Thrombocytopenia pathogenesis

Medicinal thrombocytopenia can emerge under the use of different medicines, including interferon. The main mechanism of medicinal thrombocytopenia pathogenesis is assisted by the destruction of thrombocytes by the complement which is activated during antibody preparation. On withdrawal, the content of thrombocytes in blood is normalized. The formation of antibodies to thrombocytes in patients with viral hepatitis C occurs due to the destruction of membrane glycoproteins by the viruses. 

Warkentin TE. Heparin-induced thrombocytopenia. Pathogenesis, frequency, avoidance and management. Drug Saf 1997 17(5) 325-41. 

Aster, R.H., Drug-induced immune thrombocytopenia An overview of pathogenesis, Semin. Hematol., 36 (Suppl 1), 2, 1999. 

Warkentin TE, ElavathU U, Hayward CP, Johnston MA, Russett JI, Kelton JG. The pathogenesis of venous hmb gangrene associated with heparin-induced thrombocytopenia. Ann Intern Med 1997 127(9) 804-12. 

There is a relation between MMR vaccination and thrombocytopenic purpura, but not with the measles component itself (18). Thrombocytopenic purpura after MMR has been reviewed, with discussion of pathogenesis and the vaccines and infections associated with this problem (83). Rubella vaccine is one of the most frequently reported causes of thrombocytopenia in Denmark (84). In France, a retrospective epidemiological survey (1984-92) showed that the rates of thrombocytopenic purpura per 100 000 vaccinees were 0.23 for measles vaccine, 0.17 for rubella vaccine, 0.87 for combination MR vaccine, and 0.95 for MMR vaccine (85). Thrombocytopenia was severe and always associated with purpura. Cases of recurrent thrombocytopenic purpura after repeated MMR immunization have been reported (86,87). The Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention (CDC) has recommended avoiding subsequent doses of MMR when a previous episode of thrombocytopenia occurred in close temporal proximity to the previous immunization, that is within 6 weeks (88,89). 

Wanamaker WM, Wanamaker SJ, Celesia GG (1976) Thrombocytopenia associated with long term levo-dopa therapy. JAMA 235 2217 Ward AM, Udnoon S, Watkins J (1976) Immunological mechanisms in the pathogenesis of vinyl chloride disease. Br Med J 1 936... 

The pathogenesis of thrombocytopenia will become clearer when the mechanism of production of autoimmune disease is discussed. Only a few salient points are mentioned here. A number of drugs, among them allylisopropylacetyl carbamide (Sedormid), quinine, quinidine, are known to autosensitize platelets. In affected patients, the combination of platelet, drugs, and serum leads to thrombocytopenia a large number of patients with idiopathic thrombocytopenia have antiplatelet antibodies in their blood. If the blood of such patients is injected to normal individuals, thrombocytopenia occurs. 

The haemolytic uraemic syndromes (HUSs) are a heterogeneous group of similar entities with variable expression and severity. Renovascular endothelial cell injury is central to the pathogenesis, leading to platelet activation and intravascular coagulation, haemolytic anaemia with fragmented erythrocytes, thrombocytopenia, and renal failure. 

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