idiopathic thrombocytopenic purpura
Introduction
Introduction to idiopathic thrombocytopenic purpura Idiopathic thrombocytopenic purpura (ITP) is the most common hemorrhagic disease in children. It is characterized by spontaneous bleeding, thrombocytopenia, prolonged bleeding time and poor blood clot dysfunction. This disease is an immune response-related hemorrhage. Sexual diseases can be classified into acute and chronic according to the patient's course of disease within 6 months or more than 6 months. The two types are different in age, etiology, pathogenesis and prognosis. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: iron deficiency anemia, menstrual cramps, shock
Cause
Idiopathic thrombocytopenic purpura
Autoimmune factors (50%):
Most scholars believe that ITP is a thrombocytopenia caused by the body's immune response to its own platelet-associated antigen, but the essence of platelet-associated antigen is still inconclusive. In 1982, Van Leenwen reported that autoantibodies in some ITP patients are directed against platelet membrane glycoprotein IIb. The antigenic determinant of the /IIIa (GpIIb/IIIa) molecule, and later found that the GPIb/IX complex on the platelets of some ITP patients is also the target antigen of autoantibodies, suggesting that ITP is a group of itself caused by different related antigenic determinants. In immunological diseases, the membrane antigen sites that can bind to antibodies are quite extensive. Therefore, the platelet autoantigens of ITP patients mainly include GPIIb/IIIa, GPIb/IX, and other antigen types that are not fully elucidated. The value of antiplatelet antibody testing for the diagnosis and treatment of ITP is still controversial, but there is no doubt that the production of autoantibodies plays an important role in the pathogenesis of ITP.
Reduced platelet production rate (25%):
The rate of thrombocytosis in patients with ITP can be reduced, normal or increased, and the mean platelet production rate is close to normal, but the average lifespan of platelets in the blood vessels of ITP patients is shortened (only 2.9 days, normal average is 8.0 days), mainly due to platelets. The damage is increased. Normally, the number of megakaryocytes in the ITP patients is normal or increased. The increase in the number of megakaryocytes may be related to the increase of platelet destruction and the compensatory proliferation of megakaryocytes. Because anti-platelet antibodies act on megakaryocytes or their progenitor cells at the same time. It may also cause platelets not to be produced.
Capillary permeability changes (20%):
(1) Bleeding mechanism of chronic ITP: 1 Increased platelet destruction caused by platelet-associated antibodies is the main cause of bleeding. 2 antibodies immobilized on platelet-associated antigens cause abnormal platelet function. 3 antibodies can also damage capillary endothelial cells, causing increased permeability and bleeding.
(2) Bleeding mechanism of acute ITP: 1 Platelets that bind to immune complexes are simultaneously engulfed by macrophages, and are destroyed and reduced. 2 The release of a large amount of protease during phagocytosis increases capillary permeability. (3) The immune complex can fix complement, and the cleavage of C3 and C5 can cause histamine release, resulting in vascular permeability changes and bleeding.
Pathogenesis
Platelet destruction
(1) Platelet destruction mechanism of chronic ITP: Platelet destruction of chronic ITP is caused by binding of platelet antibodies to their related antigens: PAIg binds to platelet-specific antigen through Fab segment, and its exposed Fc segment can interact with mononuclear macrophages The Fc receptors of the macrophages of the system bind, causing the platelets to be destroyed by phagocytosis. The megakaryocytes also have related antigens, so the function of generating platelets is also impaired. When the surface of the platelets has more IgG antibodies, IgG dimers can be formed. Activation of complement C1q, followed by activation of components of the complement system, C3 cleavage product C3b attached to the surface of platelets, and binding to the C3b receptor of macrophages, also leading to platelet phagocytosis, platelet destruction and macrophage activity levels It also has a relationship. For example, when a virus is infected, the number of Fc or C3b receptors on macrophages increases, affinity increases, and platelets are more easily destroyed. This may explain a clinically common phenomenon, that is, ITP patients are in the virus. When the infection is infected, the condition is often aggravated.
