The new proposed criteria derived from multinational data exhibits much improved sensitivity over the ISG criteria while maintaining reasonable specificity. It is proposed that the ICBD criteria to be adopted both as a guide for diagnosis and classification of BD.

Objective. Independent replication of the findings from genome-wide association studies (GWAS) remains the gold standard for results validation. Our aim was to test the association of Behçet's disease (BD) with the interleukin-10 gene (IL10) and the IL-23 receptor-IL-12 receptor ␤2 (IL23R-IL12RB2) locus, each of which has been previously identified as a risk factor for BD in 2 different GWAS.Methods. Six haplotype-tagging single-nucleotide polymorphisms (SNPs) in IL10 and 42 in IL23R-IL12RB2 were genotyped in 973 Iranian patients with BD and 637 non-BD controls. Population stratification was assessed using a panel of 86 ancestry-informative markers.Results. Subtle evidence of population stratification was found in our data set. In IL10, rs1518111 was nominally associated with BD before and after adjustment for population stratification (odds ratio [OR] for T allele 1.20, 95% confidence interval [95% CI] 1.02-1.40, unadjusted P [P unadj ] ‫؍‬ 2.53 ؋ 10 ؊2 ; adjusted P [P adj ] ‫؍‬ 1.43 ؋ 10 ؊2 ), and rs1554286 demonstrated a trend toward association (P unadj ‫؍‬ 6.14 ؋ 10 ؊2 ; P adj ‫؍‬ 3.21 ؋ 10 ؊2 ). Six SNPs in IL23R-IL12RB2 were found to be associated with BD after Bonferroni correction for multiple testing, the most significant of which were rs17375018 (OR for G allele 1.51, 95% CI 1.27-1.78, P unadj ‫؍‬ 1.93 ؋ 10 ؊6 ), rs7517847 (OR for T allele 1.48, 95% CI 1.26-1.74, P unadj ‫؍‬ 1.23 ؋ 10 ؊6 ), and rs924080 (OR for T allele 1.29, 95% CI 1.20-1.39, P ‫؍‬ 1.78 ؋ 10 ؊5 ). SNPs rs10489629, rs1343151, and rs1495965 were also significantly associated with BD in all tests performed. Results of meta-analyses of our data combined with data from other populations further confirmed the role of rs1518111, rs17375018, rs7517847, and rs924080 in the risk of BD, but no epistatic interactions between IL10 and IL23R-IL12RB2 were detected. Results of imputation analysis highlighted the importance of IL23R regulatory regions in the susceptibility to BD.Conclusion. These findings independently confirm, extend, and refine the association of BD with IL10 and IL23R-IL12RB2. These associations warrant further validation and investigation in patients with BD, as they may have implications for the development of novel therapies (e.g., immunosuppressive therapy targeted at IL-23p19).

Fibromyalgia (FM) is a chronic non-degenerative disease, whose nutritional therapy seems controversial. This systematic review aimed to synthesize the knowledge about the effect of dietary interventions on patient-reported outcomes (PRO) and inflammation in patients with FM. Six electronic databases -PubMed, BioMed Central, Cochrane library, EMBASE, LILACS and ISIwere searched for clinical trials, in which a dietary intervention in patients with FM diagnosed was conducted. Quality of evidence assessment was measured in accordance with GRADE methodology. Seven clinical trials -3 randomized controlled trials, 1 unrandomized clinical trial and 3 uncontrolled clinical trials were identified. Dietary approaches included gluten-free diet (n ¼ 1), raw vegetarian diet (n ¼ 2), low Fermentable oligo-, di-and monossacharides, alcohols and polyols (FODMAPs) diet (n ¼ 1), hypocaloric diet (n ¼ 2) and monosodium glutamate-and aspartamefree diet interventions (n ¼ 1). The major PRO were pain and functional repercussion, with 5 out of 7 studies reporting an improvement. The progress in secondary outcomes was reported for fatigue (2/5 studies), sleep quality (2/3 studies), depression and anxiety (3/6 studies), quality of life (4/5 studies), gastrointestinal symptoms (1/2 studies) and inflammatory biomarkers (1/1 study). However, according to Cochrane Risk of Bias, these studies had poor statistical quality. Well-designed studies should be performed to investigate the dietary interventions effect on FM. KEY MESSAGESFibromyalgia (FM) is a chronic non-degenerative disease, whose nutritional therapy seems controversial but promising. Pain and functional repercussion in FM patients seem to improve with a hypocaloric diet, a raw vegetarian diet or a low FODMAPs diet, as much as quality of life, quality of sleep, anxiety and depression and inflammatory biomarkers. Existing studies in this subject are scarce and low quality, which does not allow conclusions to be drawn.

The Portuguese version of the XI can be considered a reliable and valid instrument to measure patients' xerostomia symptoms.

Behçet's disease (BD) is a complex disease with genetic and environmental risk factors implicated in its etiology; however, its pathophysiology is poorly understood. To decipher BD's genetic underpinnings, we combined gene expression profiling with pathway analysis and association studies. We compared the gene expression profiles in peripheral blood mononuclear cells (PBMCs) of 15 patients and 14 matched controls using Affymetrix microarrays and found that the neuregulin signaling pathway was over-represented among the differentially expressed genes. The Epiregulin (EREG), Amphiregulin (AREG), and Neuregulin-1 (NRG1) genes of this pathway stand out as they are also among the top differentially expressed genes. Twelve haplotype tagging SNPs at the EREG-AREG locus and 15 SNPs in NRG1 found associated in at least one published BD genome-wide association study were tested for association with BD in a dataset of 976 Iranian patients and 839 controls. We found a novel association with BD for the rs6845297 SNP located downstream of EREG, and replicated three associations at NRG1 (rs4489285, rs383632, and rs1462891). Multifactor dimensionality reduction analysis indicated the existence of epistatic interactions between EREG and NRG1 variants. EREG-AREG and NRG1, which are members of the epidermal growth factor (EGF) family, seem to modulate BD susceptibility through main effects and gene-gene interactions. These association findings support a role for the EGF/ErbB signaling pathway in Electronic supplementary material The online version of this article