title: Posttransplantation cytotoxic immunoglobulin G is associated with a high rate of acute allograft dysfunctions in heart transplant recipients.
abstract: BACKGROUND
  The significance of anti-human leukocyte antigen immunoglobin G (IgG) detected in the posttransplantation course of heart graft recipients remains unclear.
  
  
  METHODS
  Sera from 121 cardiac allograft recipients transplanted between January 1992 and December 1994 were screened for the presence of lymphocytotoxic antibodies in the first year after transplantation. Dithiothreitol was used to differentiate IgG from immunoglobulin M.
  
  
  RESULTS
  Nineteen patients (15%) had cytotoxic IgG develop, mainly during the first month after transplantation. The percentage of women was higher in this group (42% vs 15.7%; P <.05). Donor to recipient mismatches for sex, blood typing, cytomegalovirus serology, and human leukocyte antigen typing were comparable between IgG producers and nonproducers. The frequency of acute allograft dysfunction during the first year after transplantation was significantly higher among patients producing IgG (42% vs 5.9; P <.001). Most of these acute allograft dysfunctions were independent of cellular rejection lesions but were associated with a thickening of the posterior wall and the interventricular septum during the acute episode. Finally, all the patients but one recovered. Recurrences were not uncommon and, at 1 year after transplantation, the dose of cyclosporine used in patients producing IgG was significantly greater, as was the left ventricular thickness.
  
  
  CONCLUSIONS
  Posttransplantation cytotoxic IgG is not uncommon and appears to be associated with a high rate of acute allograft dysfunction. Development of these antibodies can be caused by a previous undetected immunization, as suggested by the higher percentage of women in the producer group. Correlation with histologic lesions of humoral rejection are discussed.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, La Pitié Hospital, Paris, France.
authors.forename: P
authors.initials: P
authors.lastname: Leprince
authors.forename: C
authors.initials: C
authors.lastname: Fretz
authors.forename: R
authors.initials: R
authors.lastname: Dorent
authors.forename: A
authors.initials: A
authors.lastname: Boudifa
authors.forename: J
authors.initials: J
authors.lastname: Jourdan
authors.forename: J J
authors.initials: JJ
authors.lastname: Youssoub
authors.forename: V
authors.initials: V
authors.lastname: Bors
authors.forename: P
authors.initials: P
authors.lastname: Nataf
authors.forename: A
authors.initials: A
authors.lastname: Pavie
authors.forename: I
authors.initials: I
authors.lastname: Gandjbakhch
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D016572:Cyclosporine / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D006084:Graft Rejection / Q000276:immunology*; D016027:Heart Transplantation / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis*; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D018570:Risk Assessment; D014184:Transplantation, Homologous; D016277:Ventricular Function, Left
chemical_list: D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D016572:Cyclosporine