Physical activity and sedentary levels in children with juvenile idiopathic arthritis and inflammatory bowel disease. A systematic review and meta-analysis

The inflammatory bowel diseases (IBDs), including ulcerative colitis and Crohn disease, are chronic inflammatory disorders of the gastrointestinal tract most often diagnosed in adolescence and young adulthood, with a rising incidence in pediatric populations. These disorders are common enough in children that most pediatricians and other pediatric clinicians will encounter children with IBD in their general practice. Inflammatory bowel disease is caused by a dysregulated mucosal immune response to the intestinal microflora in genetically predisposed hosts. Although children can present with the classic symptoms of weight loss, abdominal pain, and bloody diarrhea, many present with nonclassic symptoms of isolated poor growth, anemia, or other extraintestinal manifestations. Once IBD is diagnosed, the goals of therapy consist of eliminating symptoms, normalizing quality of life, restoring growth, and preventing complications while minimizing the adverse effects of medications. Unique considerations when treating children and adolescents with IBD include attention to the effects of the disease on growth and development, bone health, and psychosocial functioning. The purpose of this review is to provide a contemporary overview of the epidemiologic features, pathogenesis, diagnosis, and management of IBD in children and adolescents.

To conduct a systematic literature review on incidence and prevalence of juvenile idiopathic arthritis and to estimate these figures in Europe for 2010. Articles on incidence or prevalence of juvenile idiopathic arthritis were searched in Medline. Pooled incidence and prevalence were calculated overall, by gender, age, classification and arthritis categories. We used the available age and gender pooled rates to standardize the incidence and prevalence on the 2010 European population and estimate the number of cases in Europe in 2010. Forty-three articles (33 on incidence, 29 on prevalence) were included. Incidence rates varied from 1.6 to 23 and prevalence from 3.8 to 400/100,000. Pooled incidence and prevalence were higher for girls (10.0 [9.4-10.7] and 19.4 [18.3-20.6]/100,000) than boys (5.7 [5.3-6.2] and 11.0 [10.2-11.9]/100,000). Oligoarthritis was the most frequent form (pooled incidence rate 3.7 [3.5-3.9] and prevalence 16.8 [15.9-17.7]/100,000). The direct standardized incidence rate was 8.2 [7.5-9.0] and prevalence 70.2 [62.9-78.1]/100,000. In Europe in 2010, the estimated number of incident cases was 6896 [5481-8578] and 59,175 [44,256-76,983] prevalent cases. Incidence and prevalence varied greatly among published reports of juvenile idiopathic arthritis, which may be explained by methodological issues, classification used, and time. Estimating the number of affected children can be useful, especially with the new treatment possibilities. Copyright © 2013 Société française de rhumatologie. Published by Elsevier SAS. All rights reserved.

Tumor necrosis factor alpha (TNFalpha) has been implicated as a mediator of muscle wasting through nuclear factor kappa B (NF-kappaB) -dependent inhibition of myogenic differentiation. The aim of the present study was to identify the regulatory molecule(s) of myogenesis targeted by TNFalpha/NF-kappaB signaling. TNFalpha interfered with cell cycle exit and repressed the accumulation of transcripts encoding muscle-specific genes in differentiating C2C12 myoblasts. Overexpression of a p65 (RelA) mutant lacking the transcriptional activation domain attenuated the TNFalpha-mediated inhibition of muscle-specific gene transcription. The ability of muscle regulatory factor MyoD to induce muscle-specific transcription in 10T1/2 fibroblasts was also disrupted by wild-type p65, demonstrating that NF-kappaB transcriptional activity interferes with the function of MyoD. Inhibition of muscle-specific gene expression by TNFalpha was restored by overexpression of MyoD, whereas endogenous MyoD protein abundance and stability were reduced by TNFalpha through increased proteolysis of MyoD by the ubiquitin proteasome pathway. Last, the inhibitory effects of TNFalpha on myogenic differentiation were demonstrated in a mouse model of skeletal muscle regeneration, in which TNFalpha caused a delay in myoblast cell cycle exit. These results implicate that TNFalpha inhibits myogenic differentiation through destabilizing MyoD protein in a NF-kappaB-dependent manner, which interferes with skeletal muscle regeneration and may contribute to muscle wasting.