Drug immune thrombocytopenic purpura

Introduction to drug-induced thrombocytopenic purpura Drug-induced thrombocytopenic purpura is caused by the immune destruction of the patient's platelets by drug-induced platelet antibodies. Antigen-antibody reactions occur on the peripheral platelet membrane, and drugs that do not generally affect megakaryocytes include plant alkalis, antipyretic and analgesic drugs. Sulfonamides. Hormone treatment is not ideal. basic knowledge The proportion of sickness: 0.001% - 0.005%, more common in allergic people Susceptible people: no special people Mode of infection: non-infectious Complications: gastrointestinal bleeding

Drug-induced thrombocytopenic purpura

(1) Causes of the disease

Drugs that cause immune thrombocytopenia:

1 plant alkalis: quinine, quinidine.

2 antibiotics: penicillin, cephalosporin, streptomycin, chloramphenicol, rifampicin, sulfonamides.

3 sedative antispasmodic drugs: barbiturates, benzalazine, chlorpromazine, reserpine, codeine, pethidine (Du Lengding), methyl propyl amide (Sirmant), phenytoin and so on.

4 antipyretic analgesic drugs: aspirin, phenylbutazone, indomethacin, antipyrine, promethazine (fetagen), sodium salicylate and so on.

5 Sulfonamide derivatives: chlorpropamide, tolbutamide, and the like.

6 other: nitroglycerin, spironolactone, expectorant, chloroquine, methyldopa, propylthiouracil, digoxin, insecticides, etc. A foreign research report reported that the drug that is most likely to cause thrombocytopenia is quinidine, followed by quinine, rifampicin, chlordiazepoxide, chloroquine, indomethacin, antipyrine and other drugs that cause immune thrombocytopenia. Not a few.

(two) pathogenesis

Platelets are immunocompromised by drug-dependent anti-platelet antibodies, and antigen-antibody reactions occur mostly on peripheral platelet cell membranes and generally do not affect megakaryocytes.

Some drugs can bind to the antibody to form a complex, adhere to the platelet membrane, and at the same time activate complement, causing platelet destruction. The binding of the complex to the platelet is not strong, and it is easy to separate from the platelets and adhere to other platelets. Therefore, A small amount of complex can cause a large number of platelets to destroy in the blood vessels, and this type can also be called "immune complex type".

In addition, some drugs can bind to platelet membrane glycoprotein, causing structural changes, exposure of new sequence sites hidden by platelet surface membrane glycoproteins, or binding of platelet surface proteins to drugs to form complexes, resulting in platelet surface New antigenicity induces antibody formation.

The drug can be combined with a macromolecular protein or a carrier in plasma to form an antigen (drug-macromolecule protein complex), and an antibody is produced by the action of the antigen. Most of the antibody is IgG, and IgM is a specific antibody. It can destroy platelets with corresponding drug combinations without destroying normal platelets. A study of 15 patients with quinine-induced thrombocytopenia showed that there are antibodies in the serum that can bind to GPIb-IX, and some patients only exist. An antibody against GPIb or GPIX, and some patients have two antibodies. In addition, there is no cross-reaction between the two platelet antibodies induced by quinine and quinidine, indicating that the drug-induced antibody has a different drug structure. Highly specific.

Drug-induced thrombocytopenic purpura prevention

Avoid or reduce the use of plant alkalis, antipyretic analgesics and sulfonamides.

Drug-induced thrombocytopenic purpura complications Complications, gastrointestinal bleeding

Severe cases can be complicated by digestive tract, urinary tract hemorrhage, fever and abnormal liver function.

Drug-induced thrombocytopenic purpura symptoms Common symptoms Freckle skin defects Platelet reduction Gum bleeding Bleeding upper gastrointestinal bleeding

Drug-induced thrombocytopenia generally has an incubation period, and its length often varies with the nature of the drug. The incubation period ranges from several hours to several years, with a median time of 14 days, for example, immune thrombocytopenia caused by quinine and quinidine. It can occur within 12 hours after taking the drug, but the incubation period can be as long as several months; cephalosporin only for several days; rifampicin for several months; nitroglycerin takes about 5 months.

The disease can lead to severe thrombocytopenia, manifested as skin spots, ecchymosis, nosebleeds, bleeding gums, etc., sometimes severe bleeding symptoms, digestive tract and urinary tract bleeding, clinical symptoms vary with the degree of thrombocytopenia, platelet destruction When increased, if the bone marrow megakaryocyte compensation is good, and the destruction of platelets is balanced with compensatory hyperplasia, the thrombocytopenia is not obvious, and there is no clinical bleeding.

In foreign statistics, 247 patients with drug-induced thrombocytopenia, 23 (9%) had obvious bleeding symptoms, 2 of which died of severe bleeding; 68 (28%) had milder bleeding symptoms; 96 cases ( 36%) only purpura, bleeding symptoms are not obvious, the remaining 60 cases (27%) no bleeding symptoms.

Drug-induced thrombocytopenic purpura

1. Peripheral blood leukocytes, hemoglobin, red blood cells have no change, platelets are generally significantly reduced, severe cases can be as low as 10 × 109 / L, even in peripheral blood is difficult to find platelets.

2. The beam arm test is positive.

3. The bleeding time is prolonged.

4. The megakaryocytes in the bone marrow are normal or increased, often accompanied by megakaryocyte maturation disorders.

Platelet agglutination test, radionuclide labeled platelet dissolution test, complement fixation test, platelet factor III release test, etc., in which the complement binding test and platelet factor III release test are most sensitive, blood clot retraction is inhibited by fresh blood plus related drugs, and blood clot is observed. The degree of contraction, if positive, indicates the presence of drug-related anti-platelet antibodies in the patient's serum, which can be used as a clinical screening test.

Diagnosis and differentiation of drug-induced thrombocytopenic purpura

diagnosis

Have a history of drugs, combined with clinical manifestations and laboratory tests.

Differential diagnosis

It is differentiated from systemic lupus erythematosus thrombocytopenia, megakaryocyte thrombocytopenic purpura, microangiopathic thrombocytopenic purpura (TTP), hypersplenism, and the like.

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