Free PMC article Baggott, J. E., Morgan, S. L. & Vaughn, W. H. Differences in methotrexate and 7-hydroxymethotrexate inhibition of folate-dependent enzymes of purine nucleotide biosynthesis.
& Kremer, J. M. Methotrexate polyglutamation in relation to infliximab pharmacokinetics in rheumatoid arthritis.
Phillips, D. C., Woollard, K. J. Hasko, G., Linden, J., Cronstein, B. & Pacher, P. Adenosine receptors: therapeutic aspects for inflammatory and immune diseases.
Thank you for visiting nature.com. Effect of aminopterin in rheumatoid arthritis and psoriasis. It's the first drug most doctors prescribe after you’re diagnosed. Despite the introduction of numerous biologic agents for the treatment of rheumatoid arthritis (RA) and other forms of inflammatory arthritis, low-dose methotrexate … Online ahead of print.Heliyon. & Aarden, L. A. Inhibition of cytokine production by methotrexate. & Channon, K. M. Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency.
Andersson, S. E., Johansson, L. H., Lexmuller, K. & Ekstrom, G. M. Anti-arthritic effect of methotrexate: is it really mediated by adenosine? II. Nature Publishing Group The demonstration in 1985 that low-dose, intermittent methotrexate is a potent and effective therapy for rheumatoid arthritis (RA) [] led to a dramatic change in the way that patients with RA are treated.Indeed, methotrexate is no less efficacious than specific anti-tumor-necrosis-factor (anti-TNF) therapy for the relief of symptomatic joint inflammation in early RA, and the …
Despite the rapid pace of change, the most commonly used drug in RA remains methotrexate, which is considered the anchor drug for this condition. Hasko, G. & Cronstein, B. Novaes, G. S., Mello, S. B., Laurindo, I. M. & Cossermelli, W. Low dose methotrexate decreases intraarticular prostaglandin and interleukin 1 levels in antigen induced arthritis in rabbits. & Blotman, F. Effects of methotrexate on leukotriene and derivated lipoxygenase synthesis in polynuclear neutrophils in rheumatoid polyarthritis. Figure 3.. Methotrexate inhibition of polyamine and… Figure 3.. Methotrexate inhibition of polyamine and lymphotoxin formation. Baggott, J. E., Vaughn, W. H. & Hudson, B. Low disease activity and remission are now frequently achieved, and this success is largely the result of the evolution of treatment paradigms and the introduction of new therapeutic agents.
2016 Oct;45(5):347-55. doi: 10.3109/03009742.2015.1105290. Hamilton, R. A. & Khan, I. U. T-cell specific defect in expression of the NTPDase CD39 as a biomarker for lupus.
Published by Elsevier Masson SAS. These include measurements of lymphocyte subsets, proliferative responses to mitogens, immunoglobulin production, rheumatoid factor and immune complexes.
Despite the rapid pace of change, the most commonly used drug in RA remains methotrexate, which is considered the anchor drug for this condition. Bressolle, F., Bologna, C., Kinowski, J. M., Sany, J. Montesinos, M. C., Desai, A. 2020 Apr 14;41(4):348-350. doi: 10.3760/cma.j.issn.0253-2727.2020.04.018. 2020 Jul 21. doi: 10.5152/eurjrheum.2020.2067. 2005 Jun;57(2):163-72. doi: 10.1124/pr.57.2.3.Perdan-Pirkmajer K, Pirkmajer S, Thevis M, Thomas A, Praprotnik S, Hočevar A, Rotar Ž, Gašperšič N, Sodin-Šemrl S, Žibert J, Omersel J, Chibalin AV, Tomšič M, Ambrožič A.Scand J Rheumatol. Ultimately, finding a clear explanation for the pathway and mechanism leading to methotrexate efficacy in RA, there may be a way to formulate more potent therapies with fewer side effects. 2016 Dec;12(12):731-742. doi: 10.1038/nrrheum.2016.175. The affinity of methotrexate for DHFR is about 1000-fold that of folate. 1997 Nov;23(4):739-55. doi: 10.1016/s0889-857x(05)70358-6.Curr Opin Rheumatol. Altindag, Z. & Cronstein, B. N. Suppression of inflammation by low-dose methotrexate is mediated by adenosine A2A receptor but not A3 receptor activation in thioglycollate-induced peritonitis. Treatment of early rheumatoid arthritis: concepts in management. A., van de Winkel, J. G., Bijlsma, J. W. & Lafeber, F. P. Down-regulation of activating Fcγ receptors on monocytes of patients with rheumatoid arthritis upon methotrexate treatment. Godfrey, C., Sweeney, K., Miller, K., Hamilton, R. & Kremer, J. & Deussen, A. COVID-19 is an emerging, rapidly evolving situation. Crabtree, M. J., Hale, A. & Matherly, L. H. The human proton-coupled folate transporter: biology and therapeutic applications to cancer. & Reichen, J. Intraindividual variability of the bioavailability of low dose methotrexate after oral administration in rheumatoid arthritis. Low disease activity and remission are now frequently achieved, and this success is largely the result of the evolution of treatment paradigms and the introduction of new therapeutic agents. Angelis-Stoforidis, P., Vajda, F. J. 2019;25(26):2859-2874. doi: 10.2174/1381612825666190710111658.Nat Rev Rheumatol. & Combe, B. 2020 Jul 21. doi: 10.5152/eurjrheum.2020.2067. 2020 Jun 18;21(12):4345. doi: 10.3390/ijms21124345.Kodidela S, Dorababu P, Thakkar DN, Dubashi B, Sundaram R, Muralidharan N, Nidanapu RP, Aribandi A, Pradhan SC, Uppugunduri CRS.Genes (Basel). B. Cronstein, B. N. Low-dose methotrexate: a mainstay in the treatment of rheumatoid arthritis. Figure 2.. Adenosine receptors and signaling pathways. Klimiuk, P. A., Fiedorczyk, M., Sierakowski, S. & Chwiecko, J. Soluble cell adhesion molecules (sICAM-1, sVCAM-1, and sE-selectin) in patients with early rheumatoid arthritis. Currently, adenosine signaling is probably the most widely accepted explanation for the methotrexate mechanism in RA given that methotrexate increases adenosine levels and on engagement of adenosine with its extracellular receptors an intracellular cascade is activated promoting an overall anti-inflammatory state. P.M.B.