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Background/Aims Acquired hypocomplementemia occurs through immune complex-mediated diseases, as seen in systemic lupus erythematosus (SLE), idiopathic membranoproliferative glomerulonephritis (MPGN) and cryoglobulinemia. Infective causes are less common, although chronic bacterial and viral infections causing glomerulonephritis (GN) and vasculitis have been reported. Bacterial infections causing chronic osteomyelitis, endocarditis and visceral abscesses have all been implicated, whilst hepatitis B is the only virus known to cause severe GN/ vasculitis leading to low complement levels. Severe meningococcal disease is an established cause of acquired hypocomplementemia, typically associated with Nisseria Meningitidis. Parvovirus B19 is an infection exclusive to humans, usually manifesting as fifth disease, a mild illness characterised by a rash, fever and runny nose. Less common systemic effects include hydrops fetalis, thrombocytopenia, neutropenia, neurological sequalae (including encephalopathy, aseptic meningitis, neuropathy and neuralgic amyotrophy), myocarditis and hepatitis. Arthropathy is by far the most common manifestation in adults, affecting 60% of females and 30% of males. Methods The literature on Parvovirus B19 and hypocomplementemia is sparse, limited to case reports and comparative studies, the pathogenicity of which stems from glomerulonephritis, consequently resulting in low complement levels. We present a case series of 2 patients with Parvovirus B19 infection and acquired hypocomplementemia between 2016-2020. Results Patient A, a 26-year-old female, presented with a vasculitic rash on her legs and arthralgia affecting her hands and knees, refractory to oral prednisolone and hydroxychloroquine. She was found to have low complement levels (C3 0.61 g/l and C4 0.03 g/l), whilst ANA, ENA and ANCA testing was negative. She also had a negative rheumatoid factor and anti-CCP antibody, and a normal serum protein: creatinine (6 mg/mmol). Immunoglobulins were within normal range (IgG 8.7 g/l, IgA 0.80 g/l, IgM 2.41 g/l) and a serum protein electrophoresis was normal. Hepatitis and HIV serology was also negative. Patient B, a 34-year-old female, 9 weeks pregnant, presented with polyarthralgia, fever and a maculopapular rash, with normal inflammatory markers and a normal serum protein: creatinine (9 mg/mmol). Her complement was low (C3 0.57 g/l and C4 Conclusion We recommend that clinicians consider acute viral illness in patients presenting with vasculitis and hypocomplementemia. If diagnosis and treatment can be established early, patients can avoid the need for long term immunosuppression. Disclosure A. Gharatya: None. C. Nelson: None. S. Melath: None.

Background Fibroblast Ggrowth factor-23 (FGF-23) is a phosphate regulator primarily expressed by osteocytes. Excess FGF-23 leads to decreased hydroxylation of 25-hydroxyvitamin D and poor renal phosphate reabsorption. This leads to hypophosphataemia and represents a rare cause of osteomalacia, resulting in bone oedema and stress fractures. Methods A 57-year-old man with known skin psoriasis presented with a two-year history of left foot and ankle pain. On examination, he had chronic dactylitis of the left, big toe associated with skin psoriasis and nail pitting. Serum inflammatory markers were normal, and autoimmune screens for RF, anti-CCP and HLA-B27 were negative. Bilateral foot and ankle X-rays showed no bony abnormality. This was diagnosed as likely psoriatic arthritis and MRI showed talar bone oedema, felt to be related to the inflammatory arthritis. Symptoms settled well on non-steroidal anti-inflammatories. However, he presented two months later with focal distal tibial pain and swelling. There was no history of trauma. Repeat MRI showed proximal migration of bone oedema with stress fractures of the left posterior talus and distal tibial metaphysis. Results Blood tests showed low phosphate, elevated PTH, normal adjusted calcium, raised ALP and low 25-hydroxyvitamin D. DEXA scan confirmed osteoporosis of the hip. The patient was commenced on intravenous three-monthly pamidronate and colecalciferol (vitamin D3) supplements. Despite this, the patient continued to have migratory joint pain affecting the ankle, hip and sacroiliac joints. Methotrexate was prescribed to improve his psoriasis, but whilst his skin improved his legs remained painful. A repeat MRI showed new insufficiency fractures to the left talus and right neck of femur. Although taking colecalciferol supplementation, his serum phosphate remained low (0.5mmol/L). On further investigation, Myeloma screen and FDG PET were normal but he was noted to have an increased fractional urinary phosphate excretion indicating poor renal phosphate reabsorption. Serum FGF-23 assay was elevated at 131 mIU/L (normal Conclusion This case illustrates the need for thorough investigation of symptomatic, treatment-refractory hypophosphataemia. Although mild hypophosphatemia could indicate adult onset rickets, rarer causes such as FGF-23 secreting tumours should be considered. These tumours are notoriously difficult to locate; 68-Gallium DOTATATE PET may offer superior specificity to other imaging modalities, including FDG-PET, in detecting these mesenchymal tumours. FGF-23 decreases hydroxylation of vitamin D3 and renal phosphate reabsorption, and calcitriol alongside phosphate supplementation is advisable for symptomatic management until definitive treatment. Disclosures K. Fisher None. S. Melath None. S. Patel None.

