Clinical Analysis Of 7 Cases Of Idiopathic Thrombocytopenic Purpura Complicated With Thrombosis

The platelet plays an important role during physiological and pathological thrombosis, and the amount of platelet parallels blood coagulatlon status. Idiopathic thrombocytopenic purpura is a hemorrhagic disease with the immunal destruction of platelete and decrease of platelet count in peripheral blood. It is characterized with extensive skin, mucosa or internal organs hemorrhage, the decrease of platelet count, failure of megakaryocyte development and maturity in bone marrow, platelet survival time shortening and appearence of platelet-associated autoantibody. Because of the decrease of platelet count and inhibition of platelet function, thrombus is not easliy formed and the patient with ITP has hemorrhagic tendency. But during the clinical therapy of the patient with ITP, individual patient appeared thrombosis, such as cerebral infarction, vein thrombosis and so on, which caused intense attention of us. The goal of this article is to increase the knowledge of ITP complicated with thrombosis. Method: Retrospectively analyse the 7 cases of ITP complicated with thrombosis in our hospital from January 1994 to December 2004, and analyse its general data, and its clinical situation, and accessory examination, and its therapy and outcome. Results: 1, The incidence rate of ITP complicated with thrombosis is very low, 0.663 percent patients of ITP complicated with thrombosis in our hospital. 2, The patient of ITP complicated with thrombosis mostly is older, smoker, or has hypertension, diabetes mellitus, malignant tumor, atrial fibrillation, operation and so on, which always lead to thrombosis. 3, The mechanism of ITP complicated with thrombosis: ①large dose glucocorticoid caused endothelial cell of blood vessel function disorder during long-term therapy. ②glucocorticoid caused lipid metabolism abnormal. ③glucocorticoid inhibited the generation of platelet-associated autoantibody, blocked reticuloendothelial system, reduced destruction of platelets, stimulated production of platelets. Glucocorticoid can increase white blood cells and red blood cells also. ④glucocorticoid heightened concentration of some coagulation factors, raised their activity, reduced the cleaning of actived coagulation factors. ⑤Cimetidine added the calcium ions in platelets, increased platelet aggregation, reinforced the reaction with inducer, caused thrombosis. ⑥C imetidine inhibited TXA2 synthase, reduced TXA2, increased PGG2 and PGH2, activated platelet. ⑦in the cases of infection evocated ITP, bacteria and virus produced toxin and immune complex which can cause thombosis, the infection of blood vessel also can injure the blood vessel endothelial cell. ⑧a part of ITP is a kind of earlier period or atypical manifestation of SLE, and SLE can cause thrombosis itself. ITP and SLE complicated with anti-phospholipid antibody positive is called secondary antiphospholipid syndrome, and anti-phospholipid antibody can cause thrombosis through many ways. 4, Clinical physician should be care of the existence of systemic lupus erythematosus and secondary antiphospholipid syndrome in the patients of ITP complicated with thrombosis, and perform related tests and follow-up to avoid misdiagnosis and missed diagnosis. 5, When large dose and long-term glucocorticoid and Cimetidine treat ITP, we should pay attention to examine blood coagulatlon routine, to avoid the formation of hematological hypercoagulable state and thrombosis, and to remove the evoking factor of bacteria and virus infection in time. 6, Because the treatment of thrombotic diseases is easy to complicated with hemorrhage, and ITP has hemorrhagic...