Antiphospholipid and Antinuclear Antibodies in Children with Idiopathic Epilepsy: A 2-Year Prospective Study.

BACKGROUND AND PURPOSE: The high prevalence of antiphospholipid antibodies (aPL) and antinuclear antibodies (ANA) in patients with epilepsy may be associated with either the disease itself or the antiepileptic treatment. The purpose of this prospective study was to determine the prevalence of aPL and ANA in children with idiopathic epilepsy before and during treatment with antiepileptic drugs. METHODS: aPL, including both anticardiolipin and anti-ß2-glycoprotein I antibodies, and ANA statuses were determined in 40 healthy children, 30 children treated with sodium valproate (VPA) monotherapy, and 20 children treated with carbamazepine (CBZ) monotherapy before and at 6, 12, and 24 months after treatment initiation. RESULTS: Fifteen children (50%) in the VPA-treated group and 7 (35%) in the CBZ-treated group showed positivity for aPL before treatment initiation, compared with only 4 of the 40 controls. Nine children (30%) in the VPA-treated group and 4 (20%) in the CBZ-treated group showed positivity for ANA before treatment initiation, compared with only 2 of the 40 controls. The subgroup analysis found nonsignificant associations at the different time points regarding the positivity of all of the autoantibodies. Only patients treated with VPA had a significantly decreased risk of aPL positivity after 6 months of treatment. CONCLUSIONS: The increased prevalence of autoantibodies in children with idiopathic epilepsy is strongly associated with the disease itself.

The emerging role of cardiovascular magnetic resonance imaging in the assessment of cardiac involvement in juvenile idiopathic arthritis.

Juvenile idiopathic arthritis (JIA) is the commonest rheumatic disease in childhood and presents several subtypes according to the ILAR classification. JIA, specifically in its systemic form, may seriously damage various structures of the cardiovascular system. Other JIA phenotypes are also of interest, as cardiovascular disease (CVD) is underestimated and understudied, but chronic systemic inflammation and risk factors remained important contributors for CVD development. The currently applied non-invasive modalities, although they are important for the initial evaluation of JIA patients, frequently fail to detect the silent, subclinical forms of CVD. Cardiovascular magnetic resonance (CMR), due to its multifaceted capability in the detection of cardiovascular disease, can offer early, reproducible, non-invasive information about cardiovascular disease in JIA, allowing risk stratification and timely initiation /modification of cardiologic and anti-rheumatic treatment. However, lack of availability/expertise and high cost still hamper its application in the clinical cardio-rheumatic practice. The aim of the current article is to present an overview of CVD in JIA emphasizing the emerging role of CMR in early diagnosis and treatment follow-up of CVD in JIA patients.

The transforming growth factor-beta/bone morphogenetic protein signalling pathway in adipogenesis.

Rising obesity epidemic makes the better understanding of transcription factor networks regulating adipogenesis very challenging. Adipogenesis begins with the commitment of pluripotent mesenchymal stem cells to the adipocyte lineage, followed by terminal differentiation of preadipocytes to mature adipocytes. Among the molecules that influence the decision of progenitor cells to become adipocytes are members of transforming growth factor-beta superfamily and particularly bone morphogenetic proteins. Transforming growth factor-beta and bone morphogenetic proteins exert their biological functions mainly through their downstream molecules, the Smads. Here, we review the role(s) of transforming growth factor-beta/bone morphogenetic protein signalling pathway in adipocyte differentiation. Unravelling the precise mechanism of each molecule/pathway is necessary for developing suitable inhibitors or mimetic agents in order to treat obesity and improve insulin resistance. Current research efforts aim at discovering drugs that reduce fat mass or change the phenotype of adipose tissue into a more thermogenic one.

Serum leptin, adiponectin and tumor necrosis factor-α in hyperlipidemic rats with/without concomitant diabetes mellitus.

We compared the lipid profiles and serum levels of leptin, adiponectin and tumor necrosis factor-α (TNF-α) in rats with/without hyperlipidemia and with/without concomitant diabetes mellitus. Forty 10-wk-old male Wistar rats were divided into four groups. Groups A and C received standard food for 12 wks. Groups B and D received a high-fat diet enriched with 2% additional cholesterol. Moreover, insulin-deficient (type I) diabetes mellitus was induced in rats in groups C and D with intraperitoneal injections of streptozotocin. Fasting serum leptin levels were decreased in diabetic groups (groups C and D) compared with controls. Fasting serum adiponectin levels were decreased in groups C and D compared with group A. Serum TNF-α levels were augmented in groups B and D, those fed with an atherogenic diet. By contrast, TNF-α levels were decreased in group C. Our data suggest that serum leptin, adiponectin and TNF-α levels may serve as markers of obesity and type I diabetes mellitus.