Correlation of in vitro antibody synthesis with the outcome of intravenous gamma-globulin treatment of chronic idiopathic thrombocytopenic purpura. Academic Article uri icon

Overview

abstract

  • Intravenous gamma-globulin (IVGG) effectively elevates the platelet count of most patients with chronic idiopathic thrombocytopenic purpura (ITP). This study examined whether this effect was related to changes in in vitro immunoglobulin secretion and suppression in coculture. Before treatment, patient in vitro immunoglobulin secretion was less than 50% of the concurrent control in all eight cases and the patients suppressed antibody synthesis in coculture an average of 39%. After treatment, increases in in vitro immunoglobulin secretion and decreases in suppression were closely related to a good response to IVGG therapy as measured both by acute increases in the platelet count (P less than 0.05) and by the long-term outcome from therapy (P less than 0.05). Decreases in platelet-associated IgG correlated with increases in in vitro immunoglobulin secretion (P less than 0.05). Data consistent with the lack of inhibition of in vitro immunoglobulin secretion following IVGG included long-term increases in both serum IgM and IgG (independent of transfused IgG) and maintenance of the percentage of total IgG that was IgG3. T-cell numbers and subsets and lymphocyte proliferation were unaffected by IVGG. IVGG tends to normalize in vitro immunoglobulin secretion and its suppression in those ITP patients with good clinical responses in conjunction with decreased levels of autoantibody. This evidence suggests that good responders to IVGG may have inhibition of antiplatelet antibody production. IVGG does not appear to interfere with normal antibody production.

publication date

  • January 1, 1986

Research

keywords

  • Antibody Formation
  • Purpura, Thrombocytopenic
  • gamma-Globulins

Identity

Scopus Document Identifier

  • 0023039645

Digital Object Identifier (DOI)

  • 10.1007/BF00915364

PubMed ID

  • 2420817

Additional Document Info

volume

  • 6

issue

  • 1