IA rAAV2-TNFR:Fc resulted in administration site reactions after 12% of injections. A fatal SAE, disseminated histoplasmosis, was considered not related to study agent. Patient-reported outcome measures of clinical response showed greater improvement in treated patients than placebo patients.

Though the efficacy of intraarticular (IA) corticosteroid administration in the therapeutic management of rheumatoid arthritis (RA) has been well documented, its immunomodulatory effects have not been defined. Categorization of these effects is important to develop safe derivative therapeutic strategies with a more targeted mechanism of action as they relate to the pathophysiology of RA. We describe here a broad spectrum immune response to inflammation as evidenced by rapid transient systemic inhibitory effects on key inflammatory regulators induced by the effects of IA administration of triamcinolone acetonide in a case of active RA who failed to respond to methotrexate.

A unique case of adult-onset synchronous cyclic neutropenia and thrombocytopenia occurring at six-week intervals is presented. Periods of cytopenia were associated with fever, myalgias, gastrointestinal symptoms, and mild mucocutaneous bleeding. Alternate-day steroid treatment failed to correct the periodic fluctuations in peripheral blood counts but ameliorated symptoms during cytopenia. The treatment of cyclic hematopoiesis is reviewed.

We composed a model from autoimmune serologic findings, HLA antigens, and clinical findings that explains, at least partially, the clinical heterogeneity of 40 patients with systemic lupus erythematosus (SLE). In these patients, anti–Ro (SS‐A) was related to the HLA–DQ1/DQ2 heterozygotes, anti–La (SS‐B) was related to HLA–B8 and HLA–DR3, and anti–nuclear RNP (Sm) was related to HLA–DR4. Lymphopenia was associated with anti–Ro (SS‐A) and, secondarily, with anti‐single‐stranded DNA. Renal disease in these SLE patients was inversely associated with anti–La (SS‐B) and was positively associated with anti–double‐stranded DNA. There were no associations between the HLA antigens and these clinical manifestations. The results support a model of disease expression in which individuals are nonspecifically potentiated for SLE. Their HLA antigen composition influences the production of particular autoantibodies that are related in complex ways to the different particular clinical findings of SLE manifested in individual patients.