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Etanercept (Enbrel, Immunex, Seattle) is a soluble tumor necrosis factor (TNF) receptor fusion protein that binds and inactivates TNF, a proinflammatory cytokine that is overproduced in the joints of patients with rheumatoid arthritis. 1 Etanercept reduces disease activity in adults and children with chronic rheumatoid arthritis who have had an inadequate response to other therapies. 2 – 5 TNF also stimulates the production of other proinflammatory cytokines, increases cell migration by increasing the production of cellular adhesion molecules, and increases the rate of tissue remodeling by matrix-degrading proteases. 6 – 8 In addition to reducing symptoms of rheumatoid arthritis, inhibition of the action of TNF . . .

Juvenile rheumatoid arthritis is the most common rheumatic condition in children. 1 , 2 In approximately one third of patients, the disease is controlled with nonsteroidal antiinflammatory drugs and an appropriate program of physical and occupational therapy. The remainder are candidates for more aggressive therapy with antirheumatic drugs. Methotrexate was shown to have a therapeutic advantage over placebo, with an acceptable safety profile, in a randomized, controlled trial in children with juvenile rheumatoid arthritis who had polyarticular involvement (regardless of the type of onset). 3 Long-term studies showed that methotrexate is efficacious and well tolerated in most children with juvenile rheumatoid arthritis. 3 – . . .

Etanercept, a tumour-necrosis-factor inhibitor, has shown efficacy in the treatment of rheumatoid arthritis. Psoriatic arthritis and psoriasis are disease states in which tumour necrosis factor, a proinflammatory cytokine, is present in increased concentrations in joints and in the skin. Therefore, psoriatic arthritis and psoriasis may be appropriate therapeutic targets for etanercept. This randomised, double-blind, placebo-controlled, 12 week study assessed the efficacy and safety of etanercept (25 mg twice-weekly subcutaneous injections) or placebo in 60 patients with psoriatic arthritis and psoriasis. Psoriatic arthritis endpoints included the proportion of patients who met the Psoriatic Arthritis Response Criteria (PsARC) and who met the American College of Rheumatology preliminary criteria for improvement (ACR20). Psoriasis endpoints included improvement in the psoriasis area and severity index (PASI) and improvement in prospectively-identified individual target lesions. In this 12 week study, 26 (87%) of etanercept-treated patients met the PsARC, compared with seven (23%) of placebo-controlled patients. The ARC20 was achieved by 22 (73%) of etanercept-treated patients compared with four (13%) of placebo-treated patients. Of the 19 patients in each treatment group who could be assessed for psoriasis (≥3% body surface area), five (26%) of etanercept-treated patients achieved a 75% improvement in the PASI, compared with none of the placebo-treated patients (p=0·015). The median PASI improvement was 46% in etanercept-treated patients versus 9% in placebo-treated patients; similarly, median target lesion improvements were 50% and O, respectively. Etanercept was well tolerated. Etanercept offers patients with psoriatic arthritis and psoriasis a new therapeutic option for control of their disease.

The interaction of B7-related molecules on antigen-presenting cells with CD28 or CTLA-4 antigens on T cells provides a second signal for T cell activation. Selective inhibition of the B7-CD28 or B7-CTLA-4 interactions produces antigen-specific T cell unresponsiveness in vitro and suppresses immune function in vivo. To determine whether selective inhibition of the B7-CD28 or B7-CTLA-4 interactions could suppress spontaneous autoimmune disease, a B7-binding protein was generated by genetic fusion of the extracellular domain of murine CTLA-4 to the Fc portion of a mouse immunoglobulin G2a monoclonal antibody (muCTLA4Ig). In lupus-prone NZB/NZW filial generation (F 1 ) mice, treatment with muCTLA4Ig blocked autoantibody production and prolonged life, even when treatment was delayed until the most advanced stage of clinical illness. These findings suggest a possible role for human CTLA4Ig in the treatment of autoimmune diseases in humans.

The interaction of B7-related molecules on antigen-presenting cells with CD28 or CTLA-4 antigens on T cells provides a second signal for T cell activation. Selective inhibition of the B7-CD28 or B7-CTLA-4 interactions produces antigen-specific T cell unresponsiveness in vitro and suppresses immune function in vivo. To determine whether selective inhibition of the B7-CD28 or B7-CTLA-4 interactions could suppress spontaneous autoimmune disease, a B7-binding protein was generated by genetic fusion of the extracellular domain of murine CTLA-4 to the Fc portion of a mouse immunoglobulin G2a monoclonal antibody (muCTLA4lg). In lupus-prone NZB/NZW filial generation (F$_1$) mice, treatment with muCTLA4lg blocked autoantibody production and prolonged life, even when treatment was delayed until the most advanced stage of clinical illness. These findings suggest a possible role for human CTLA4lg in the treatment of autoimmune diseases in humans.

Increasingly, HIV-infected patients seek the advice of primary care physicians while they are still asymptomatic. Many patients are well informed about the disease and are interested in treatment protocols. Others seek information about prognosis and infectivity and about social and psychological support. To address these concerns, physicians need to evaluate each patient's clinical status. Because many patients present with subtle signs and symptoms of HIV infection, is the patient truly asymptomatic? Is there evidence of a treatable coinfection? What health maintenance measures should be taken? Is the patient eligible for any treatment protocols? Is the patient using \"alternative\" or experimental therapies--drugs such as dextran sulfate--obtained from community sources?