Henoch-Schonlein purpura is caused by allergies. When some allergens enter allergic constitution, after an incubation period of about two weeks, allergic inflammation will occur in capillaries, which will increase the permeability of capillaries, and blood and lymph will penetrate into tissues, causing exudative bleeding and edema of subcutaneous mucosa or visceral tissues. Thrombocytopenic purpura may be related to autoimmunity, and thrombocytopenia affects hemostasis function.
In addition, allergic purpura and thrombocytopenic purpura have the following differences, which are described as follows.
First, the clinical manifestations are different.
Henoch-Schonlein purpura
Most of the children had a history of upper respiratory tract infection 1-3 weeks before onset. In most cases, cutaneous purpura is the first symptom, and rash is the main manifestation. Mainly distributed in the weight-bearing parts, mostly at the distal end of the lower limbs, densely around the ankle joint; Secondly, it is found in the buttocks.
The characteristic rash is higher than the skin, which is small urticaria or pink maculopapular rash at first, and purpura when pressed. Hemorrhagic blisters can also form at the lesion site, even necrosis, leading to ulcers. Purple blends into pieces and finally turns brown. It generally disappears within 1-2 weeks, leaving no trace; It can also be postponed for weeks or months.
About two-thirds of children have digestive tract symptoms. Usually occurs in the rash 1 week. The most common symptom is abdominal pain, mostly manifested as paroxysmal periumbilical colic, which can also spread to any part of the abdomen. About half of the children were positive for occult blood in stool, and some even vomited blood in stool.
The urinary system can be gross hematuria or microscopic hematuria and proteinuria, or tubular urine. It can occur at any stage of the course of allergic purpura, but it usually occurs 2-4 weeks after purpura, and it can also occur after the rash subsides or the disease is still. Most children have only some joint pain or arthritis.
? Thrombocytopenic purpura
The disease is found in children of all ages and can be divided into acute (≤6 months) and chronic (> 6 months) types.
Acute onset is sudden, bleeding is serious, and respiratory infection often occurs shortly before or at the same time of bleeding. Chronic cases have no obvious peak age, but most of them are in school age. Most of them have hidden onset and mild bleeding symptoms. About 10% of children turn from acute to chronic. Its bleeding is characterized by extensive bleeding of skin mucosa, mostly scattered needle-like skin or subcutaneous bleeding spots, forming petechiae or ecchymosis; There are many limbs, but it can also be a systemic hemorrhage or hematoma; Some children complain of nosebleeds (about 20%-30%) or bleeding gums.
Common hematemesis or melena are mostly caused by swallowing when the mouth and nose are bleeding, and real gastrointestinal bleeding is rare. Subconjunctival hemorrhage is also a common symptom. About 1% children suffer from intracranial hemorrhage, which is the main cause of death in thrombocytopenic purpura.
Second, the laboratory results are different.
Henoch-Schonlein purpura
Platelet count is normal or elevated. The bleeding time, coagulation time and clot contraction time are all normal. The total number of white blood cells in some children is as high as 20× 109/L, and the nucleus is shifted to the left. The erythrocyte sedimentation rate can be accelerated, and C-reactive protein and anti-streptolysin can be positive.
? Thrombocytopenic purpura
(1) Blood routine: The most important change in peripheral blood is that platelets drop below 100× 109/L, and the degree of bleeding is directly proportional to the level of platelets. The other two lines are basically normal, with occasional hemorrhagic anemia.
(2) Bone marrow smear: The main manifestation is megakaryocyte maturation disorder. Classification of megakaryocytes: the percentage of original megakaryocytes and immature megakaryocytes is normal or slightly higher; The number of mature megakaryocytes without platelet release increased significantly, reaching 80%. However, few mature megakaryocytes release platelets.
(3) Detection of platelet antibody: The main reason is the increase of platelet surface IgG(PA IgG), and the positive rate is 66%- 100%. Simultaneous detection of anti-platelet antibodies (PAIgG, PAIM, PAIgA) can improve the positive rate.
Third, the treatment plan is different.
? Henoch-Schonlein purpura
Use antihistamines and calcium when you stay in bed in the acute stage and have urticaria or angioneurotic edema. Antiplatelet drugs (aspirin or dipyridamole) and anticoagulant therapy (heparin sodium or heparin calcium) can be used. When there are serious gastrointestinal diseases (such as gastrointestinal bleeding), nephrotic syndrome and acute nephritis, glucocorticoid can be used for treatment. When renal failure occurs, plasma exchange and dialysis can be used, and severe cases can be treated with large doses of gamma globulin.
? Thrombocytopenic purpura
Reduce activities and avoid trauma. Glucocorticoid is used for treatment, and gamma globulin can be used for children with bleeding or more. Transfusion of fresh platelets can only be used as an emergency treatment for severe bleeding. If the hormone is ineffective, try immunosuppressants such as vincristine and cyclophosphamide. Splenectomy has a certain remission rate for chronic children, but the surgical indications should be strictly controlled.
The above are the main differences between allergic purpura and thrombocytopenic purpura. A comprehensive understanding of these can accurately distinguish and treat them scientifically.
However, it should be noted that the recovery period of these two diseases is relatively long. In the meantime, we must pay special attention to related life care, such as strengthening nutrition, moderate exercise and ensuring adequate sleep. To promote the recovery of the disease.