Immune thrombocytopenic purpura in the elderly

Introduction to immune thrombocytopenic purpura in the elderly Immune thrombocytopenic purpura (ITP) is a group of clinical syndromes caused by the shortening of platelet life caused by the combination of autoreactive antibodies and platelets. The common features are: 1 peripheral blood platelet reduction; 2 the main cause is immune mediation. Excessive damage caused by the lead; 3 bone marrow megakaryocytes often increase or normal, mostly associated with maturity disorders, it includes two groups: one group is autoantibody-induced thrombocytopenia (idiopathic); the other group is allogeneic antibody Guided thrombocytopenia. basic knowledge The proportion of illness: 0.001% Susceptible people: the elderly Mode of infection: non-infectious Complications: anemia

The cause of immune thrombocytopenic purpura in the elderly

(1) Causes of the disease

The cause of this disease has not been fully elucidated.

(two) pathogenesis

Acute type

Most patients have a history of viral infection, such as rubella, measles, chickenpox, herpes, mumps or upper respiratory tract, 1 to 3 weeks before the onset of the disease. The relationship between infection and thrombocytopenia has not been fully elucidated. The body produces the corresponding antibody and forms an immune complex (IC). IC binds to the Fc receptor (FcR) on the platelet, causing destruction of the target cell. In addition, the virus infection may also change the structure of the platelet, and make it Platelets are immunogenic, produce autoantibodies, react with platelet membrane antigens, bind to FcR of mononuclear-phagocytic system and be phagocytosed; viral infection can directly damage megakaryocytes, affect platelet production and reduce thrombocytopenia, application closure Both macrophage Fc receptors and splenectomy can increase platelets and indicate that they play a role in the pathogenesis of ITP.

2. Chronic type

(1) Immune-mediated factors: In 1951, when Harrington found that he was infused with plasma from patients with ITP, hepatic platelet depletion rapidly appeared, confirming the presence of anti-platelet factor in ITP patients; this factor was later proved to be a globulin in serum. Its physical and chemical properties are IgG. Currently, anti-platelet antibodies are recognized as the main cause of thrombocytopenia in patients with ITP. After years of research, anti-platelet antibodies are mainly targeted at glycoprotein (Gp) on platelet membranes, and anti-platelet antibodies can be combined with GpIIb/. IIIa, GpIb/IX, GpIIb and other antigenic sites bind, and can also interact with cardiolipin antigens, MHC class I molecules. In recent years, autoantibodies of integrin subfamily member 3 have also been discovered, indicating that there are various antigens recognized by antiplatelet antibodies. Therefore, the disease may be a group of syndromes that produce anti-platelet antibodies with different antigens.

(2) Mechanism of thrombocytopenia: It is currently believed that platelets bind to autoantibodies and bind to FcR on mononuclear macrophages and eventually phagocytose, causing thrombocytopenia; when platelet-bound antibody is abundant, IgG can be formed. The aggregate, activated complement binds to C3bR (mainly expressed in liver) on macrophages through C3b, and is finally phagocytosed; the expression of FcR and C3bR on mononuclear macrophages increases when viral infection occurs, platelet destruction accelerates, and the virus also Directly damage megakaryocytes to reduce platelet production; megakaryocytes and platelets have a common antigen, so in addition to binding to platelets, antibodies also act on megakaryocytes, causing maturity to occur, and platelet production is reduced or rapidly destroyed in the marrow.

(3) Immunoregulatory disorders: Inhibition of T cell function in patients with ITP increases the production of antibodies by activated B cells; CD5+ B cells in peripheral blood of active ITP patients are significantly increased, and the multi-reactive antibodies produced by them also have autoantibodies. effect.

(4) The role of liver and spleen in the pathogenesis of ITP: The spleen has been proved to be the main site of platelet antibody production. In vitro tissue culture confirmed that the spleen can synthesize IgG, and the ability of spleen to synthesize IgG in ITP patients is more than 7 times that of normal people. IVIG is applied. Treatment of closed macrophage FcR and spleen treatment is effective, indicating that the spleen is the main site of platelet destruction; antibodies on the platelets form dense dimers, activate complement to produce C3b, and the liver is blocked by C3bR, the platelets are destroyed, in addition, the bone marrow is also A place where target cells are destroyed.