(2) Platelet destruction mechanism of acute ITP: Acute ITP is more common in children and is often associated with viral infection. Acute type is an immune complex disease caused by natural immune defense response after viral infection. The mechanism of platelet destruction is:
1 virus infection can directly damage megakaryocytes and platelets: it can also cause platelet membrane antigenic changes, induce the production of autoantibodies.
2 sequestration and destruction of platelets by mononuclear macrophage system: A. formation of immune complexes (IC) in vivo: antiviral antibodies bind to platelet-adsorbed viruses, and can also bind antibodies to circulating non-platelet antigens, and then to platelet membranes. The Fc receptor binds, binds to and eliminates circulating immune complexes that are normally normal mononuclear macrophages, but causes thrombocytopenia; B. Antiplatelet autoantibodies are also present in acute ITP patients, except for GPIIb/ In addition to IIIa and GPIb/IX autoantibodies, there may also be GPV autoantibodies.
Anti-platelet antibody
(1) Detection of anti-platelet antibodies: In 1975, Dixon and Rosse first directly used quantitative methods to detect immunoglobulins on the platelet surface of patients with ITP, called platelet-associated antibodies (PAIgG), and found a negative correlation between PAIgG and platelet count. Relationship, after that, with the improvement of methodology, RIA, ELISA and other methods have been successively introduced. The concentration of normal human PAIgG/106 platelets is 1-11 ng, while the platelet PA IgG content of ITP patients is 4-13 times higher than that of normal people. Although the results vary from report to report, the results of different reports have been shown to be significantly higher in most ITP patients (78.6% to 100%) than in the normal population. The number of PAIgG is negatively correlated with platelet count and also with platelets. Life expectancy is negatively correlated; PAIgG levels reflect clinical signs and are associated with the severity of the disease, and as the platelet count increases, PAIgG decreases or falls to normal as treatment is effective.
Further studies have found that bacterial sepsis, active systemic lupus erythematosus (SLE), infectious mononucleosis with thrombocytopenia, Graves disease, Hashimoto's thyroiditis, lymphoma, chronic lymphocytic leukemia and other diseases of PAIgG The level may increase. It is considered that PAIgG is not a specific antibody related to ITP. The interpretation of PAIgG should be cautious. In 1983, Lo Bugli and other 125I-labeled monoclonal antibody-anti-human IgG were used to determine PAIgG, and normal control platelet surface was found. PAIgG is (169±79) IgG molecules; ITP patients have platelet surface PAIgG of 79013095 IgG molecules; non-immune thrombocytopenic patients have platelet surface PAIgG of (246±156) IgG molecules, this data suggests that although PAIgG is elevated It is not a specific indicator of ITP diagnosis, but it still has important reference value in the diagnosis of ITP. Combined with clinical signs, thrombocytopenia, elevated PAIgG, if other secondary diseases (such as SLE, thyroid disease, lymphoproliferative disorders) And infection, etc.), should be highly suspected of the possibility of ITP; if PAIgG is negative, it is likely not ITP.
(2) Types of platelet-related antibodies: With the in-depth study of ITP, it was found that not all ITP thrombocytopenia is mediated by PAIgG, and there may be other factors affecting thrombocytopenia, such as PAIgM, PAIgA and PAC3, PAIgM High binding rate and cohesive ability, 1 molecule of IgM can activate complement and promote platelet destruction. It is reported that PAIgM level has the strongest correlation with platelet count. PAIgM may have a dominant role in the pathogenesis of ITP, and there are reports that patients only There is an increase in PAC3 and no increase in PAIgG, suggesting that complement can destroy platelets alone in the absence of platelet-associated antibodies, but many patients have platelet surface-associated antibodies belonging to PAIgG. In most cases, PAIgG is present alone, accounting for approximately 70%, as well as PAIgG and PAIgM. And (or) PAIgA coexist, a small number of patients, especially acute ITP, PAIgM antibody alone, IgG1 is most common in IgG antibody subtypes, IgG1 often coexists with IgG3, IgG4, and IgG2 coexisting is rare.
