title: CD55 and CD59 deficiency in transplant patient populations: possible association with paroxysmal nocturnal hemoglobinuria-like symptoms in Campath-treated patients.
abstract: Campath-1H therapy is directed to CD52, a small mw protein that has a glycosylphosphatidylinositol (GPI) anchor, which has a conventional structure similar to other GPI anchors such as CD55 and CD59. Paroxysmal nocturnal hemoglobinuria (PNH) results when cells have a somatic defect in the synthesis of GPI anchors and lack CD55 and CD59, as well as CD52. Several patients treated with Campath developed PNH-like symptoms with hemolysis and thrombosis. These patients were followed after therapy by measurement of peripheral CD55 and CD59 levels and showed an increased number of cells deficient in the expression of these molecules. Thereafter we instituted a screening program for the presence of CD55/59 levels in all pretransplant patients. Our results show that 17.3% of all pretransplant samples contained abnormal (9.7% of samples) or slightly abnormal (7.6% of samples) levels of granulocytes deficient in CD55 or CD59. This high prevalence of CD55/59 deficiency in Campath-treated patients with PNH-like symptoms suggests that a lack of these molecules (including CD52) could predispose to a complication of this immunosuppressive therapy.
authors.affiliation: Department of Pathology, University of Miami School of Medicine, 1611 NW 12th Avenue, JMH Holtz Center #2101, Miami, FL 33136, USA. pruiz@med.miami.edu
authors.forename: P
authors.initials: P
authors.lastname: Ruiz
authors.forename: D
authors.initials: D
authors.lastname: Weppler
authors.forename: P
authors.initials: P
authors.lastname: Tryphonopoulos
authors.forename: S
authors.initials: S
authors.lastname: Nishida
authors.forename: J
authors.initials: J
authors.lastname: Moon
authors.forename: T
authors.initials: T
authors.lastname: Kato
authors.forename: G
authors.initials: G
authors.lastname: Selvaggi
authors.forename: D
authors.initials: D
authors.lastname: Levi
authors.forename: J
authors.initials: J
authors.lastname: Madariaga
authors.forename: J
authors.initials: J
authors.lastname: DelaGarza
authors.forename: S
authors.initials: S
authors.lastname: Tuteja
authors.forename: M
authors.initials: M
authors.lastname: Garcia
authors.forename: A
authors.initials: A
authors.lastname: Tzakis
mesh_terms: D000074323:Alemtuzumab; D000743:Anemia, Hemolytic / Q000209:etiology; D000911:Antibodies, Monoclonal / Q000009:adverse effects*; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm / Q000009:adverse effects*; D015703:Antigens, CD / Q000235:genetics; D019002:CD56 Antigen / Q000235:genetics*; D018957:CD59 Antigens / Q000235:genetics*; D017353:Gene Deletion; D006457:Hemoglobinuria, Paroxysmal / Q000139:chemically induced*; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects; D013927:Thrombosis / Q000209:etiology
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm; D015703:Antigens, CD; D019002:CD56 Antigen; D018957:CD59 Antigens; D007166:Immunosuppressive Agents; D000074323:Alemtuzumab