The role of dual energy computed tomography in the differentiation of acute gout flares and acute calcium pyrophosphate crystal arthritis

Objectives To analyse the diagnostic impact of dual energy computed tomography (DECT) in acute gout flares and acute calcium pyrophosphate (CPP) crystal arthritis when compared to the gold standard of arthrocentesis with compensated polarised light microscopy. Microscopy results were also compared to musculoskeletal ultrasound (MUS), conventional radiographs, and the suspected clinical diagnosis (SCD). Methods Thirty-six patients with a suspected gout flare (n = 24) or acute CPP crystal arthritis (n = 11, n = 1 suffered from neither) who received a DECT and underwent arthrocentesis were included. Two independent readers assessed DECT images for signs of monosodium urate crystals or calcium pyrophosphate deposition. Results Sensitivity of DECT for gout was 63% (95% CI 0.41–0.81) with a specificity of 92% (0.41–0.81) while sensitivity and specificity for acute CPP arthritis were 55% (0.23–0.83) and 92% (0.74–0.99), respectively. MUS had the highest sensitivity of all imaging modalities with 92% (0.73–0.99) and a specificity of 83% (0.52–0.98) for gout, while sensitivity and specificity for acute CPP crystal arthritis were 91% (0.59–1.00) and 92% (0.74–0.99), respectively. Conclusion DECT is an adequate non-invasive diagnostic tool for acute gout flares but might have a lower sensitivity than described by previous studies. Both MUS and SCD had higher sensitivities than DECT for acute gout flares and acute CPP crystal arthritis. Key Points• DECT offers a lower sensitivity for acute gout flares than previously described.• DECT sensitivity for acute CPP crystal arthritis is less than the already validated ultrasound.

The role of Interleukin-1 receptor antagonist as a treatment option in calcium pyrophosphate crystal deposition disease

Calcium Pyrophosphate Crystal Deposition (CPPD) disease is characterized by the deposition of calcium pyrophosphate crystals in the cartilage. In most cases, it can manifest as a subclinical condition named chondrocalcinosis, often revealed by joint x-ray examination. In other cases, deposition can cause flares of arthritis, known as acute CPP crystal arthritis. In the last few years, many pathogenic pathways have been discovered. Interleukin-1 (IL-1) plays a key role in the pathogenesis of CPPD disease, both as a mediator of inflammatory response to crystals and as a promoter of damage to articular cartilage. In this review, we investigated the role of IL-1R inhibitor, such as Anakinra, as an alternative to the various therapeutic strategies for CPPD disease, especially among patients resistant to traditional treatment with NSAIDs, corticosteroids and colchicine.

P100 Acute crystal arthritis: a leading cause of hospital admission, yet poorly recognised and mistreated

Background/Aims Crystal arthritis is the commonest inflammatory arthritis in adults. A common mimic is septic arthritis. Without appropriate synovial fluid analysis, a mis-diagnosis of sepsis can be made with resultant unnecessary hospitalization, inappropriate intravenous antibiotic therapy and excess cost. Such cases are frequently described as ‘culture-negative’ septic arthritis. We aimed to examine and analyse the cases of acute arthritis requiring acute hospital admission in a tertiary referral centre in Dublin. Methods A retrospective review of database between Jan - Dec 2019 at the Mater Misericordiae University Hospital, Dublin, was carried out. All cases of acute arthritis requiring acute hospital admission were identified. Cases treated at the Emergency Department, Acute Medical Unit or Outpatients which did not require hospital admission were excluded. Results 30 patients were identified during this period, 16 (53%) had an ultimate diagnosis of crystal arthritis, 8 (27%) had confirmed septic arthritis and 6 (20%) had other arthritides (e.g. haemoarthrosis). The median age for crystal arthritis was significantly higher (85.5 y) compared to septic arthritis (47 y). Apart from age, the clinical profile and biomarkers for crystal and septic arthritis were comparable. The majority of crystal arthritis cases were due to pseudogout (69 %), ultimately diagnosed by rheumatology. Septic arthritis led to more days in hospital than crystal arthritis (median 14 vs 5.5 days). All 30 patients received IV antimicrobial therapy for presumed septic arthritis. Conclusion This retrospective study showed crystal arthritis, especially pseudogout, was the commonest cause of hospital admission (53%) with acute arthritis particularly among elderly patients. Accurate diagnosis by synovial fluid analysis with appropriate equipment is extremely useful in the assessment of these cases. More awareness and training among orthopedic, emergency and acute clinicians is needed in order to avoid unnecessary admissions and interventions. Disclosure A. Abdalla: None.

NEUTROPHIL EXTRACELLULAR TRAPS RELEASE IN GOUT AND PSEUDOGOUT DEPENDS ON THE NUMBER OF CRYSTALS REGARDLESS OF LEUKOCYTE COUNT

Objectives Microcrystal-induced arthritis is still an unresolved paradigm for medicine. Overt inflammation may be absent even when crystals occur in synovial fluid. Recently, the production of neutrophil extracellular traps (NETs) embedding monosodium urate crystals (MSU) has been proposed as a possible mechanism of the auto-resolution of the inflammatory phase during gout. We aimed to verify and quantify the release of NETs in synovial fluids during gout and pseudogout attacks and to compare any differences with respect to crystals and neutrophils number, and to analyze activation of necroptosis pathway in synovial fluid from crystal-induced arthritis. Methods Synovial fluid samples were obtained by arthrocentesis from 22 patients presenting acute crystal-induced arthritis, gout or pseudogout (n = 11 each group), and from 10 patients with acute non-crystal arthritis as controls. NETosis was quantified in synovial fluid by nucleic acid stain and by quantification of human neutrophil elastase. Activation of p-MLKL was assessed by western blot. Results We observed that synovial fluid neutrophils encountering MSU and CPPD crystals during episodes of gout and pseudogout release NETs in relation to the number of crystals in synovial fluid and irrespective of neutrophil density and type of crystal. This release was accompanied by necroptosis through the activation of the MLKL pathway. Conclusions Our findings suggest that a role of NETs in crystal-induced arthritis is to “trap extracellular particles”, including microcrystals. Embedding crystals in aggregates of NETs may be the basis of tophi and CPPD deposition and may have implications for disease evolution, rather than for spontaneous resolution of the acute attack.