(3) Anti-platelet antibody production and platelet destruction: PAIgG is known to be mainly produced in the spleen. Other lymphoid tissues and bone marrow may also be important sites for the production of PAIgG. It is currently believed that the main organs of ITP and platelet destruction are in the spleen, liver and Bone marrow, in which the spleen is the most important, the normal spleen contains a large number of macrophages, which retains more than 1/3 of the platelets in the human body. The IgG content in the spleen of ITP patients is 5 to 35 times that of the normal control, and the anti-platelet antibody binds to the relevant antigen. Increased phagocytosis and destruction by spleen macrophages, and immediate increase in platelet count after splenectomy in most ITP patients also indicates that the spleen plays a central role in the pathogenesis of ITP, while in some patients, ITP still recurs after splenectomy, PAIgG is obvious Increased, it may be related to lymphoid tissue and bone marrow can still produce anti-platelet antibodies, and become the main destruction site of platelets.
Prevention
Idiopathic thrombocytopenic purpura prevention
First, prevention:
Prevent colds, closely observe changes in purple spots, such as density, color, size, etc., pay attention to body temperature, consciousness and bleeding, help to understand the prognosis and outcome of the disease, so as to deal with it in time to avoid trauma, severe bleeding must be absolutely Bed rest, chronic patients, according to the actual situation, appropriate exercise, avoid seven emotions, maintain a good mood, diet should be soft, if there is gastrointestinal bleeding, should be semi-liquid or fluid, do not eat spicy and spicy food, Spotted itch, can be rubbed with calamine lotion or Jiuhua powder lotion, pay attention to skin hygiene, avoid scratching the skin bow with infection.
Second, conditioning:
(1) Life conditioning
1. The incidence is more urgent, severe bleeding needs to be absolutely in bed, should pay attention to rest during the remission period, avoid overwork and avoid trauma.
2. Chronic purpura, you can exercise according to physical strength.
(two) diet conditioning
1. The diet should be soft and fine. If there is gastrointestinal bleeding, it should be given a semi-liquid or liquid diet. It should not be cold.
2. Can give vegetables and fruits, mung bean soup, lotus seed porridge, avoid using hair such as fish, shrimp, crab, astringent food.
3. Those who have a history of drug allergies should pay attention to avoid the use of sensitizing drugs when using the drug. The purple spleen has skin itching. It can be rubbed with calamine lotion or Jiuhua powder lotion. Pay attention to the skin clean and avoid the sage. You prevent the infection.
(3) Mental conditioning: regulate emotions and avoid mood swings or mental stimulation.
Complication
Idiopathic thrombocytopenic purpura complications Complications iron deficiency anemia menstruation and more shock
1, iron deficiency anemia: common young women with more menstruation.
2, visceral bleeding: including the digestive tract, urinary tract, uterine bleeding, general visceral bleeding is rare, once bleeding occurs, severe cases can cause hemorrhagic shock, intracranial hemorrhage is less common, but the main cause of death, acute ITP patients concurrent There are 3% to 4% of intracranial hemorrhage, and 1% of deaths due to intracranial hemorrhage.
Symptom
Idiopathic thrombocytopenic purpura symptoms Common symptoms Nasal bleeding Platelet life shortened Freckle bone marrow megakaryocyte maturation disorder Black stool spleen gingival bleeding Booger thrombocytopenia Shock
symptom
Clinically, hemorrhage was the main symptom, no obvious liver, spleen and lymph nodes were enlarged, platelet count was <100×109/L, bone marrow nucleus cells were dominant, megakaryocyte count increased or normal, anti-platelet antibody was detected in serum (PAIgG, M , A), platelet life is shortened, and other diseases that cause thrombocytopenia can be diagnosed.
