What is the cause of immune thrombocytopenic purpura

First of all, everyone should understand that purpura is a physical sign, and the main cause of this sign is a decrease in platelets in the body. Immune thrombocytopenic purpura is the most common sign of thrombocytopenia, and there are several reasons for this sign.

Disease Overview

Purpura is a common clinical sign, often caused by a decrease in platelet count, so it is generally called thrombocytopenic purpura. Among them, immune thrombocytopenic purpura is the most common. Although thrombotic thrombocytopenic purpura has a lower incidence, the mortality rate is higher.

Idiopathic thrombocytopenic purpura has always been considered a hemorrhagic disease of unknown cause. In recent years, a large number of studies have confirmed that the disease is related to immune response, so it should be called autoimmune thrombocytopenic purpura (also referred to as ITP). The hematological characteristics of this disease are thrombocytopenia in the peripheral blood, antiplatelet antibodies bound to the platelet surface, shortened platelet lifespan, and compensatory increase in bone marrow megakaryocytes, resulting in impaired platelet production.

Multiple factors

The exact cause of this disease has not yet been fully elucidated. It may be caused by a combination of factors, which are described as follows:

1. Immune factors. The direct cause of thrombocytopenia is increased platelet destruction, that is, the platelet survival time is significantly shortened. The cause is the presence of antiplatelet antibodies in the patient's plasma, which have a destructive effect on both the same and one's own platelets.

2. Vascular factors. Clinically, it is found that the degree of bleeding in some patients is disproportionate to the decrease in platelet count, which may be related to the bleeding of this disease and capillary dysfunction. For example, after splenectomy, although the platelet count does not increase in some cases, bleeding phenomena may improve; after treatment with adrenal cortical hormones, the platelet count may not increase, but the capillary fragility test will turn negative and bleeding may also be alleviated. All of these are sufficient to illustrate the importance of capillary defects in bleeding in this disease.

3. Spleen factors. Studies have shown that the spleen may be one of the important sites for the production of antiplatelet antibodies. When the spleen produces a large amount of antiplatelet antibodies, normal platelets become sensitized by combining with the antiplatelet antibodies through the spleen. The sensitized platelets are easily phagocytosed by macrophages, so the platelet count in the patient's peripheral blood is significantly reduced.

4. Genetic factors. Studies have shown that patients and their immediate healthy family members have varying degrees of immunological deficiencies, suggesting that the disease may be closely related to genetics.