis Play an important role in. In the 21st century, there have been many new understandings of the role of platelets in blood coagulation, especially their aggregation mechanism, which has led to Detection technology Development of. In general, platelets have adhesion, aggregation, release, coagulation promotion Clot constriction And maintain the integrity of vascular endothelium. platelet Function test It can be divided into general platelet function test platelet adhesion 、 platelet aggregation And the determination of release function and flow cytometry (FCM) analysis. General PLT function measurement includes platelet count 、 Clot constriction test (CRT), whole blood coagulation assay (WBCA) (detection instrument: whole blood coagulation analyzer), activated coagulation time assay（ ACT ）(Detection instrument: coagulation analyzer), platelet count ratio (PCR) (platelet counter), rapid platelet function analysis (RPFA), etc. These methods are clinical evaluation It is a commonly used auxiliary means for platelet function.

platelet adhesion test

A certain amount of blood and a certain amount of Surface area A considerable number of platelets adhere to the surface of the foreign body immediately after the foreign body is contacted. The difference between the number of platelets before and after the surface contact can be measured to determine the percentage of platelets in the total number of platelets percentage Namely, platelet adhesion rate. Prompt of increased platelet adhesion rate Thrombotic diseases The exists of.

Measurement of platelet aggregation function

Aggregation function is another important physiological characteristic of platelets. It refers to the adhesion between platelets, which shows the characteristics of activated platelets interacting and forming clusters. It is one of the important factors for platelets to participate in the process of hemostasis and thrombosis. The measurement of platelet aggregation function is of great significance for clinical diagnosis of prethrombotic state and thrombotic diseases. Adding an inducer to PRP or whole blood for continuous stirring can induce platelet aggregation. The aggregation reaction has two phases: Phase I: platelet adhesion at the injured part of the vascular wall, resulting in the release of ADP through the injured tissue or red blood cells. It is characterized by rapid and reversible aggregation, that is, the platelet after aggregation separates itself (called depolymerization); Phase II: aggregation is induced by ADP released by platelets themselves, characterized by slow and irreversible aggregation process. The principle of platelet aggregation detection is to add an inducer in PRP to make platelets aggregate, so as to change the blood turbidity accordingly. The degree and speed of platelet aggregation can be calculated according to the tracing curve, mainly including filter pressure method Turbidimetry Shear induced platelet aggregation assay, scattering particle assay, whole blood Electrical impedance Method, platelet count method and micro reaction plate method.

Platelet release test

Including dense granule release (platelet ATP release, 5-TH determination) and a granule release (PF4 detection β- TG detection, GMp-140 determination).

Platelet arachidonic acid (AA) Metabolites determination

Including plasma TXB2 determination, plasma malondialdehyde Determination and determination of AA metabolites in urine.

platelet Membrane protein testing

Including PLT membrane GPI determination and platelet membrane G P Ilb/Illa determination.

Diagnosis mode

1. Peripheral blood cell count is used to determine thrombocytopenia and seriousness Critical inspection, and Blood smear examination It can provide clues for the etiological examination. If thrombocytopenia is not accompanied by other diseases that affect hemostasis (such as liver disease or Disseminated intravascular coagulation ）The hemostatic function screening test is one of the normal diagnostic methods of thrombocytopenia.

two Myelogram Examination: If any abnormality other than thrombocytopenia is seen on the blood smear, this examination is applicable. This examination can provide information on the number and morphology of megakaryocytes, and determine whether there is or is not a disease that causes bone marrow failure (such as myelodysplasia). Antiplatelet antibody The examination is of little clinical significance. If the patient's medical history or examination provides the basis for the risk of hiv infection, they should be tested for hiv antibody.

three viral infection Acute thrombocytopenia, Viremia It can cause platelet aggregation and destruction and reduce the number, not caused by immune mechanism. The characteristic is that thrombocytopenia occurs at the initial stage of infection, the degree of reduction is proportional to the severity of infection, and the platelet increases with the improvement of infection. PA - IgG No increase. These can be compared with ITP identify.

4. Infection complicated with thrombocytopenia also occurs in infection acute stage , bleeding symptoms and systemic symptoms are more serious than acute ITP, thrombocytopenia progresses faster, and prothrombin time Extension Fibrinogen Lower 3P test Positive, etc laboratory examination Abnormality can be identified. The onset is often accompanied by chills fever 、 headache , vomiting and other systemic symptoms, as well as laboratory tests can be identified.

Research progress

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July 13, 2018, Japan Kyoto University union Nagoya University 、 Keio University 、 Shiga Medical University And other research teams announced that they have successfully developed iPS cells（ Inducible pluripotent stem cells ）A technique for making large numbers of platelets. The team used iPS cells to artificially cultivate platelets, and then purified them to finally obtain high-quality platelets that can be used for blood transfusion. Before this study, only 40% of artificially cultivated platelets could be used for blood transfusion, with low clinical utilization rate and high cost. The research results were published in the United States science In the journal Cell. Jiang Tenghao, the leader of the research team and professor of Kyoto University, said that the research team will basically complete the preparation for clinical application in 2019 and will steadily promote the practical application of artificial platelets according to the needs of patients. In the future, we will take the research of mass production platelet technology as the main goal to deal with the situation of insufficient blood donation and platelet shortage in the future, and consider applying it to Blood transfusion treatment Under study.^[4]

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