ITP hemorrhage is characterized by extensive bleeding of the skin and mucous membranes. Most of them are intradermal or subcutaneous hemorrhages of scattered needle size, forming sputum or ecchymosis; more limbs, but also systemic hemorrhage or hematoma; some patients A large number of snot (about 20% to 30%) or gum bleeding is the main complaint, common hematemesis or melena, mostly caused by swallowing during nose and mouth bleeding, the occurrence of true gastrointestinal bleeding is rare, under the bulbar conjunctiva Bleeding is also a common symptom, occasionally gross hematuria, about 1% of patients with intracranial hemorrhage, become the main cause of ITP death, adolescent girls can see more menstruation, other parts of the bleeding such as chest, abdominal cavity, joints, etc., extremely rare.
In addition to skin and mucous membrane hemorrhage, only 10% to 20% of patients have mild splenomegaly. Acute exposure is often accompanied by fever. Hemorrhagic anemia may occur in patients with severe hemorrhagic disease. Hemorrhagic shock may occur on the side, often accompanied by local hematoma. The corresponding symptoms, intracranial hemorrhage manifested as headache, lethargy, coma, convulsions, paralysis and other symptoms, acute fulminant patients in addition to thrombocytopenia, often accompanied by damage to the blood vessel wall, so hemorrhage is heavier.
Type
Clinically, ITP is classified into acute type and chronic type according to the patient's course of disease. Those with a disease duration of less than 6 months are called acute type, those with a history of more than 6 months are called chronic type, and some acute ITP may be converted to chronic type.
Acute ITP usually has a sudden onset of symptoms, systemic skin, mucosal hemorrhage, and often first skin ecchymosis on the onset of the disease. In severe cases, some ecchymoses can be fused into pieces or form blood blister, and bleeding or blood blister often occurs in the oral mucosa. Gingival and nasal mucosal hemorrhage often occur. A small number of patients have digestive tract and urinary tract bleeding or retinal hemorrhage. In mild cases, only skin scattered spots and ecchymoses are seen. Acute ITP is self-limited, and 80% to 90% of patients are After the disease recovered within half a year, most of them improved within 3 weeks, and a small number of patients were delayed and turned into chronic ITP.
About 30% to 40% of patients with chronic ITP have no symptoms at the time of diagnosis. Generally, the onset is slow or insidious. It often shows different degrees of skin and mucous membrane bleeding. The bleeding symptoms are often persistent or recurrent, skin purpura and ecchymosis. Can occur in any part of the body, more common in the distal extremities, especially after scratching the skin or trauma, prone to purpura and ecchymosis, mucosal bleeding varies, oral mucosa, gums, nasal mucosa bleeding and female menstruation More common, hematuria or gastrointestinal bleeding can also occur, general bleeding symptoms and platelet count, ITP patients often lack other signs besides bleeding symptoms and signs, generally no splenomegaly, occasionally in chronic patients (less than 3% ) mild spleen enlargement.
Examine
Examination of idiopathic thrombocytopenic purpura
Blood picture
Bleeding is not heavy, no red, white blood cell changes, occasionally abnormal lymphocytes, suggesting that due to viral infection, red blood cells and hemoglobin are often reduced after acute bleeding or repeated hemorrhage, white blood cells are increased, reticulocytes after massive bleeding Can increase, the most important thing in the peripheral blood is that the platelet is reduced to below 100 × 109L, the hemorrhage is directly proportional to the platelet height, the platelet <50 × 109L can be seen from the spontaneous blood, <20 × 109L when the bleeding is obvious, <10 × 109L The bleeding is severe. Chronic patients can see that the platelets are large and loose, and the staining is shallow; the bleeding time is prolonged, the clotting time is normal, the blood clot is poorly contracted or not shrinks; the prothrombin consumption is reduced, the thromboplastin is poorly formed, and the platelets are extremely reduced. Due to the lack of platelet factor 3, prolonged clotting time, platelet life is very short, platelet number is reduced to varying degrees, and there may be morphological abnormalities, such as increased volume, special morphology, reduced particles, and excessive staining, unless massive bleeding occurs. Generally no significant anemia and leukopenia.
