Background:Interferon-α (IFN-α) is known for its antiviral and antiproliferative effects, used mainly for the treatment of chronic hepatitis C infection [1]. Immunomodulatory effects have been reported in patients treated with IFN-α, including hematological, immunological, rheumatological and dermatological disorders [2]. In fact, IFN-α may lead to the induction or exacerbation of autoimmune diseases such as psoriasis, systemic lupus erythematosus, and rarely rheumatoid arthritis (RA).Objectives:We report the case of a Caucasian who developed anticyclic citrullinated peptide antibody (anti-CCP)-positive RA following treatment of chronic hepatitis C infection with pegylated IFN-α2a.Methods:A 57-year-old women was diagnosed of chronic hepatitis C infection after detection of abnormal liver function. She has a genotype Ib with a high viral load: RNA was 100,000 UI/ml. Liver histology showed advanced fibrosis and portal fibrosis (A3 F4 according to metavir score). A history of blood transfusion was found. The patient was placed on a 24-week course of PEGylated -IFN-α2a 180 µg weekly and a 1000 mg daily dose of ribavirin. After two months of antiviral treatment, she developed symmetrical polyarthritis, with pain and edema in the wrists, elbows, shoulders and metacarpophalangeal joints, associated with prolonged morning stiffness. The musculoskeletal examination was notable for active synovitis of the proximal phalangeal joints, metacarpophalangeal joints, wrists, elbows. Distal interphalangeal joints were spared. She had no musculoskeletal symptoms prior to antiviral therapy. Review of systems was otherwise unremarkable. X-ray showed no remarkable findings. Ultrasonography of the hands revealed diffuse synovitis as well as tenosynovitis of the ulnar extensor tendons in both wrists. Laboratory results revealed a normal C-reactive protein, elevated liver enzymes: ALAT (alanin-aminotransferase) 119,ASAT (aspartat-aminotransferase) 66, Gamma-GT 203 and undetectable cryoglobulins. Anti-CCP was 21 IU/ml (negative < 20 IU/ml), antinuclear antibodies were positive 1280 (negative<160), rheumatoid factor was 192 (normal < 30 IU/ml).A diagnosis of rheumatoid arthritis (RA) was made on the basis of clinical and ultra-sonographic evidence as well as Rheumatoid Factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibody positivity. Moreover, an autoimmune thyroiditis was found that evolved into hypothyroidism treated with thyroxine.Results:The patient developed a sustained virological response as evidenced by persistent undetectable HCV RNA and normal aminotransferase activities. Upon completion of a 12-week course of antiviral therapy, The rheumatoid syndrome disappeared after cessation of IFN therapy. By that time, antinuclear antibodies were in a titre of 1 /180, rheumatoid factor and Anti-CCP were negative.Conclusion:The present case suggests that biological agents, affecting the cytokine network, may work as triggering factors for the development of RA in previously predisposed individuals. Screening for RF and anti-CCP may be considered before treating with IFN. In addition, a close surveillance for the occurrence of autoimmune phenomena during and after treatment should be worthy, for early diagnosis and adequate clinical management.References:[1]DARICE YANG,DANIEL ARKFELDandTSE-LING FONG TreatmentforChronic Hepatitis C Infection.DevelopmentofAnti-CCP-positive Rheumatoid Arthritis Following Pegylated Interferon-alpha. J Rheumatol 2010;37;1777Volume 37, no. 8. 2a[2]Okanoue T, Sakamoto S, Itoh Y, Minami M, Yasui K, Sakamoto M, et al. Side effects of high-dose interferon therapy for chronic hepatitis C. J Hepatol 1996;25:283-91.Disclosure of Interests:None declared

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Background:Poncet disease (PD) is defined as an inflammatory rheumatism associated with visceral tuberculosis without direct bacteriological involvement of the joints [1]. It is classified as a parainfectious rather than a reactive arthritis [2].Objectives:Here by a first case of PD who presented with sterile arthritis and tuberculous spondylodiscitis.Methods:We report a case of a 40-year-old women who presented with polyarthritis in 2014. On physical examination, she had synovitis in both wrists, the metacarpophalangeal joints and the fifth proximal interphalangeal joint of the right hand. Her serum was negative for Rheumatoid Factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibody. Her C-reactive protein (CRP) was 24,5mg/l. Ultrasound revealed tenosynovitis of the superficial and deep flexor tendons on both hands with Doppler signal. The Magnetic resonance imaging (MRI) of the hands showed active synovitis in the wrists mainly in the distal radioulnar joint, erosions in the ulnar styloid as well as edematous infiltration of the soft tissue of the hands. Since she fulfilled the new ACR/EULAR 2010 criteria for RA, a diagnosis of rheumatoid arthritis (RA) was made and the patient was put on Methotrexate (MTX) 15 mg/week/po in January 2015. Eight months later, the patient developed high temperature 38°c and lumbar stiffness. A chest CT performed as part of the etiologic investigation didn’t show pulmonary manifestations but revealed a lytic vertebrae lesion. Lumbar spine MRI showed prevertebral edema and soft tissue enhancement with abnormal marrow signal in L2 and L3 which was concerning for infectious etiology. MTX was stopped. A CT-guided core needle biopsy concluded to a tuberculous spondylodiscitis. The patient was initiated on an antituberculous-therapy (ATT) for 15 months. The course was marked by the reoccurrence of low back pain. MRI of the spine was then performed and revealed persistence of spondylodiscitis and multiple abscesses at the levels of L2-L3. The ATT was resumed.Results:The patient received four drugs for 4 months, followed by isoniazid and rifampicin for 1 year. At follow up, the patient responded well to treatment with complete resolution of symptoms without sequelae. She did not present neither polyarthritis nor synovitis. Moreover, she sustained a negative CRP (2mg/dl). Ultrasound control of the wrists did not show synovitis or tenosynovitis Doppler signal. Similarly, a disappearance of effusion as well as synovitis was noted on the MRI at follow up.Conclusion:We report a unique case of Poncet disease with tubercular spondylodiscitis. It is important to recognize PD in a patient presenting with polyarthritis in order to avoid unnecessary long-term disease-modifying antirheumatic treatment. Future research is indicated to understand the etiopathogenesis of Poncet’s disease and to educate clinicians as to the importance of maintaining a high index of suspicion about this rare, yet potentially easily treatable disease.References:[1]Sood R, Wali JP, Handa R. Poncet’s disease in a north Indian hospital. Trop Doctor. 1999; 29: 33-6.[2]Bloxham CA, Addy DP. Poncet’s disease: parainfective tuberculous polyarthropathy. Br Med J. 1978; 1: 1590.Disclosure of Interests:None declared