No abstract

One hundred and forty‐nine women received a suburethral woven polypropylene mesh insertion for urodynamic stress incontinence. Eleven patients (7.5%) presented between 4 and 17 months after surgery (mean 10 months) with symptoms of retropubic infection. Ten patients required surgical exploration, drainage of the collection and removal of the tape either unilaterally (six) or bilaterally (four). Bacterial cultures were negative in nine women. Following removal of the tape, eight patients reported residual incontinence, either stress leakage (five) or de novo urge incontinence (three). Multifilament polypropylene meshes appear to be more at risk of infection, usually requiring sling removal, which may be related to pore size of the mesh. Our data reinforce the importance of proper evaluation of new surgical procedures by rigorously designed randomised trials with adequate follow up to identify rare but potentially serious complications.

No abstract

A monoclonal antibody (mAb) directed against the extracellular domain of the IFNAR1 chain of the human interferon-alpha (IFN-alpha) receptor (IFN-alphaR), which inhibits activation of the Jak-Stat signal transduction pathway, administered together with a subeffective dose of cyclosporine induced prolonged survival of skin allografts in major histocompatibility complex (MHC) divergent cynomolgus monkeys. Skin biopsies from animals treated with anti-IFN-alphaR mAb and cyclosporine revealed very low levels of MHC class I and class II antigen expression and the absence of histologic signs of rejection. Monkey antibodies (IgG) to the mouse antihuman IFN-alphaR mAb were not detected in the serum of any of the animals treated with the anti-IFN-alphaR mAb either alone or together with cyclosporine. The anti-IFN-alphaR mAb abrogated activation of the Jak-Stat signal transduction pathway in IFN-treated cells. These results, which show that selective and long-lasting immunosuppression can be obtained by short-term administration of an IFN-alpha antagonist together with a subeffective dose of cyclosporine, may have important implications for the therapy of human allograft rejection.