We are analyzing https://link.springer.com/article/10.1007/s40265-018-0956-9.

Title:
Adult-Onset Still’s Disease: Molecular Pathophysiology and Therapeutic Advances | Drugs
Description:
Adult-onset Still’s disease (AOSD) is a rare inflammatory disorder of unknown etiology generally characterized by persistent high spiking fever, evanescent rash, and polyarthritis. The pathogenesis of AOSD is only partially known. The pivotal role of macrophage cell activation, which leads to T-helper 1 (Th1) cell cytokine activation, is now well-established in AOSD. Moreover, pro-inflammatory cytokines such as interleukin (IL)-1, -6, and -18 seem to play a key role in this disorder, giving rise to the development of new targeted therapies. For years, treatment of AOSD has been largely empirical, using nonsteroidal anti-inflammatory drugs, corticosteroids, and disease-modifying antirheumatic drugs. Patients with steroid- and methotrexate-refractory AOSD can now benefit from efficient and well-tolerated biologic agents such as IL-1, IL-6, and tumor necrosis factor-α antagonists.
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Keywords {🔍}

pubmed, disease, google, scholar, article, stills, cas, adultonset, rheumatol, adult, arthritis, patients, rheum, central, treatment, clin, chen, onset, refractory, interleukin, clinical, syndrome, systemic, ann, dis, juvenile, study, idiopathic, exp, efficacy, tocilizumab, med, case, sfriso, macrophage, activation, cytokine, res, lin, hsieh, anakinra, drugs, aosd, pathogenesis, therapy, rev, oxford, lee, response, van,

Topics {✒️}

month download article/chapter sara bindoli & paola galozzi macrophage-colony stimulating factor anti-cd20 monoclonal antibody nonsteroidal anti-inflammatory drugs steroidal anti-inflammatory drugs ifn-gamma-producing lymphocytes autologous stem-cell transplantation tnf-alpha-producing macrophages anti-il1 drug anakinra macrophage activation syndrome disease-modifying antirheumatic drugs article drugs aims full article pdf conventional treatment-refractory adult-onset van rossum ma line disease-modifying therapy il-1r inhibitor anakinra anti-interleukin-1 treatment distinguishes gerfaud-valentin privacy choices/manage cookies autoinflammatory disease reloaded anti-tnf-alpha active systemic features nlrp3 inflammasome van der veen high serum level liver biopsy illustrating open label treatment pro-inflammatory cytokines van damme-lombaerts long-acting inhibitor reduced perforin expression article sfriso anti-tnf switching connect tissue res hemophagocytic syndrome anti-interleukin-1 agents nold-petry ca european economic area 5ème édition paris nationwide epidemiological survey toxoplasma gondii infection intercellular adhesion molecule-1 serum cx3cl1 level sampalis js arthritis res ther arthritis care res rare inflammatory disorder tolerated biologic agents

Questions {❓}

Is anti-TNF switching in refractory Still’s disease safe and effective?
Targeting interleukin-1 b in CAPS (cryopyrin-associated periodic) syndromes: what did we learn?

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         description:Adult-onset Still’s disease (AOSD) is a rare inflammatory disorder of unknown etiology generally characterized by persistent high spiking fever, evanescent rash, and polyarthritis. The pathogenesis of AOSD is only partially known. The pivotal role of macrophage cell activation, which leads to T-helper 1 (Th1) cell cytokine activation, is now well-established in AOSD. Moreover, pro-inflammatory cytokines such as interleukin (IL)-1, -6, and -18 seem to play a key role in this disorder, giving rise to the development of new targeted therapies. For years, treatment of AOSD has been largely empirical, using nonsteroidal anti-inflammatory drugs, corticosteroids, and disease-modifying antirheumatic drugs. Patients with steroid- and methotrexate-refractory AOSD can now benefit from efficient and well-tolerated biologic agents such as IL-1, IL-6, and tumor necrosis factor-α antagonists.
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      description:Adult-onset Still’s disease (AOSD) is a rare inflammatory disorder of unknown etiology generally characterized by persistent high spiking fever, evanescent rash, and polyarthritis. The pathogenesis of AOSD is only partially known. The pivotal role of macrophage cell activation, which leads to T-helper 1 (Th1) cell cytokine activation, is now well-established in AOSD. Moreover, pro-inflammatory cytokines such as interleukin (IL)-1, -6, and -18 seem to play a key role in this disorder, giving rise to the development of new targeted therapies. For years, treatment of AOSD has been largely empirical, using nonsteroidal anti-inflammatory drugs, corticosteroids, and disease-modifying antirheumatic drugs. Patients with steroid- and methotrexate-refractory AOSD can now benefit from efficient and well-tolerated biologic agents such as IL-1, IL-6, and tumor necrosis factor-α antagonists.
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