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JAK-STAT pathway. A frequent side effect of these drugs is arthralgia, which occurs in up to 26% of patients. Methods: We present a 62-year-old man who developed florid inflammatory arthritis following initiation of eltrombopag for ITP. Results: The patient was first diagnosed with ITP in 1997 and underwent splenectomy in 1998. Rituximab treatment in 2014 was ineffective for his persistent thrombocytopaenia. Eltrombopag was then commenced and titrated to 50 mg daily. Three months later he developed new-onset left knee pain with an effusion. Following a dose increase to 50/75 mg (alternate days), the arthritis progressed to involve the shoulders, wrists and hands bilaterally. He noted joint stiffness, worse in the mornings, particularly in the small joints of the hands, with associated swelling and difficulty making a fist. On examination, he displayed bilateral swollen wrists, MCP joints and PIP joints with reduced range of movement. Blood tests showed CRP <5 mg/l, ESR 16 mm/h, uric acid 326 mmol/l, with RF, anti-CCP antibodies and ANA all being negative. Plain radiographs identified moderate degenerative changes in the hands, however, MRI of the left Downloaded from https://academic.oup.com/rheumatology/article/55/suppl_1/i65/1794220 by guest on 30 September 2021 knee showed a significant joint effusion. Ultrasonography showed moderately severe synovitis of the right wrist and mild synovitis of the left wrist, with increased power Doppler signal. Three months after eltrombopag dose reduction to 50 mg daily, the arthritis in the hands improved such that he could form a fist. Eltrombopag was weaned with the aim of stopping and this led to further improvement in his symptoms. Conclusion: To our knowledge, this is the first case of a patient developing inflammatory arthritis following treatment with JAK stimulation. Interestingly, our patient was seronegative for both RF and anti-CCP, but had synovitis on US. The temporal and dose-related correlation between eltrombopag initiation and inflammatory arthritis in the absence of other causes suggests an association. Mechanistically this is likely to be via the binding of eltrombopag to dendritic cell thrombopoietin receptors with subsequent JAK2-STAT5 activation. Conversely, inhibition of JAK signalling by MTX or the JAK inhibitors tofacitinib and baricitinib is used in the treatment of inflammatory arthritis. While most rheumatologists are aware of the therapeutic benefits of JAK inhibitors, the effects of potential stimulators of the pathway are less well known. It is possible that the increasing use of these drugs may result in an increase in inflammatory arthritis. Disclosure statement: The authors have declared no conflicts of interest.

007 JAK-STAT PATHWAY STIMULATION: A NEW CAUSE OF INFLAMMATORY ARTHRITIS Maliha F. Shaikh1, Ruth L. Gilliver1, Melanie A. Hopper2 and Andrew J. K. O¨ sto¨ r1 1Rheumatology and 2Radiology, Addenbrooke’s Hospital, Cambridge University Hospitals, Cambridge, UK

Background: Downregulation of the JAK-STAT signalling pathway with agents such as tofacitinib (a JAK inhibitor) is emerging as an effective tool in the management of RA. It is conceivable therefore that upregulation of this pathway could result in inflammatory arthritis. The thrombopoietin receptor agonists eltrombopag and romiplostim, used in the treatment of immune thrombocytopaenia (ITP), stimulates the