2. Bone marrow
In severe cases of hemorrhage, reactive hematopoietic function is strong. The number of megakaryocytes in acute cases is normal or slightly higher. The megakaryocytes in chronic patients are increased more than 0.2×109L (200/mm3) or even 0.9×109L (normal value (0.025~). 0.075) × 109L], megakaryocyte classification: the percentage of proto-megakaryocytes and naive megakaryocytes is normal or slightly higher; megakaryocytes with mature platelets are not significantly increased, up to 80%; and megakaryocytes with mature platelet release are rare, A bone marrow examination is required to confirm the disease and exclude leukemia or aplastic anemia.
3. Platelet antibody test
Mainly platelet surface IgG (PA IgG) increased, the positive rate was 66% ~ 100%, simultaneous detection of PAIgG, PAIgM, PAIgA can increase the positive rate of detection, PAIgG increased is not a specific change of the disease, in other immune diseases can also Increased, but non-immune thrombocytopenic purpura PAIgG does not increase, in addition, systematic observation of PAIgG changes have a guiding significance for the prognosis of ITP, generally the platelet rises when PAIgG decreases, it is reported that the amount of PAIgG per platelet is >1.1×10-12g Cases with hormone therapy are ineffective, and the amount of PAIgG per platelet is (0.5 ~ 1.0) × 10-12g. The hormone effect is good. If the PAIgG is extremely high before cutting the spleen, it indicates that the operation is not good, such as hormone therapy or spleen surgery. If the PAIgG returns to normal, the prognosis is good. If the PAIgG is continuously increased, the treatment is invalid.
In addition, serum platelet antibodies can be measured, and about 54% to 57% of patients have serum antibodies, but the free platelet antibodies in serum are not parallel to the positive rate of platelet surface IgG.
4. Shortened platelet life
Application of isotope 51Cr or 111In labeled platelets to patients with ITP: for the determination, the patient's platelet life is significantly shortened, even only a few hours (1 to 6 hours, normal 8 to 10 days), can also be measured using the companion body surface counting method Platelet retention and destruction sites (spleen, liver, lung, bone marrow), platelet adhesion and aggregation tests can sometimes detect platelet dysfunction in patients with chronic ITP.
5. Coagulation test
Prolonged bleeding time, positive capillary fragility test, poor blood clot retraction, poor prothrombin consumption, low platelet aggregation and adhesion.
6. Determination of platelets by radionuclide
Platelet life is significantly shortened, this test is specific for the diagnosis of ITP, but due to the lack of simple and easy detection methods, it can not be widely used in clinical practice.
According to the condition, clinical manifestations, symptoms, signs, B-ultrasound, X-ray, CT, MRI, liver and kidney function tests.
Diagnosis
Diagnosis and differentiation of idiopathic thrombocytopenic purpura
diagnosis
The main diagnosis of ITP is based on clinical signs of bleeding, decreased platelet count, no swelling of the spleen, changes in the quality and quantity of bone marrow megakaryocytes, and anti-platelet antibodies. In December 1986, the first Chinese Society of Hematology National Thrombosis Hemostatic Conference was presented. The following ITP diagnostic criteria: multiple test platelet count <100 × 109 / L; bone marrow examination megakaryocytes increased or normal, there are maturity disorders; spleen is not large or slightly increased; any of the following 5 points: 1 Prednisone (prednisone) treatment is effective; 2PA IgG increase; 3PAC3 increase; 4 spleen effective; 5 platelet life measurement shortened; can exclude secondary thrombocytopenia, elderly ITP should be associated with other secondary thrombocytopenic purpura Identification, such as drugs, infections, etc.; if accompanied by splenomegaly, should be alert to other diseases that may cause thrombocytopenia.
1. Diagnostic criteria and basis
Domestic diagnostic criteria (the first China Society of Hematology National Conference on Thrombosis and Hemostasis, 1986).
(1) Multiple tests to check for a decrease in platelet count.
(2) The spleen does not increase or only slightly increases.
(3) Bone marrow examination of megakaryocytes increased or normal, there are maturity disorders.
(4) At least one of the following five items:
1 Adrenal glucocorticoid treatment is effective.
2 splenectomy is effective.
3PA IgG increased.
4PAC3 increased.
5 platelet life is shortened.