Background Fibroblast growth factor-23 (FGF-23) is a phosphate regulator primarily expressed by osteocytes. Excess FGF-23 leads to decreased hydroxylation of 25-hydroxyvitamin D and poor renal phosphate reabsorption. This leads to hypophosphatemia and represents a rare cause of osteomalacia, resulting in bone oedema and stress fractures. Methods A 57-year-old man with known skin psoriasis presented with a two-year history of left foot and ankle pain. On examination, he had chronic dactylitis of the big toe and extra-articular features included skin psoriasis on the scalp, elbows, knees, and nail pitting. Serum inflammatory markers were normal, and autoimmune screens for RF, anti-CCP and HLA-B27 were negative. Bilateral foot and ankle X-rays showed no bony abnormality. This was diagnosed as likely psoriatic arthritis and MRI showed talar bone oedema, felt to be related to inflammatory arthritis. Symptoms settled well on non-steroidal anti-inflammatories. However, he presented with focal distal tibial swelling and pain, two months later. There was no history of trauma, Repeat MRI2 showed proximal migration of bone oedema with stress fractures of the left posterior talus and distal tibial metaphysis. Bloods tests showed low phosphate, elevated PTH, normal adjusted calcium, raised ALP and low 25-OH vitamin D. DEXA scan confirmed osteoporosis of the hip. The patient was commenced on bisphosphonate with 25-hydroxyvitamin D and phosphate supplementation. Despite this, the patient continued to have migratory joint pain affecting the ankle, hip and sacroiliac joints. Methotrexate was started for psoriasis and whilst his skin improved, his pain remained and further MRI showed left talar and right neck of femur insufficiency fractures. Results Although taking vitamin D3 supplementation, he remained hypophosphateamic 0.5mmol/L. Myeloma screen and PET FDG were normal. However, he was noted to have an increased fractional urinary phosphate excretion indicating poor renal phosphate reabsorption. One possible cause of this is elevated FGF-23, which was confirmed with FGF-23 assay (include levels and normal range). The patient underwent PET Ga-DOTATE imaging, utilising a tracer specific for somatostatin receptors found on neuroendocrine tumours. This showed a T9 pedicle lesion and a CT-guided biopsy confirmed a mesenchymal tumour as the cause of FGF-23 secretion, resulting in TBMO and insufficiency fractures. The patient has become asymptomatic on calcitriol and phosphate supplementation. He is now being considered for radiofrequency ablation therapy. Conclusion This case illustrates the need for a thorough investigation of symptomatic, treatment-refractory hypophosphataemia. Although mild hypophosphatemia could indicate adult-onset rickets, rarer causes such as FGF-23 secreting tumours should be considered. These tumours are notoriously difficult to locate; Ga-DOTATE PET is probably superior to other imaging modalities including FDG-PET in isolating mesenchymal tumours. Disclosures K. Fisher None. S. Melath None. S. Patel None.