I. Diagnostic considerations for ITP
1. So far, the diagnosis of ITP is still a diagnosis of exclusion. More emphasis is placed on history, physical examination, blood count (repeated several times), blood smear examination, autoantibody screening, etc.
2, If splenomegaly is found in the diagnosis of ITP other diagnoses should be considered first.
3, Peripheral blood smear microscopy can help to exclude EDTA-dependent platelet aggregation caused by pseudo-thrombocytopenia, microangiopathic hemolysis, leukemia or other malignancy-related thrombocytopenia, etc.
4. Bone marrow aspiration should still be routinely performed in patients with suspected ITP. The main purpose of this test is to exclude other diseases that cause thrombocytopenia, so that misdiagnosis can be avoided to the greatest extent possible.
5. Autoimmune series antibody tests (rheumatic series, antiphospholipid antibodies, anti-thyroid antibodies, etc.) should be done as routine screening tests in the diagnosis of ITP.
6, platelet glycoprotein (GP) is more specific and can distinguish between immune and non-immune thrombocytopenia, which helps in the diagnosis of ITP.
7.TPO level test can help to distinguish ITP from atypical remitting disease or hypoproliferative MDS.
II. Current clinical diagnostic criteria
No specific criteria. It mainly relies on medical history, physical examination, blood routine and blood smear, bone marrow cytology and other comprehensive judgment.
1, manifestations of bleeding.
2, decreased platelet count on multiple examinations.
3, a small or mildly large spleen.
4, normal or increased number of megakaryocytes in the bone marrow with impaired maturation.
5, Prednisone treatment is effective or splenectomy treatment is effective.
III. Differential diagnosis of ITP
The following points need to be noted.
1. Due to the widespread use of automated blood cell counters, reports of pseudo-thrombocytopenia due to platelet aggregation caused by anticoagulants (EDTA) are gradually increasing and must be taken seriously.
2.For pregnant women, the incidence of pregnancy thrombocytopenia (benign disease) is a hundred times higher than that of ITP.
3, For pediatric patients with ITP, attention should be paid to differentiate it from congenital or hereditary thrombocytopenia and AA.
All patients with ITP should be distinguished from other autoimmune diseases and lymphoproliferative diseases, and should be carefully asked whether they have taken other drugs to understand the possibility of drug-induced thrombocytopenia (e.g., heparin, quinine, etc.).
IV. Treatment strategy for ITP
The ideal goal for the treatment of this disease is to raise platelets above 100×109/L, and the minimum goal is no bleeding manifestations. In principle, overtreatment should be avoided as much as possible.
1. Follow-up observation is recommended for those with platelets above 30×109/L.
2. For those with platelets of 30×109/L and bleeding or with treatment requirements, the following options are available.
①Dexamethasone 40mg/d×4 (newly recommended) and repeat in two weeks if necessary. If platelets are above 30×109/L, enter the follow-up observation program. Or
②Prednisone 1~1.5mg/d (traditional use), gradually reduce and maintain until discontinuation after platelets are close to normal.
3. For platelets 10×109/L, severe bleeding or risk of severe bleeding, take the acute treatment described below.
4.If hormone therapy is not sensitive and platelets are 30×109/L and there is bleeding, consider splenectomy.
5. If splenectomy is indicated but the patient refuses surgery or there is a contraindication to surgery, consider
① TPO± Danazol.
② Meroval.
③ Cyclosporine A.
④ Clinical trial of Chinese medicine.
6. If the above treatments are not effective, refer to non-conventional treatment. See Treatment of refractory ITP (to be continued).
V. Emergency management of ITP
1. Platelet suspension infusion: Repeatable according to the abundance of the condition.
2.Intravenous gammaglobulin: 0.4g/kg/d for 5 days.
3, plasma replacement: can effectively remove PAIg from the patient’s drug plasma. 3000ml per replacement, more than 3 times in a row.
4, high-dose methylprednisolone: can play a therapeutic role by inhibiting the destruction of platelets by the monocyte-macrophage system. Use 1000 mg/d×3.
The above methods can be chosen according to the patient’s specific situation.