(5) Exclusion of secondary thrombocytopenia.
2. Diagnostic evaluation
(1) According to the immunological pathogenesis of idiopathic thrombocytopenic purpura, idiopathic thrombocytopenic purpura is called immunic thrombocytopenic purpura, and ITP abbreviation is still used. Currently, the literature will The phenomenon of mixed use is more common, but from the point of view of several authoritative hematology monographs abroad, the connotation of the two should not be the same. Idiopathic thrombocytopenic purpura should be referred to as no explicit predisposing factors. Immune thrombocytopenic purpura with other immune diseases, is part of immune thrombocytopenic purpura, and immune thrombocytopenic purpura also includes secondary immune thrombocytopenic purpura, such as associated with systemic lupus erythematosus, drugs Sexual immune thrombocytopenic purpura, neonatal alloimmune thrombocytopenic purpura, diagnosis of ITP is a diagnostic method, in addition to the exclusion of secondary immune thrombocytopenic purpura, should also exclude other causes Thrombocytopenia.
(2) Multiple tests to check the reduction of platelet count is very important: the illusion caused by one test error can be excluded. In addition, other illusions should be noted, such as significant reduction of platelets, but no bleeding tendency, except for anticoagulant EDTA-mediated Pseudo-platelet reduction, according to foreign literature, the incidence of EDTA-mediated pseudo-thrombocytopenia in "normal" is 0.09% to 0.11%, more common in critically ill or hospitalized patients, the incidence rate is 1.9% There is no relevant data in China.
(3) related to bone marrow examination: controversial is the number of megakaryocytes, typical megakaryocytes increase, maturity disorders, some patients with megakaryocyte counts can be normal, but megakaryocyte reduction can rule out the diagnosis is debatable, first, a bone marrow examination The reduction of megakaryocytes does not necessarily represent the real situation in the body. Secondly, most of the target antigens targeted by anti-platelet antibodies are also present in megakaryocytes, which may have an effect on the proliferation and differentiation of megakaryocytes.
(4) Most ITP patients can detect antibodies on the surface of platelets: PAIg, most of which is PAIgG, but it should be noted that PAIg is not a specific antibody related to ITP, and some immune diseases such as systemic lupus erythematosus, rheumatoid Arthritis, Sjogren's syndrome (Sjogren's syndrome), etc. also often increase PAIg, in addition, the level of elevated PAIg is not necessarily parallel with the degree of thrombocytopenia, some patients have high PAIg levels, but platelet counts are only mild Decreased, PAIg in different ITP patients may target different target antigens, including glycoprotein Ib, IIb/IIIa, phospholipids, etc. Some of these target antigens are related to platelet adhesion and aggregation functions. Therefore, in addition to platelet reduction, ITP patients Platelet function abnormalities can be combined, which may partly explain why some patients have a low platelet count, but heavier bleeding, while some patients have low platelet counts but no bleeding.
(5) Diagnostic criteria for refractory ITP: Foreign standards generally include at least the following two points: glucocorticoid therapy is ineffective and splenectomy is not effective. The actual situation in China is that patients do not usually receive splenectomy or Spleen resection is not accepted. Patients often receive other immunosuppressive agents or other treatments when glucocorticoid therapy is ineffective. Therefore, there is almost no refractory ITP in China, but in addition to splenectomy, There are many patients who are ineffective in multiple therapies. Therefore, the criteria for refractory ITP in China should be formulated according to the actual situation in China.
Differential diagnosis
Clinically, it is often necessary to identify the following diseases:
(1) Aplastic anemia: manifested as fever, anemia, bleeding, three major symptoms, liver, spleen, lymph nodes, similar to idiopathic thrombocytopenic purpura with anemia, but generally anemia, the total number of white blood cells and The number of neutrophils is reduced, the reticulocytes are not high, the bone marrow is red, the blood function of the granulosa system is reduced, and the megakaryocytes are reduced or extremely difficult to find.
(2) Acute leukemia: ITP is especially needed to identify leukemia with no increase in white blood cells. It can be confirmed by bloody smear showing various stages of immature white blood cells and bone marrow examination.
