Etanercept in rheumatoid arthritis

Abstract

Etanercept (Enbrel, Immunex Corporation, Seattle, Washington, USA) is a new biological disease-modifying antirheumatic drug (DMARD) for the treatment of active rheumatoid arthritis (RA). It is one of two TNF-alpha blockers to be licensed for the treatment of active RA and is classified as a recombinant human soluble TNF receptor. The drug competitively inhibits the binding of TNF to cell surface receptors and thus renders TNF biologically inactive. In doing so, etanercept inhibits the pro-inflammatory effects of TNF and results in a reduction of joint inflammation in patients with RA. Etanercept has shown a statistically significant reduction in swollen and inflamed joint counts, biochemical markers such as erythrocyte sedimentation rate and C-reactive protein and shown significant improvements in quality of life measures (HAQ and global assessment scores) in all studies. In early disease, etanercept has shown a reduction in joint space narrowing equal to methotrexate (MTX) and a reduction in the appearance of new erosions significantly better than MTX after 1 year of treatment. Etanercept has a rapid onset of action which is significantly faster than standard DMARDs. Etanercept was well-tolerated in clinical trials. The commonest side effects were injection site reactions and upper respiratory tract infections. Etanercept therapy has resulted in serious infections in some patients and should be used with caution in any patient with a history of recurring infections or with disease states that may predispose to infections. In summary, etanercept is an effective and well-tolerated agent that is a significant breakthrough in the treatment of this disabling condition.

Therapeutic Effects of <i>Hominis placenta</i> Injection into an Acupuncture Point on the Inflammatory Responses in Subchondral Bone Region of Adjuvant-Induced Polyarthritic Rat

“…2,28,29) Thus far, only two drugs targeting TNF-a were developed and licensed to clinically treat rheumatoid arthritis patients, in a form of modified protein of soluble TNF receptor or monoclonal antibody to TNF-a. 30,31) Our results also indicated that those cytokines were significantly secreted in arthritic joints of the legs, which means that the inflammatory cells, mainly macrophages, were infiltrated into the arthritic joints as the arthritis proceeded. Because the inflammatory cytokines such as TNF-a and IL-1b were specifically stained on the bone section, the immunopositive cells could indirectly represent the inflammatory cells infiltrated.…”

Tumor Necrosis Factor-α Mediates Oligodendrocyte Death and Delayed Retinal Ganglion Cell Loss in a Mouse Model of Glaucoma

“…The toxic effects of TNF-␣ are mediated via TNFR2 receptors on CD11b ϩ microglia, which are likely to be the final killers of oligodendrocytes and, indirectly, of RGCs. Interference with TNF-␣ by using a blocking antibody has been applied in the treatment of other inflammatory diseases (De Keyser et al, 2006); other possible approaches include the use of a soluble receptor (Alldred, 2001) or a TACE (TNF-␣-converting enzyme) inhibitor (Moss et al, 2001). Blockade of TNF-␣ function and downstream microglial activation may be an important approach for the treatment of glaucoma.…”

Two distinct cellular mechanisms of osteoclast formation and bone resorption in periprosthetic osteolysis

“…by OPG or RANK:Fc) is unlikely to be completely successful in the treatment of wear particle-associated bone resorption where inflamed tissues have elevated levels of T N F r and IL-la. Anti-T N F drugs (such as etanercept and infliximab) are currently being used in the treatment of rheumatoid arthritis and have been shown to reduce the formation of marginal erosions [2,57]. They have also been found to inhibit wear-induced osteolysis in experimental animals [9].…”