MR imaging demonstrated the wide spectrum of findings of central nervous system involvement in patients with Wegener granulomatosis and was particularly useful for the evaluation of direct intracranial spread from orbital, nasal, or paranasal disease.

Conventional immunosuppression for systemic vasculitides is limited by substantial side-effects, cumulative drug toxicity and refractoriness in some patients. Six Wegener's granulomatosis patients who had been refractory to conventional therapy for at least 6 months, were treated with humanized monoclonal antibodies specific to lymphocyte CD52 or CD4 antigens. Diagnosis was on clinicopathological grounds, supported by the presence of autoantibodies to Proteinase 3. Histological evidence of persistent disease activity was obtained for each patient. Humanized monoclonal anti-CD52, with or without anti-CD4, was given intravenously up to 40 mg/day for up to 10 days. Remission, (programmed withdrawal of drug therapy without return of refractory disease) was achieved in all patients. Cytotoxic drugs were discontinued at the time of monoclonal antibody treatment and not used again; steroids were withdrawn gradually. Four patients relapsed at 1.5, 5, 10 and 18 months, and were treated successfully with further monoclonal antibody therapy alone. Three years after the study began, five patients are well; one patient died at surgery whilst in remission. Humanized monoclonal antilymphocyte antibodies may provide an effective treatment in patients with systemic vasculitis which is refractory to steroids or cytotoxic agents, or who are intolerant of these drugs.

ANCA not directed against classical antigens (MPO and PR3) may be found in PiZZ patients. However, these patients do not develop systemic vasculitis features. Therefore, alpha1-antitrypsin deficiency is not sufficient to induce ANCA positive vasculitides, and may only act as a second hit amplifying factor.

No abstract

Results: There was a homocysteine dose-related reduction in A23 187stimul eNOS ictivity was lower in non-stimulated cells and no cansistent pattern of inhibition by homocysieine was observed eNOS mass ranged from ?.I 10 2.9 optical density units per mg protein; there was no reduction in enzyme mass as a result of incubation with homocysteine. either as a function of time or of concentration. Concluqions: Homocysleinr, at concentrations commonly found in mild hyperhomocysteinaemia. reduces endothelial eNOS activity by a mechantsin that involves enzyme inhibition rather than a reduction in enzyme mass. MODULATIONOF ERYTHROCYTE SODIUM-UTHIUM COUNTERTRANSPORT (Na-Li CT) BY PROTEIN KlNASE C AND PROTEIN PHOSPHATASES E PARKINSON (introduced). H LEITCH (introduced), R COLEMAN (introduced), J WILLIAMS (introduced)

No abstract