(5) Decreased platelet production: A study of platelet autoreplication rate indicates that platelet turnover is normal or decreased in most ITP patients. We integrated light for Gp Ib, IIb, IIIa in the development of bone marrow megakaryocytes in ITP patients. Density values were measured and found that the integrated light-density values of megakaryocytes Gp Ib, IIb, IIIa were significantly lower than those of normal controls (P < 0.005). The above conclusions indicate that the thrombocytopenia of ITP is not only excessively damaged, but also insufficiently generated. the elements of.

(6) Stem cell defects: A study using an animal model of autoimmune disease in W/BF1 male mice demonstrated this: a lethal dose of whole body irradiation (8.5 Gy) to mice, followed by BABL/C input to T cells. In the bone marrow cells of mice, the platelets of the surviving mice returned to normal after transplantation; on the contrary, the bone marrow of male W/BF1 mice de-celled were transplanted to healthy mice after lethal irradiation, and the surviving mice gradually showed thrombocytopenia. The above test indicates that stem cells are defective in autoimmune mice.

(7) the role of estrogen: this disease is more common in women of childbearing age, easy to relapse during pregnancy, speculation that estrogen may be involved in the disease, it is believed that estrogen can enhance the phagocytosis of the spleen on platelets.

Elderly immune thrombocytopenic purpura prevention

Acute patients with severe bleeding tendency should stay in bed to avoid trauma, and it is forbidden to take antiplatelet drugs such as aspirin.

Elderly patients with immune thrombocytopenic purpura Complications anemia

Common anemia, severe cases may have digestive tract, urinary tract bleeding, the most serious can occur intracranial hemorrhage, symptoms can be automatically relieved within six months, followed by infection.

Elderly patients with immune thrombocytopenic purpura symptoms Common symptoms thrombocytopenic recurrent bleeding platelet life shortening nasal bleeding ecchymosis lymphadenopathy intracranial hemorrhage blister enlargement

Acute type

More common in children, no gender differences, acute onset, 1 to 3 weeks before the onset of virus infection, respiratory infections, etc., some children after vaccination, patients with hemorrhage, except for visible skin spots, ecchymoses In addition, mucosal blood blister can still be seen, severe cases may have digestive tract, urinary tract bleeding, the most serious can occur intracranial hemorrhage, symptoms can be automatically relieved within six months, the severity and location of physical bleeding depends on the majority, most patients have no lymph nodes Swelling, no liver and spleen, a small number of children may have mild splenomegaly.

2. Chronic type

More common in adult women, the ratio of male to female incidence is about 1:3, insidious onset, bleeding is mild, mucosal blister and digestive tract are rare, urinary tract bleeding, nasal bleeding or menorrhagia, such as repeated Hemorrhage can occur anemia, the degree is consistent with bleeding, physical signs in addition to sputum, ecchymosis, generally no liver and spleen, swollen lymph nodes.

Examination of immune thrombocytopenic purpura in the elderly

1. Platelet count: the acute type is more than 20×109/L, and the chronic type is mostly in the range of (30-80)×109/L.

2. Hemoglobin concentration: It can be reduced only when the chronic blood loss is large, and the acute type is normal.

3. Beam arm test: more positive.

4. Bleeding time: normal or prolonged.

5. Clot retraction test: normal or poor.

6. Bone marrow examination: The main change is megakaryocyte increase or normal, mostly accompanied by maturity disorder, and the production of platelet-type megakaryocytes is significantly reduced.

7. Platelet-related antibodies: PAIgG, PAIgM, PAIgA, PAC3 are often increased.

8. Platelet life: shortened.

9. Antigen capture experiment: The glycoprotein monoclonal antibody coated template is used to capture the corresponding antigen on the platelet, and the autoantibody in the patient's serum is also bound to the corresponding antigen, and then the enzyme-labeled anti-human IgG is added to determine the presence or absence of autoimmune anti-platelet antibody. This test is more meaningful.

Diagnosis and diagnosis of immune thrombocytopenic purpura in the elderly

Diagnostic criteria

The standards set by the National Conference on Thrombosis and Hemostasis in 1986 were:

1. Multiple tests for thrombocytopenia.

2. No spleen or only slight increase.

3. Bone marrow examination shows an increase or normal megakaryocyte with a maturation disorder.

4. Exclude secondary thrombocytopenia.

5. Have any of the following 5 items:

1 prednisone treatment is effective;

2 splenectomy is effective;

3 platelet-related antibody positive;

4PAC3 positive;

5 platelet life is shortened.

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