(3) allergic purpura: for symmetrical hemorrhagic rash papules, the lower limbs are more common, platelets are many, generally easy to identify.
(4) lupus erythematosus: early manifestations of thrombocytopenic purpura, suspected of anti-nuclear antibodies and lupus cells (LEC) can help identify.
(5) Wiskortt-Aldrich syndrome: in addition to hemorrhage and thrombocytopenia, combined with extensive eczema throughout the body and easy to infect, reduced platelet adhesion, no agglutination reaction to ADP, adrenaline and collagen, attribute concealed hereditary disease, The incidence of male infants is more than one year old.
(6) Evans syndrome: characterized by simultaneous autoimmune thrombocytopenia and hemolytic anemia, Coomb s test is positive, the condition is more serious, most patients are effective by hormone or splenectomy.
(7) Thrombotic thrombocytopenic purpura, seen at any age, the basic pathological changes are eosinophilic embolization of small arteries, previously thought to be platelet embolism, and confirmed by fibrin embolization by fluorescent antibody test, this vascular damage can occur in each Organs, clinical manifestations of thrombocytopenic hemorrhage and hemolytic anemia, hepatosplenomegaly, hemolysis is more urgent, fever, and abdominal pain, nausea, diarrhea and even coma, convulsions and other neurological symptoms, increased reticulocytes, Nuclear red blood cells appear in the surrounding blood, serum anti-human globulin test is generally negative, can show renal dysfunction, such as hematuria, proteinuria, azotemia, acidosis, serious prognosis, only temporary combination of adrenal cortex hormones .
(8) secondary thrombocytopenic purpura: severe bacterial infections and viremia can cause thrombocytopenia, various splenomegaly diseases, bone marrow infections, chemical and drug allergies and poisoning (drugs can directly destroy platelets or inhibit Its function, or combined with plasma components, to form antigen complexes, followed by antibody production, and then allergic reactions by antigen antibodies, destroying platelets, chills, fever, headache and vomiting can be seen at the beginning of allergic reactions, hemolytic anemia can be accompanied There is thrombocytopenia, should be carefully examined to find out the cause to identify with idiopathic thrombocytopenic purpura.
(9) pseudo-thrombocytopenia: can be seen in normal people or other patients, the incidence rate is 0.09% ~ 0.21%, the patient does not have any clinical signs of bleeding, the most common in EDTA anticoagulant caused by platelet aggregation in vitro (platelets, platelets and Between the white blood cells), the erroneous recognition of the cytometer, the mechanism of causing pseudo-thrombocytopenia is the presence of an EDTA-dependent lectin (usually IgG) in the plasma of these individuals, capable of recognizing platelet surface antigen in the presence of anticoagulation in vitro. (eg GPIIb/IIIa) and/or neutrophil FcIII receptor, causing platelet-platelet or platelet-neutrophil aggregation, for those patients with clinically unexplained thrombocytopenia, anticoagulation with citrate The number of platelets was verified under a microscope or with a blood cell automatic counter.
(10) Chronic liver disease accompanied by hypersplenism: patients with liver disease manifestations, splenomegaly, etc. can be identified.
(11) Myelodysplastic syndrome (MDS): Some patients with MDS-RA only have thrombocytopenia as the main manifestation in the early stage. They need to be differentiated from ITP. Bone marrow examination shows that venous hematopoiesis of multiple hematopoietic cells is the main identification point.
(12) Chronic DIC: Patients often have certain underlying diseases. In addition to thrombocytopenia, there are some abnormalities in DIC laboratory tests (aPTT, PT, fibrinogen, D-Dimer, etc.), which are not difficult to identify with ITP. .
(13) Drug-induced thrombocytopenia: such as heparin, quetnidin, antipyretic analgesics, etc. sometimes cause acute thrombocytopenia, often due to the involvement of immune mechanisms, by carefully asking about the history of medication and the platelets after stopping the drug can generally be compared Fast recovery, can be identified with ITP.
