Persistent inflammatory monoarthritis is inflammation of one joint, with symptoms lasting beyond 3 months. Approximately 50 % of cases are self-limiting; others will transform into oligo- or polyarticular disease, but a significant minority remain as a persistent inflammatory monoarthritis, which are often resistant to standard therapies used for oligo- or polyarticular disease and constitute a difficult therapeutic problem. However, there are no clear guidelines for treatment of this category of patients or an evidence-based consensus view on best treatment. A literature search was done through PubMed using 'monoarthritis', 'chronic synovitis' and 'persistent inflammatory monoarthritis' as search terms. Reports were located using references to related articles; reports in humans and animals, published in English, were included. Persistent inflammatory monoarthritis has a variable disease course, generally with a better prognosis than polyarthritis. There is no clear evidence for the use of traditional DMARDS in monoarthritis, and treatment algorithms are extrapolated from oligo- or polyarticular disease. Intra-articular anti-tumour necrosis factor (TNF) has been used with similar efficacy to intra-articular corticosteroids, and as yet, there are no reported cases of systemic anti-TNF use in monoarthritis. Synovectomy may be of use, with lower risk of recurrent disease, in open synovectomy. There is paucity of evidence for best practice in the management of chronic monoarthritis. Questions remain concerning the indications for invasive procedures and the balance between toxicity of systemic therapies versus the intended benefits to prevent disability. There is a pressing need for further studies and randomised controlled trials to be performed in this subset of patients.

Background Treatment strategies in chronic hepatitis B (CHB) are evolving as more potent oral antivirals become available. However, drug resistance remains a major challenge and policy guidelines on management are limited by the evidence base. This study aims to review the implications of the National Institute for Health and Clinical Excellence (NICE) guidelines in a cohort of unselected CHB patients in the United Kingdom and to evolve a management algorithm for their treatment. Methods In total, 783 unselected hepatitis B surface antigen-positive patients, were assessed of whom 212 (27%) underwent liver biopsy. Age, alanine aminotransferase, hepatitis B virus DNA and necroinflammatory score were analysed to determine their value as predictors of fibrosis. Patients with biopsy evidence of fibrosis were offered treatment and followed longitudinally. Six-month on-treatment virologic response was evaluated to determine the validity of this strategy in predicting the early emergence of resistance. Results Age, gender and necroinflammatory score were predictors of fibrosis in CHB patients, whereas age >40 years was a predictor of cirrhosis in both hepatitis B e antigen (HBeAg)-positive ( P<0.03) and HBeAg-negative patients ( P<0.003). A total of 81% of HBeAg-positive and 65% of HBeAg-negative CHB patients who required adefovir add-on therapy were identifiable after 6 months of lamivudine monotherapy, by continuing HBV DNA positivity ( P<0.002 and P<0.0001, respectively). Conclusions Advanced liver disease was present in patients falling outside current treatment guidelines, highlighting the importance of liver histology in identifying fibrosis and the need for antiviral therapy. While 6 month on-treatment virologic response as a trigger for instituting add-on therapy may be an improvement on the current recommendations, such a strategy should be integrated into any new treatment algorithm, likely to consist of entecavir and tenofovir.

BackgroundThe significance of reduced vitamin D (25-OHD) to skeletal health, as assessed by radiological changes and fracture risk, is not known in detail. The uncertainty of this nutritional interaction becomes critical for instance in cases of potential non-accidental fracture. In order to provide an insight into this area we studied a paediatric group at high risk of low vitamin D levels.AimsWe aimed to estimate the incidence of radiological bony changes in patients attending a paediatric tuberculosis clinic, many of whom have chronically low vitamin D levels. Secondary outcomes were to assess whether serological markers of bone health can be used to identify those at greater risk of osteopenia and rickets.MethodsChildren attending a paediatric TB clinic between 01/01/2008 and 31/12/2011 had blood samples, including serum vitamin D levels, and chest radiograph taken as part of routine investigation at diagnosis. All radiographs were reported independently and retrospectively by two consultant radiologists, who were blinded to the child’s vitamin D status, on the presence of osteopenia or rickets.Results174 children were included in this study (46.6% male, median age 7 years range, 0.25–16y). At the point of diagnosis, 35 children were 25-OHD deficient (levels <25nmol/l), 57 were insufficient (levels 25–49nmol/l). During the study none of the cases suffered fracture and none had clinical evidence of rickets. Osteopenia was reported in one child by one radiologist. This child had a vitamin D level of 22 nmol/l and a raised PTH at 36.9.PTH levels were normal in 92 children, unavailable in 45 and raised in 30 children, of whom 29 had normal radiological skeletal appearances. A significant correlation between 25-OHD and PTH was identified (r=–0.371, 95% CI –0.5105 to –0.2123, p value <0.0001). Two children had hypocalcaemia with vitamin D deficiency but had normal PTH and alkaline phosphatase levels. There was no correlation between serum 25-OHD levels and alkaline phosphatase levels.ConclusionThe low incidence of radiographic bony abnormality and absence of fractures in a cohort of children with vitamin D deficiency, suggests many children with low serum vitamin D levels are unlikely to develop rickets and fractures.