The Experts below are selected from a list of 48 Experts worldwide ranked by ideXlab platform

Taede Sminia - One of the best experts on this subject based on the ideXlab platform.

Dona M.h. Hameleers - One of the best experts on this subject based on the ideXlab platform.

Jeike Biewenga - One of the best experts on this subject based on the ideXlab platform.

Douglas J Norman - One of the best experts on this subject based on the ideXlab platform.

  • reduced human igg anti atgam Antibody Formation in renal transplant recipients receiving mycophenolate mofetil
    Transplantation, 1995
    Co-Authors: J A Kimball, Mark D Pescovitz, B K Book, Douglas J Norman
    Abstract:

    Exposure to the equine-derived polyclonal antithymocyte preparation, ATGAM, frequently elicits human anti-ATGAM Antibody Formation. The influence of concomitant immunosuppressants on this antiAntibody response has not been established. We therefore evaluated IgG Antibody Formation to ATGAM in 47 patients receiving ATGAM as part of a prospective, randomized, double-blinded study of mycophenolate mofetil versus azathioprine for maintenance immunosuppression after primary cadaveric renal transplantation. All patients received ATGAM for induction of immunosuppression plus methylprednisolone, prednisone, and cyclosporine. In addition, patients were randomized to receive maintenance immunosuppression consisting of either azathioprine (AZA) 1-2 mg/kg/day, mycophenolate mofetil 2 gm/day (MMF2), or mycophenolate mofetil 3 gm/day (MMF3). Patient sequential sera were independently tested for IgG anti-ATGAM Antibody by 2 laboratories, which were blinded to treatment arm assignments, using enzyme-linked immunosorbent assays. Both laboratories found significantly greater anti-ATGAM Antibody Formation in group AZA compared with groups MMF2 and MMF3 : laboratory 1 reported sensitization rates in the 3 groups of 94% (AZA), 50% (MMF2) (P<0.02 vs. AZA), and 60% (MMF3) (P<0.05 vs. AZA) ; and laboratory 2 reported rates of 67% (AZA), 17% (MMF2) (P<0.02 vs. AZA), and 10% (MMF3) (P<0.02 vs. AZA). In addition, fewer patients formed high titer Antibody in the MMF arms compared to the AZA arm : 56% (AZA), 0% (MMF2)(P<0.02 vs. AZA), and 20% (MMF3) (P<0.02 vs. AZA) of patients for laboratory 1 ; and 20% (AZA), 0% (MMF2) (P<0.05 vs. AZA), and 0% (MMF3) (P<0.05 vs. AZA) of patients for laboratory 2. Differences in test results between the 2 laboratories were explained by differences in the sensitivity of their respective immunoassays and in the criteria used for assigning a positive result to test specimens. In this protocol, MMF at 2-3 gm/day was associated with a reduced incidence and titer of IgG anti-ATGAM Antibody Formation compared with standard azathioprine dosing. Although MMF previously has been reported to inhibit T cell responses that mediate acute cellular rejection, this is the first demonstration that MMF significantly inhibits human B cell responses to antigen in vivo.

Gertjan Wolbink - One of the best experts on this subject based on the ideXlab platform.

  • Decreased clinical response to adalimumab in ankylosing spondylitis is associated with Antibody Formation.
    Annals of the rheumatic diseases, 2009
    Co-Authors: M.k. De Vries, Elisabeth Brouwer, I E Van Der Horst-bruinsma, Anneke Spoorenberg, J.c. Van Denderen, Anna Jamnitski, M.t. Nurmohamed, B A C Dijkmans, Lucien A. Aarden, Gertjan Wolbink
    Abstract:

    Treatment with anti-tumour necrosis factor (TNF) is very effective in most patients with ankylosing spondylitis (AS), but inefficacy occurs in about 40% of cases.1 Antibody Formation against TNF blocking agents is an increasingly recognised problem;2 however, no data have yet been reported on Antibody Formation against adalimumab (anti-adalimumab) in AS. Lack of response can be explained in two ways: (1) TNF might not be important for disease activity in certain patients; and (2) TNF inhibition might be insufficient. The latter could be caused by excessive production of TNF, low compliance of the patient, insufficient dosing or an enhanced clearance of adalimumab due to Antibody Formation. Adalimumab is a fully human monoclonal Antibody against TNF but, despite this fact, an immune response …