Update on the diagnosis and management of gout.

Gout is a common clinical problem encountered by both general and specialist clinicians. The key principles in gout management include establishing a definitive diagnosis, the swift treatment of acute attacks, and using urate-lowering therapies appropriately to prevent further attacks and joint damage. The gold standard diagnostic tool for gout remains the identification by polarised light microscopy of monosodium urate crystals in synovial fluid or in a tophus. Emerging diagnostic imaging techniques and novel therapies show promise in the diagnosis and treatment of gout. In most cases, using existing therapies judiciously remains the key determinant of success in managing gout.

Australian and New Zealand recommendations for the diagnosis and management of gout: integrating systematic literature review and expert opinion in the 3e Initiative.

AIM: To develop evidence-based recommendations for the diagnosis and management of gout in Australia and New Zealand as part of the multi-national 3e Initiative. METHOD: Using a formal voting process, a panel of 78 international rheumatologists selected 10 key clinical questions pertinent to the diagnosis and management of gout. An additional question was also developed by participating Australian and New Zealand rheumatologists. Each question was investigated with a systematic literature review. MEDLINE, EMBASE, Cochrane CENTRAL and abstracts from 2010 to 2011 European League Against Rheumatism and American College of Rheumatology meetings were searched in each review. Relevant studies were independently reviewed by two individuals for data extraction and synthesis and risk of bias assessment. Using this evidence, 47 Australian and New Zealand rheumatologists developed national recommendations. For each recommendation the level of agreement was assessed and the level of evidence graded. RESULT: Eleven recommendations were produced relating to the diagnosis of gout, different aspects of the management of gout, cardiovascular and renal comorbidities and the management of asymptomatic hyperuricemia. The mean level of agreement with the recommendations was 9.1 on a 1-10 scale, with 10 representing full agreement. CONCLUSION: Eleven Australian and New Zealand recommendations on the diagnosis and management of gout were developed combining systematically reviewed evidence with local expertise, enhancing their utility in clinical practice.

Isotretinoin-induced skeletal hyperostosis.

We describe a case of skeletal hyperostosis in a 29 year old man presenting with non-inflammatory back pain with a past history of isotretinoin therapy for acne. The development of skeletal hyperostosis, predominantly of the spine, has been reported in association with isotretinoin use and has a radiographic picture similar to diffuse idiopathic skeletal hyperostosis. The prevalence and severity of this condition appears to correlate with duration of therapy. Isotretinoin is a well-established treatment for severe acne. It is important for the rheumatologist be aware of this phenomenon when assessing young patients with musculoskeletal symptoms and evidence of radiological abnormalities.

South Australian Scleroderma Register: autoantibodies as predictive biomarkers of phenotype and outcome.

AIM: To investigate the relationship between scleroderma-specific autoantibodies and clinical phenotype and survival in South Australian patients with scleroderma. METHOD: Two cohorts of patients were studied from the South Australian Scleroderma Register (SASR). In the first, the sera of 129 consecutive patients were analyzed for anticentromere (ACA), anti-Scl70, anti-RNA polymerase III, anti-U1RNP, anti-Th/To, anti-Pm/Scl, anti-Ku and anti-fibrillarin antibodies using the Euroline immunoblot assay. Statistical analysis was performed to look for a significant association between specific antibodies and various clinical features. In the second cohort survival from first symptom onset was analyzed in 285 patients in whom the autoantibody profile was available, including ACA, Anti-Scl70, anti-U1RNP and anti-RNA polymerase III measured using multiple methods. Survival analysis compared mortality between different groups of patients with specific antibodies. RESULTS: ACA, Th/To and Ku antibodies were associated with limited scleroderma, Scl70 and RNA Pol III antibodies were associated with diffuse scleroderma and antibodies to U1RNP were associated with overlap syndrome. Significant associations between Scl70 and interstitial lung disease (P = 0.004), RNA Pol III and renal crisis (P = 0.002), U1RNP and pulmonary hypertension (P = 0.006) and Th/To and pulmonary hypertension (P = 0.034) were seen. Trends were observed with an increased frequency of lung disease with Pm/Scl and Th/To and an increased frequency of myositis with Ku. The presence of Scl70, RNA Pol III and U1RNP was associated with significantly reduced survival as compared with patients with ACA. CONCLUSIONS: Scleroderma-specific autoantibodies are associated with clinical phenotype and survival.

Low copy number of the FCGR3B gene and rheumatoid arthritis: a case-control study and meta-analysis.

INTRODUCTION: Low copy number (CN) of the Fc gamma receptor 3B (FCGR3B) gene has been associated with systemic autoimmune disease. This receptor for IgG is present almost exclusively on neutrophils and plays a role in their interaction with immune complexes. At present the relationship between FCGR3B and rheumatoid arthritis (RA) is unclear. The aim of the present study was to investigate whether low CN of the FCGR3B gene is associated with susceptibility to RA. METHOD: The FCGR3B CN was determined using a custom Taqman® CN assay (Hs04211858; Applied Biosystems, Foster City, CA, USA) in 197 RA patients, recruited from a tertiary setting, and in 162 population matched controls. Odds ratios for low CN (< 2) and high CN (> 2), both relative to the normal diploid 2CN, were estimated by logistic regression. RESULTS: A significant association between RA and low FCGR3B CN was observed, with frequencies of 13.7% in RA patients compared with 6.2% in controls (odds ratio 2.5, 95% confidence interval 1.2 to 5.4, P = 0.017). No association was observed between low CN and the presence of rheumatoid factor, anti-cyclic citrullinated peptide antibodies or radiographic erosions in RA patients. A meta-analysis including six previous studies confirmed an association between RA and low FCGR3B CN (odds ratio 1.47, 95% confidence interval 1.13 to 1.92, P = 0.004). CONCLUSIONS: The present study confirms that a low CN of the FCGR3B gene is associated with susceptibility to RA. The association may be stronger in patients recruited from a tertiary setting, which may relate to disease severity and/or complications. The mechanism of susceptibility remains unclear and further study is required.