112 A SIMPLE CASE OF HOUSEMAID’S KNEE? 1 and Muhammad Kazmi 1 Sheffield Teaching Hospitals, Sheffield, UNITED Background: Pre-patellar bursitis is most commonly caused by recurrent minor injury, for example, kneeling to scrub floors. It can also be caused by major trauma, infection or crystal arthropathy. Rarely is it caused by sarcoidosis which, although known to affect any organ, presents in more than 90% of cases with lymph-node enlargement, pulmonary, skin or ocular symptoms. Methods: We describe a 49 year old lady, who presented to orthopaedics with left knee pain and swelling over the patella. There was no bony abnormality or significant effusion on X-ray. Pre-patellar bursitis was diagnosed. A week later she was admitted with abdominal pain. CT scan showed faecal loading. She was prescribed laxatives and discharged. After another week she was admitted generally unwell. A thorough history revealed she had been ill for the preceding three months with a constellation of symptoms, including red eyes, rash, dyspnoea, fevers and one stone weight loss. On examination there was suprapatellar swelling and a small effusion on the left knee, and bilateral ankle synovitis. There was a maculopapular rash on the back and right arm but no erythema nodosum on the legs. Results: CRP was normal and ESR 70 (1-15mm/hr). Rheumatoid factor, anti-CCP, ANA, ENA and ANCA were negative. dsDNA and complement levels were normal. An infection screen was negative except for positive hepatitis B surface antibodies. Quantiferon was negative. A chest X-ray was reported as normal but on hindsight did show bulky hila. The left knee joint aspirate was sterile. An intramuscular depomedrone injection was given for a likely reactive illness with follow-up appointment arranged. Before the appointment, she was re-admitted with pleuritic chest pain. D-dimer was raised at 570 (0-500ug/L). CTPA showed no pulmonary embolus but did show widespread lymphadenopathy, raising the possibility of lymphoma or sarcoidosis. Serum ACE was 146 (20-70 IU/L). PET CT showed intense activity in the parotid glands, lymph nodes above and below the diaphragm and uptake around the knee joints. Biopsy of the parotid gland showed granulomatous inflammation. Sarcoidosis was diag- nosed and our patient was commenced on 20mg prednisolone daily. She responded well. The joint inflammation and systemic features settled but the left knee pre-patellar swelling persisted. Knee MRI showed thickening of the pre-patellar soft tissues but no focal fluid collection. A biopsy of the bursa showed fibrous tissue containing multiple epithelioid granulomata consistent with sarcoidosis. We plan to commence our patient on methotrexate. Conclusion: The main causes of pre-patellar bursitis are repeated minor or major trauma, infection and crystal arthropathy. A rare cause is sarcoidosis. Sarcoidosis is a multi-system disease and therefore it is important not to focus on a single system, but to undertake a thorough systemic history and examination as was eventually done in our patient. Disclosures: R. Smith: None. M. Kazmi: None. 113 HEPATITIS E AS A CAUSE OF VERY ABNORMAL LIVER FUNCTION TESTS IN PATIENTS ATTENDING RHEUMATOLOGY CLINICS: AN EMERGING PROBLEM? Robert D. Sandler 1 , Muhammad F. Kazmi 1 and James R. Maxwell 1 1 Rheumatology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UNITED KINGDOM Background: Hepatitis E is a single stranded RNA virus, which causes acute, self-limiting infection in most patients. Newly- identified cases should be reported to Public Health England. An increase in cases was highlighted in the media in August 2017, associated with the consumption of infected pork. In most patients the virus causes non-specific symptoms, with the diagnosis made after abnormal LFT detected on screening, usually with very high transaminases. Patients receiving immunosuppressive medication are at an increased risk of chronic infection, leading to liver fibrosis and cirrhosis. Methods: Retrospective review of patients attending rheumatology outpatient clinic for blood monitoring, who had abnormal liver function tests and positive hepatitis E serology between 2010 and 2018. Results were gathered from the ICE computer system and clinical notes were reviewed. Results: We identified 7 patients attending the rheumatology clinic in Sheffield, confirmed as having acute infection with hepatitis E. There were 4 males and 3 females, with an age range of 48 to 73. The patients were all receiving disease modifying or biologic medications, ranging from hydroxychloroquine to anti-TNF treatment, and under- went their blood tests as part of routine monitoring. In all cases