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Publication Detail
The treatment of chronic idiopathic thrombocytopenia with anti-D (Rho) immunoglobulin: its effectiveness, safety and mechanism of action.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Boughton BJ, Chakraverty R, Baglin TP, Simpson A, Galvin G, Rose P, Rohlova B
  • Publication date:
    1988
  • Pagination:
    275, 284
  • Journal:
    Clin Lab Haematol
  • Volume:
    10
  • Issue:
    3
  • Status:
    Published
  • Country:
    England
  • Print ISSN:
    0141-9854
  • Language:
    eng
  • Keywords:
    Adult, Aged, Chronic Disease, Erythrocytes, Female, Humans, Immunization, Passive, Immunoglobulin G, Immunoglobulins, Isoantibodies, Male, Middle Aged, Rho(D) Immune Globulin, Spleen, Thrombocytopenia
Abstract
Twenty-three courses of i.v. anti-D (Rho) immunoglobulin were administered to 13 Rh D-positive patients with chronic idiopathic thrombocytopenia (ITP). Clinically significant responses were seen in a proportion of patients treated with 500-2500 i.u. anti-D, but all those treated with 12,500 i.u. (180 i.u./kg) responded. Patients refractory to other forms of treatment responded well to anti-D, and previous splenectomy did not influence the clinical response. No adverse reactions were observed. The anti-D response was preceded by a lag period of 3-16 days and was maintained for 14-145 days. Platelet-associated IgG was increased after treatment, due to improved survival of immunosensitized platelets or platelet Fc receptor binding of high molecular weight IgG in the therapeutic material. There was no clinical or biochemical evidence of haemolysis. The erythrocyte direct Coombs' test remained positive for 3-45 days, and histological examination of splenic material showed no erythrophagocytosis. We conclude that anti-D (Rho) immunoglobulin is a safe and effective treatment for chronic ITP and that the therapeutic dose is now established in standardized units. The mechanism of action appears to be complex and is probably not due to macrophage Fc receptor blockade with immunosensitized red cells.
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