Splenectomy in relapsing and plasma-refractory acquired thrombotic thrombocytopenic purpura

Haematologica. 2004 Mar;89(3):320-4.

Abstract

Background and objectives: Acquired thrombotic thrombocytopenic purpura (TTP) is often due to autoantibodies inhibiting ADAMTS-13 activity resulting in impaired processing of very large von Willebrand factor multimers. TTP usually presents with an acute onset and a fulminant, sometimes fatal course. With appropriate treatment including plasma exchange, and fresh frozen plasma replacement, often supplemented by immuno-suppressive therapy, the acute episode generally resolves within days to weeks.

Design and methods: We describe the clinical course of 3 patients with acquired TTP. One was refractory to PE, the other 2 relapsed after this treatment. All three were treated with splenectomy. ADAMTS-13 activity and inhibitor levels were monitored.

Results: ADAMTS-13 activity was initially < 5% in all 3 patients. After splenectomy the inhibitor against ADAMTS-13 disappeared rapidly in 2 patients and there was full recovery of ADAMTS-13 activity in all 3 patients.

Interpretation and conclusions: Splenectomy, by eliminating a source of pathogenic autoantibody production, can be a successful treatment for patients with relapsing or plasma-refractory acquired TTP due to autoantibody-mediated ADAMTS-13 deficiency.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADAMTS13 Protein
  • Adolescent
  • Adult
  • Aged
  • Autoantibodies / immunology
  • Female
  • Follow-Up Studies
  • Humans
  • Male
  • Metalloendopeptidases / antagonists & inhibitors
  • Metalloendopeptidases / immunology
  • Metalloendopeptidases / metabolism
  • Plasma Exchange
  • Purpura, Thrombotic Thrombocytopenic / etiology
  • Purpura, Thrombotic Thrombocytopenic / immunology
  • Purpura, Thrombotic Thrombocytopenic / surgery*
  • Splenectomy*

Substances

  • Autoantibodies
  • ADAMTS13 protein, mouse
  • Metalloendopeptidases
  • ADAMTS13 Protein