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thrombocytopenic purpura[¦thräm·bō¦sīd·ō¦pē·nik ′pər·pə·rə]
(purpura hemorrhagica), a widespread disease of man and animals; one of the group of hemorrhagic diatheses. It is caused by a decrease in the blood platelet count and by disturbances in blood clotting.
Thrombocytopenic purpura may occur as an independent disease (idiopathic thrombocytopenic purpura, or Werlhof’s disease), which is encountered mainly in women and is often chronic. Important in the genesis of thrombocytopenic purpura are the transformation of autoantibodies into platelets, intensified decomposition of platelets in the spleen, and changes in the vascular wall caused by the disappearance of the marginal layer of platelets, which results in hemophilia. Drug-induced thrombocytopenic purpura, which may result from the ingestion of such substances as analgesics, sulfanilamides, or quinine, is characterized by an instantaneous intravascular decomposition of platelets resulting from the formation of antibodies to counter the drug-thrombocyte complex. Symptomatic thrombocytopenic purpura may occur in typhoid, protracted septic endocarditis, splenomegaly, collagen diseases, aplastic anemia, leukemia, and carcinomatous metastases in bone marrow.
The principal clinical symptoms of thrombocytopenic purpura are hemorrhages in the skin and a tendency toward bleeding in the mucous membranes. The type of thrombocytopenia is determined through a biopsy of the bone marrow. Treatment is effected by administering corticosteroids and hemostatics or by removing the spleen.
REFERENCEKassirskii, I. A., and G. A. Alekseev. Klinicheskaia gematologiia, 4th ed. Moscow, 1970.
A. N. SMIRNOV