Thrombocytopenia autoantibody-induced

IgG autoantibody-coated platelets induce Fey receptor-mediated phagocytosis by mononuclear macrophages, predominantly in the spleen and liver. Thrombocytopenia develops as a consequence of megakaryocyte inability to increase platelet production and maintain a normal number of circulating platelets. Currently used treatments are directed at different aspects of the antibody production, platelet sensitization, and the clearance and production cycle.30... 

Another type of autoantibody leading to thrombocytopenia that is induced by ti-clopidine is directed against von Willebrand factor metalloproteinase [45 ]. This prevents the normal clearance of large multimers of von Willebrand this can lead to platelet aggregation, and in some cases, to thrombotic thrombocytopenic purpura, commonly referred to as TTP. Many other drugs have been implicated as cases of TTP, but the mechanism is unclear and appears to differ with different drugs [46],... 

Heparin-induced thrombocytopenia (HIT), characterised by arterial thromboemboli and haemorrhage, occurs in about 2-3% of patients who receive standard heparin for a week or more (less in patients on LMW heparins). It is due to an autoantibody directed against heparin in association with platelet factor 4, causing platelet activation, and occurs most commonly with heparin derived from bovine lung. HIT should be suspected in any patient in whom the platelet count falls by 50% or more after starting heparin, and usually occurs 5 or more days after starting therapy (or sooner if the patient has previously been exposed to heparin). Up to 30% of patients may require amputation or may die. 

Treatments with recombinant therapeutic cytokines occasionally induce autoimmune phenomena. In particular, IFN-a may cause or exacerbate autoimmune effects, in particular thyroiditis, but also autoimmune thrombocytopenia or autoimmune hepatitis, and systemic lupus erythematosus has been reported. Relationships between IFN-a treatment and dermatomyositis (Dietrich et al., 2000) and diabetes mellitus (Fabris et al., 2003) have been observed. In addition, increased levels of various autoantibodies have been found in patients receiving IFN-a (Vial et al., 2002). Monzani et al. 

Garratty G, Amdt P, Prince HE, Shulman lA (1993) The effect of methyldopa and procainamide on suppressor cell activity in relation to red cell autoantibody production. Br J Haematol 84 310-315 Gottschall JL, Elliot W, Lianos E, McFarland JG, Wolfmeyer K, Aster RH (1991) Quinine-induced immune thrombocytopenia associated with hemolytic uremic syndrome a new clinical entity. Blood 77 306-310... 

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