scholarly journals Effects of Janus kinase inhibitor tofacitinib on circulating serum amyloid A and interleukin-6 during treatment for rheumatoid arthritis

2014 ◽  
Vol 175 (2) ◽  
pp. 208-214 ◽  
Author(s):  
K. Migita ◽  
Y. Izumi ◽  
Y. Jiuchi ◽  
H. Kozuru ◽  
C. Kawahara ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interleukin 6 ◽  
Serum Amyloid A ◽  
Kinase Inhibitor ◽  
Janus Kinase ◽  
Serum Amyloid ◽  
Janus Kinase Inhibitor ◽  
Amyloid A

Influence of Janus Kinase Inhibition on Interleukin 6-mediated Induction of Acute-phase Serum Amyloid A in Rheumatoid Synovium

2011 ◽  
Vol 38 (11) ◽  
pp. 2309-2317 ◽  
Author(s):  
KIYOSHI MIGITA ◽  
TOMOHIRO KOGA ◽  
ATSUMASA KOMORI ◽  
TAKAFUMI TORIGOSHI ◽  
YUMI MAEDA ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Acute Phase ◽  
Interleukin 6 ◽  
Intracellular Signaling ◽  
Serum Amyloid A ◽  
Janus Kinase ◽  
Serum Amyloid ◽  
Western Blots ◽  
Amyloid A ◽  
Acute Phase Serum

Objective.Inhibition of intracellular signal transduction is considered to be a therapeutic target for chronic inflammation. The new Janus kinase (JAK)3 inhibitor CP690,550 has shown efficacy in the treatment of rheumatoid arthritis (RA). We investigated the influence of JAK/STAT inhibition using CP690,550 on the induction of acute-phase serum amyloid A (SAA), which is triggered by interleukin 6 (IL-6) stimulation in rheumatoid fibroblast-like synoviocytes (RA-FLS).Methods.IL-6-stimulated gene expression of the acute-phase serum amyloid A genes (A-SAA; encoded by SAA1+SAA2) and SAA4 was analyzed by reverse transcriptase-polymerase chain reaction. The intracellular signaling pathway mediating the effects of CP690,550 on IL-6-stimulated JAK/STAT activation was assessed by measuring the phosphorylation levels using Western blots.Results.IL-6 trans-signaling induced A-SAA messenger RNA (mRNA) expression in RA-FLS. By contrast IL-6 stimulation did not affect SAA4 mRNA expression, which is expressed constitutively in RA-FLS. IL-6 stimulation elicited rapid phosphorylation of JAK2 and STAT3, which was blunted by CP690,550. CP690,550 abrogated IL-6-mediated A-SAA mRNA expression in RA-FLS. Similarly, CP690,550 inhibited IL-6-mediated A-SAA mRNA expression in human hepatocytes.Conclusion.Our data indicated that CP690,550 blocked IL-6-induced JAK2/STAT3 activation, as well as the induction of A-SAA. Inhibition of IL-6-mediated proinflammatory signaling pathways by CP690,550 may represent a new antiinflammatory therapeutic strategy for RA and AA amyloidosis.

scholarly journals Oral Janus Kinase Inhibitor for the Treatment of Rheumatoid Arthritis: Tofacitinib

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Han Ni ◽  
Soe Moe ◽  
Kay Thi Myint ◽  
Aung Htet
Keyword(s):  
Rheumatoid Arthritis ◽  
Safety Profile ◽  
Kinase Inhibitor ◽  
Meta Analysis ◽  
Janus Kinase ◽  
Serious Adverse Events ◽  
Janus Kinase Inhibitor ◽  
Immune Modulators ◽  
Serious Infections

Since the introduction of immune modulators in the treatment of rheumatoid arthritis (RA), there has been hope that orally effective biologic agents would be developed. Tofacitinib, a Janus kinase inhibitor, has become the first oral biologic to receive approval for use in active RA patients. This paper reviews the efficacy and safety profile of Tofacitinib at dosages of 5 mg and 10 mg twice daily. Remarkable improvement in terms of ACR 20 response and HAQ-DI score was noted at month 3 and month 6. DAS 28-4 ESR < 2.6 achievement was noticeably obvious at month 6 for both dosages. No significant serious adverse events, serious infections, neutropenia, or anaemia were observed compared to placebo. In fact, Tofacitinib 5 mg was even found to have significant protective effect of anaemia in the meta-analysis (P=0.004). Tofacitinib has a noticeable efficacy in controlling disease activity in RA with a manageable safety profile. However, longer studies are needed for its long-term safety profile.

scholarly journals Extensive Tinea Associated with Tofacitinib Therapy Masquerading as New-Onset SCLE

2020 ◽  
Vol 4 (5) ◽  
pp. 456-459
Author(s):  
Connor R Buechler ◽  
Elena Kurland ◽  
Jesse Veenstra
Keyword(s):  
Rheumatoid Arthritis ◽  
Tinea Capitis ◽  
Kinase Inhibitor ◽  
Autoimmune Disorder ◽  
Connective Tissue Disorder ◽  
Janus Kinase ◽  
Immunomodulatory Agents ◽  
Janus Kinase Inhibitor ◽  
Infection Monitoring ◽  
New Onset

Rheumatoid arthritis is a chronic autoimmune disorder that often requires treatment with immunomodulatory agents, however, such interventions are not without risk of opportunistic infection.  Monitoring for such conditions is critical, whereas recognition and treatment can prove challenging at times, as they may manifest with an atypical presentation or masquerade as another condition entirely. We present here a case of extensive tinea corporis with concomitant tinea capitis masquerading as new-onset connective tissue disorder in a patient being treated for rheumatoid arthritis with the Janus kinase inhibitor tofacitinib.

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