the presentation was characterised by a marked and unexpected rise in transaminases. In all cases the blood tests returned to baseline after 4- 6 weeks, with no apparent long term sequelae. Conclusion: We would like to present this case series to raise awareness of hepatitis E as a cause of abnormal transaminases, particularly in those patients receiving DMARD medication. All patients recovered completely and were able to safely restart their DMARD medications. Disclosures: R.D. Sandler: None. M.F. Kazmi: None. J.R. Maxwell: None. 114 A CONUNDRUM: PRIMARY ANGIITIS OF THE CENTRAL NERVOUS SYSTEM ASSOCIATED WITH KIKUCHI-FUJIMOTO DISEASE AND UNDIFFERENTIATED CONNECTIVE TISSUE DISEASE Yihui Goh 1 , Leonard L. L. Yeo 2 , Gim Gee Teng 3 , Amy M. L. Quek 2 , Clement W. T. Tan 4 and Anita Y. N. Lim 3 1 Internal Medicine, National University Health System, Singapore, SINGAPORE, 2 Neurology, National University Health System, Singapore, SINGAPORE, 3 Rheumatology, National University Health System, Singapore, SINGAPORE, and 4 Ophthalmology, National University Health System, Singapore, SINGAPORE Background: Primary angiitis of the central nervous system (PACNS) is a rare form of vasculitis affecting the brain and spinal cord. Often posing a diagnostic challenge, it has yet to be described in conjunction with other autoimmune diseases - rather, systemic vasculitides are part of the differential diagnosis for PACNS. We describe a case of PACNS associated with Kikuchi-Fujimoto disease (KFD) and undiffer- entiated connective tissue disease (UCTD). Methods: A 48 year old Chinese male presented in 2012 with a left pure sensory stroke, in the absence of cardiovascular risk factors. Magnetic resonance angiogram showed two fusiform aneurysms. He was discharged well but re-presented with fever and weight loss five months later, with leucopenia, thrombocytopenia, raised inflammatory markers, transaminitis and generalised lymphadenopathy. Histology of a cervical lymph node showed histiocytic necrotizing lymphadenitis. He responded to prednisolone with improvement in cell counts, inflammatory markers, transaminitis and fevers. Fevers recurred with correspondingly high inflammatory markers when immunosuppression was tapered, a year after his initial presentation for KFD. Anti-nuclear antibody was elevated at 1:160 (homogenous and speckled), with anti- Smith antibody being transiently positive. He had mild proteinuria, with haematuria and casts on urine microscopy but did not fulfill other criteria for systemic lupus erythematosus. He was treated as for concomitant UCTD with hydroxychloroquine, prednisolone and azathioprine. In 2013, he presented with intermittent headaches and a left abducens nerve palsy when prednisolone was reduced to less than 5 mg daily. Magnetic resonance angiography showed fusiform aneurysms with beading of vasculature, with an ectactic left vertebral artery coursing along the abducens nerve. Positron emission tomo- graphy did not demonstrate FDG-avid signals in other large vessels. Antineutrophil cytoplasmic antibodies were negative. Lumbar puncture showed raised protein and positive paired oligoclonal bands, with no infections or malignancy. He received increased steroids and intravenous cyclophosphamide, with improvement in his abducens nerve palsy. With tapering of steroids to 5mg prednisolone daily in spite of maintenance azathioprine, cranial neuropathies recurred - abducens nerve palsy in 2016 and 2017, followed by right inferior oblique weakness in 2016 and left trochlear nerve palsy in 2017. These resolved completely with increased steroid dose and intravenous cyclophosphamide. Serial imaging demonstrated stable intracranial aneurysms. He declined brain biopsy. In 2018, he developed giddiness and torsional nystagmus while on mycophenolate mofetil and 2.5mg prednisolone daily. Results: Magnetic resonance imaging of intracranial vessel walls showed inflammation of the posterior circulation. Upon review of his clinical presentation over the years and imaging findings, he was diagnosed with PACNS and treated with intravenous methylpredniso- lone and cyclophosphamide. Conclusion: Our patient illustrates the challenges faced in the diagnosis of PACNS, and the use of newer imaging modalities (magnetic resonance imaging of vessel walls) for diagnosis and monitoring of central nervous system vasculitis. Disclosures: Y. Goh: None. L.L.L. Yeo: None. G. Teng: None. A.M.L. Quek: None. C.W.T. Tan: None. A.Y.N. Lim: None. iii88 Wednesday 1 May 2019 INVITED SPEAKERS ABSTRACTS Downloaded from https://academic.oup.com/rheumatology/article/58/Supplement_3/kez108.021/5444322 by guest on 14 January 2024