title: Effect on lymphocyte subsets of clotting factor therapy in human immunodeficiency virus-1-negative congenital clotting disorders. The Transfusion Safety Study Group.
abstract: Patients with hemophilia A without human immunodeficiency virus type 1 (HIV-1) infection have lower CD4+ counts and CD4+/CD8+ ratios than controls. This is usually interpreted as a therapy-induced immunodeficiency. Our data re-examine the effect of therapy on peripheral blood mononuclear cell immunophenotypic subpopulations in all congenital clotting disorders. Since late 1985 we have prospectively observed HIV-1 uninfected persons with all types and severity of disorder. Controls were household members without clotting disorders or HIV-1 infection. Analyses of immunophenotype and treatment included a longitudinal random effects model. Compared with controls, age-adjusted CD4+ counts were significantly lower in treated patients (P < .0001) and in patients with all types of clotting disorders who were seldom or never treated (P = .0005). Significantly lower values among both treated and untreated clotting disorder subjects (P < .05) were likewise found for total lymphocytes, several other T-cell subsets, and the CD4+/CD8+ ratio. For most indexes, including the CD4+ count and CD4+/CD8+ ratio, the type of clotting deficiency was not a significant variable. Comparing persons who had no or minimal therapy with those having the most showed increases in CD8+ (P = .0017) and CD20+ CD21- counts (P = .0255), and a lower CD20+ CD21+/CD20+ ratio (P = .0106) in the latter. Controls and persons with clotting disorders differ in CD4+ count. Among those with clotting factor disorders, there is no difference attributable to type of clotting disorder or factor therapy. Large amounts of treatment increased CD8+ and CD20+ CD21- counts, but were not associated with a change in CD4+ count.
authors.affiliation: Mount Sinai Medical Center, New York, NY.
authors.forename: J
authors.initials: J
authors.lastname: Hassett
authors.forename: G F
authors.initials: GF
authors.lastname: Gjerset
authors.forename: J W
authors.initials: JW
authors.lastname: Mosley
authors.forename: M A
authors.initials: MA
authors.lastname: Fletcher
authors.forename: E
authors.initials: E
authors.lastname: Donegan
authors.forename: J W
authors.initials: JW
authors.lastname: Parker
authors.forename: R B
authors.initials: RB
authors.lastname: Counts
authors.forename: L M
authors.initials: LM
authors.lastname: Aledort
authors.forename: H
authors.initials: H
authors.lastname: Lee
authors.forename: M C
authors.initials: MC
authors.lastname: Pike
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D001778:Blood Coagulation Disorders / Q000151:congenital* / Q000276:immunology / Q000628:therapy; D001779:Blood Coagulation Factors / Q000627:therapeutic use*; D006679:HIV Seropositivity / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007153:Immunologic Deficiency Syndromes / Q000276:immunology / Q000628:therapy*; D016131:Lymphocyte Subsets / Q000502:physiology*; D008297:Male
chemical_list: D015703:Antigens, CD; D001779:Blood Coagulation Factors