What is idiopathic thrombocytopenic purpura

Generally, when thrombocytopenia occurs, idiopathic thrombocytopenic purpura may easily occur, which is a common symptom. Generally, idiopathic thrombocytopenic purpura can be divided into chronic and acute, and the manifestations of the two are different.

Idiopathic thrombocytopenic purpura is an immune syndrome and a common bleeding disease. The characteristic is the presence of antiplatelet antibodies in the blood circulation, which causes excessive platelet destruction and causes purpura; while the megakaryocytes in the bone marrow are normal or increase in number and become immature. Clinically, it can be divided into acute and chronic types, and the pathogenesis and manifestations of the two are significantly different.

Overview

Idiopathic thrombocytopenic purpura is a hemorrhagic disease caused by immune destruction of platelets, leading to thrombocytopenia in peripheral blood. Bacterial or viral infection is closely related to the onset of this disease. 80% of acute ITP patients have a history of respiratory tract infection about two weeks before the onset of the disease. Infection cannot directly lead to the onset of ITP. The involvement of immune factors may be an important cause of the onset of ITP. Platelet antibodies can be detected on the surface of platelets in more than 80% of ITP patients. In addition, platelets adsorbed with such antibodies are easily phagocytosed by macrophages in the liver and spleen (mainly in the spleen), which shortens the life of platelets.

The degree of thrombocytopenia is directly proportional to the amount of antiplatelet antibodies in the circulation, that is, the more antiplatelet antibodies there are, the more severe the thrombocytopenia is. The mother of a newborn patient may suffer from the same disease. Since antibodies can pass through the placenta and enter the fetus, it can cause thrombocytopenia in the newborn. The above characteristics all support that ITP is a disease caused by immune mechanism. The spleen is not only the main site for platelet destruction, but also the main organ for the production of antiplatelet antibodies. The antiplatelet antibody titer of patients with effective splenectomy decreased significantly after surgery.