Cardiovascular Disease in Juvenile Idiopathic Arthritis.

Juvenile idiopathic arthritis (JIA), is a term used to describe a group of inflammatory disorders beginning before the age of 16 years. Although for the majority of children remission is achieved early, those with systemic or polyarticular form of the disease may present persistent symptoms in adulthood. Considering that there is overlap in the pathogenesis of JIA with adult rheumatic diseases, concerns have been raised as to whether JIA patients could be at increased cardiovascular (CV) risk in the long-term. In this review, we summarize evidence for CV involvement in JIA and present data on CV risk factors and surrogate markers of arterial disease. We also provide information on beneficial and harmful CV effects of anti-inflammatory medications in the context of JIA and suggest strategies for CV screening. Overall, patients with systemic forms of JIA demonstrate an adverse lipid profile and early arterial changes relevant to accelerated arterial disease progression. Although there is paucity of data on CV outcomes, we recommend a holistic approach in the management of JIA patients, which includes CV risk factor monitoring and lifestyle modification as well as use, when necessary, of antiinflammatory therapies with documented CV safety.

Fatty acid profile of plasma NEFA does not reflect adipose tissue fatty acid profile.

Adipose tissue (AT) fatty acid (FA) composition partly reflects habitual dietary intake. Circulating NEFA are mobilised from AT and might act as a minimally invasive surrogate marker of AT FA profile. Agreement between twenty-eight FA in AT and plasma NEFA was assessed using concordance coefficients in 204 male and female participants in a 12-month intervention using supplements to increase the intake of EPA and DHA. Concordance coefficients generally showed very poor agreement between AT FA and plasma NEFA at baseline SFA: 0·07; MUFA: 0·03; n-6 PUFA: 0·28; n-3 PUFA: 0·01). Participants were randomly divided into training (70 %) and validation (30 %) data sets, and models to predict AT and dietary FA were fitted using data from the training set, and their predictive ability was assessed using data from the validation set. AT n-6 PUFA and SFA were predicted from plasma NEFA with moderate accuracy (mean absolute percentage error n-6 PUFA: 11 % and SFA: 8 %), but predicted values were unable to distinguish between low, medium and high FA values, with only 25 % of n-6 PUFA and 33 % of SFA predicted values correctly assigned to the appropriate tertile group. Despite an association between AT and plasma NEFA EPA (P=0·001) and DHA (P=0·01) at baseline, there was no association after the intervention. To conclude, plasma NEFA are not a suitable surrogate for AT FA.

Epilepsy biomarkers.

A biomarker is defined as an objectively measured characteristic of a normal or pathologic biologic process. Identification and proper validation of biomarkers of epileptogenesis (the development of epilepsy) and ictogenesis (the propensity to generate spontaneous seizures) might predict the development of an epilepsy condition; identify the presence and severity of tissue capable of generating spontaneous seizures; measure progression after the condition is established; and determine pharmacoresistance. Such biomarkers could be used to create animal models for more cost-effective screening of potential antiepileptogenic and antiseizure drugs and devices, and to reduce the cost of clinical trials by enriching the trial population, and acting as surrogate markers to shorten trial duration. The objectives of the biomarker subgroup for the London Workshop were to define approaches for identifying possible biomarkers for these purposes. Research to identify reliable biomarkers may also reveal underlying mechanisms that could serve as therapeutic targets for the development of new antiepileptogenic and antiseizure compounds.