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Papulosquamous Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Melek Aslan Kayıran, Jordan V. Wang, Ayşe Serap Karadağ
Various biologic agents can target specific molecules and pathways in the psoriasis pathway. They generally have more systemic side effects and risks than other systemic immunosuppressant regimens. Common biologic agents include tumor necrosis factor-alpha inhibitors (e.g., adalimumab, etanercept, certolizumab), IL-17 inhibitors (e.g., secukinimab, ixekizumab, brodalumab), IL-12/23 inhibitors (e.g., ustekinumab) and IL-23 inhibitors (e.g., guselkumab, risankizumab). Biologic treatments are mainly approved for psoriasis vulgaris and psoriatic arthritis and are generally not as effective for pustular psoriasis.
Immune Modulation In Sepsis
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Janet M. J. Hammond, Peter D. Potgieter
The results of these studies are suggestive of the potential benefit of administration of anti-tumor necrosis factor alpha therapies, although much of the work is still in a preliminary phase. In animal studies there have generally been some degree of protection and an increased survival rate from septic shock when the TNF antagonist is given before or during the infusion of endotoxin or bacteria [46,192]. There have, however, been several studies that have shown no effect, or deleterious effects, of TNF antagonists in murine models of peritonitis, including cecal ligation/puncture [56,194], The clinical importance of this model is uncertain, and further studies are needed to clarify this issue.
Hematopoietic Stem Cell Transplantation in the Treatment of Chronic Inflammatory Demyelinating Polyradiculoneuropathy
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
George Hutton, Yu Oyama, Richard K. Burt, Uday Popat
Antibodies alone are not a sufficient explanation for the production of demyelination because they would not penetrate the blood nerve barrier unless it were first rendered leaky. It is likely that a T cell response is also involved. CIDP patients had increased percentages of activated circulating T lymphocytes34 and raised serum concentrations of both IL-2 and IL-2 receptors.35,36 In a single study, primary T cell proliferated responses to P2 and PO proteins or peptides were recorded in almost half of the patients studied.37 Tumor necrosis factor alpha (TNF-alpha) is a cytokine secreted by both macrophages and T cells which has toxic effects on myelin, Schwann cells and endothelial cells. Elevated serum TNF-alpha levels were found in 25% of CIDP patients.38 TNF-alpha levels correlated with clinical severity and electrophysiologic abnormalities, and decreased after immunotherapy.3
The role of pharmacotherapy in the treatment of endometriosis across the lifespan
Published in Expert Opinion on Pharmacotherapy, 2020
Kaia Schwartz, Natalia C. Llarena, Jenna M. Rehmer, Elliott G. Richards, Tommaso Falcone
Tumor necrosis factor is a major player in the inflammatory milieu of endometriosis. There are many drugs that target tumor necrosis factor alpha including etanercept, infliximab, and imiquimod. Small trials have tested these drugs in animal models of endometriosis with successful results. A rat model comparing etanercept and infliximab found that both successfully decreased endometrial implant size, etanercept more so than infliximab [83]. There are many other small studies looking at newer targets such as janus kinase inhibitors and mTOR inhibitors [85]. The side effects from these drugs seem to be tolerable and they warrant further investigation with clinical trials. Furthermore, with continued improvements in single-cell deep sequencing technology, a knowledge of the individual immune environment may allow for novel targeted treatment options.
Real-world utilization of methotrexate or prednisone co-therapy with etanercept among Canadian patients with rheumatoid arthritis: a retrospective cohort study
Published in Current Medical Research and Opinion, 2019
Majed Khraishi, Jelena Ivanovic, Yvonne Zhang, Brad Millson, Marie-Josee Brabant, John Woolcott, Heather Jones, Cinzia Curiale
Over the past several decades, pharmacologic treatment using disease-modifying anti-rheumatic drugs (DMARDs) has become increasingly recognized among rheumatologists in treating patients with RA because of their well established effects on the signs and symptoms of disease11. Current evidence-based guidelines recommend initiating patients on methotrexate immediately post-diagnosis, with the discretionary addition of glucocorticoids to manage symptoms and as a bridging therapy while the DMARD takes effect12,13. The guidelines also recommend rapid tapering of prednisone and, if patients respond insufficiently to methotrexate, adding a biologic DMARD (bDMARD). However, both methotrexate and prednisone are associated with toxicity, and many patients, even with aggressive treatment, do not achieve adequate therapeutic responses13. In addition, tumor necrosis factor alpha (TNF-α) inhibitors, a class of bDMARD, have been associated with adverse events (AEs) such as infection and injection-site reactions14,15. Therefore, the ability to discontinue methotrexate, or to reduce prednisone in cases requiring methotrexate/prednisone combination, as two therapeutic options, may decrease the potential for toxicities12,13.
A case of Loeffler’s endocarditis after initiation of adalimumab
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Nooreen Hussain, Preeti Patel, Jonathan Yin, Rachael Davis, Ossama Ikladios
Tumor necrosis factor alpha is a proinflammatory cytokine and is active in the systemic immune response. Anti-TNF therapy is used in diseases such as rheumatoid arthritis, ankylosing spondylitis, and inflammatory bowel disease. This therapy is known to be relatively safe, however reported side effects include infection, malignancy, and a variety of skin lesions [4]. Previous reports of Anti-TNF therapy associated with sarcoid-like granulomatosis have been reported with pulmonary, cutaneous, and interstitial nephritic involvement [4,5]. These findings were seen 10 to 18 months after onset of therapy with adalimumab or etanercept. Our patient began experiencing symptoms related to her cardiomyopathy almost two years after beginning therapy with adalimumab. While currently there are no consensus guidelines for treatment, prompt administration of steroids and removal of the offending agent is recommended.