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Behçet’s disease (BD) is a chronic, relapsing, multisystemic inflammatory disorder with unanswered questions regarding its etiology/pathogenesis and classification. Distinct manifestation based subsets, pronounced geographical variations in expression, and discrepant immunological abnormalities raised the question whether Behçet’s is “a disease or a syndrome”. To answer the preceding question we aimed to display and compare the molecular mechanisms underlying distinct subsets of BD. For this purpose, the expression data of the gene expression profiling and association study on BD by Xavier et al (2013) was retrieved from GEO database and reanalysed by gene expression data analysis/visualization and bioinformatics enrichment tools. There were 15 BD patients (B) and 14 controls (C). Three subsets of BD patients were generated: MB (isolated mucocutaneous manifestations, n = 7), OB (ocular involvement, n = 4), and VB (large vein thrombosis, n = 4). Class comparison analyses yielded the following numbers of differentially expressed genes (DEGs); B vs C: 4, MB vs C: 5, OB vs C: 151, VB vs C: 274, MB vs OB: 215, MB vs VB: 760, OB vs VB: 984. Venn diagram analysis showed that there were no common DEGs in the intersection “MB vs C” ∩ “OB vs C” ∩ “VB vs C”. Cluster analyses successfully clustered distinct expressions of BD. During gene ontology term enrichment analyses, categories with relevance to IL-8 production (MB vs C) and immune response to microorganisms (OB vs C) were differentially enriched. Distinct subsets of BD display distinct expression profiles and different disease associated pathways. Based on these clear discrepancies, the designation as “Behçet’s syndrome” (BS) should be encouraged and future research should take into consideration the immunogenetic heterogeneity of BS subsets. Four gene groups, namely, negative regulators of inflammation (CD69, CLEC12A, CLEC12B, TNFAIP3), neutrophil granule proteins (LTF, OLFM4, AZU1, MMP8, DEFA4, CAMP), antigen processing and presentation proteins (CTSS, ERAP1), and regulators of immune response (LGALS2, BCL10, ITCH, CEACAM8, CD36, IL8, CCL4, EREG, NFKBIZ, CCR2, CD180, KLRC4, NFAT5) appear to be instrumental in BS immunopathogenesis.

Background:Alopecia areata (AA) is an autoimmune-mediated hair follicle disorder. In the literature, there is no study evaluating metabolic syndrome and levels of ischemia-modified albumin (IMA) which is proposed as an oxidative stress biomarker in patients with AA.Aims:The aim was to investigate the presence of metabolic syndrome and the levels of IMA, small dense low-density lipoprotein (sd-LDL), and visfatin levels in AA patients.Settings and Design:A hospital-based cross-sectional study was undertaken among AA patients and controls.Subjects and Methods:Thirty-five patients with AA and 35 sex-, age-, and body mass index-matched healthy controls were enrolled. Clinical and laboratory parameters of metabolic syndrome were examined in all participants. Furthermore, IMA, sd-LDL, and visfatin levels were assessed and analyzed with regard to disease pattern, severity and extent, severity of alopecia tool score, duration, and recurrence.Results:The median IMA and adjusted IMA levels were significantly increased compared with controls (P<0.05 and P=0.002, respectively). Patients with pull test positivity displayed higher levels of adjusted IMA levels (P<0.05). In AA group, there was a positive correlation between adjusted IMA and waist circumference (r=0.443, P=0.008), adjusted IMA and triglyceride levels (r=0.535, P=0.001), and adjusted IMA and sd-LDL levels (r=0.46, P<0.05). We observed no statistically significant difference in fasting blood glucose and lipid profile, sd-LDL, and visfatin levels of the patients and healthy controls.Conclusions:AA patients and controls have similar metabolic profile. Raised levels of adjusted IMA levels may be associated with antioxidant/oxidant imbalance and with risk of cardiovascular disease.

No abstract

For the prediction of preterm labor/PPROM, the relatively high AGEs levels in the first trimester might be a useful marker.

Abstract:Objective: C-reactive protein (CRP) is a well-known marker of infl ammation and infection in clinical practice. This study is designed to evaluate CRP levels in diff erent phases of menstrual cycle, which might end up with misleading conclusions especially when used for cardiovascular risk assessment. Methods: Twenty-seven women were eligible for the cross-sectional study. Venous blood samples from each participant were collected twice during the menstrual cycle. The fi rst sampling was held at 2nd to 5th days of the menstrual cycle for FSH, estradiol, CRP, and sedimentation, and the second was done at 21st to 24th days of the menstrual cycle for measurement of progesterone, CRP, and sedimentation values. Results: CRP values were signifi cantly higher in the early follicular phase compared to luteal phase (1.8 mg/L [0.3-7.67] vs. 0.7 mg/L [0.1-8.3], p < 0.001, respectively). In both phases of the menstrual cycle, sedimentation rate was similar (12.1 ± 6.7 vs. 12.3 ± 7.7; p = 0.717, respectively). Conclusions: CRP levels in early follicular phase of the menstrual cycle (menstruation) are signifi cantly higher than CRP levels in luteal phase of the same cycle. In reproductive age women, detection of CRP for cardiovascular risk assessment during menstruation might not be appropriate.

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Summary Background Vitamin D has significant effects on the immune system and thereby on the pathogenesis of rosacea. However, there is a lack of information on the vitamin D status and vitamin D receptors (VDRs) of patients with rosacea. Aim To evaluate the role of vitamin D in rosacea susceptibility. Methods A case–control study was conducted, enrolling patients with rosacea and healthy controls (HCs). Five VDR gene single nucleotide polymorphisms (SNPs) (Cdx2, FokI, ApaI, BsmI and TaqI) and serum 25‐hydroxyvitamin D3 [25(OH)D3] levels were compared between patients and HCs. Results The study enrolled 60 patients (M/F: 14/46) and 60 age‐ and sex‐matched HCs (M/F: 14/46). Age (mean ± SD) was 48 ± 11 years for both groups. The serum 25(OH)D3 levels (median ± interquartile range) were higher in patients with rosacea (12.9 ± 6.8 ng/mL) than in HCs (10.5 ± 3.7 ng/mL) (P < 0.001). Subjects with high serum 25(OH)D3 levels had a 1.36‐fold increased risk of rosacea (95% CI 1.17–1.58). Heterozygous and mutant ApaI polymorphisms increased rosacea risk by 5.26‐fold (95% CI 1.51–18.35) and 3.69‐fold (95% CI 1.19–11.48), respectively, whereas mutant TaqI polymorphisms decreased the risk by 4.69 times (95% CI 1.37–16.67). Heterozygosity for Cdx2 alleles increased rosacea risk, whereas wildtype ApaI and mutant TaqI alleles decreased it. Conclusions The present study suggests that an increase in vitamin D levels may contribute to the development of rosacea. ApaI and TaqI polymorphisms, and heterozygous Cdx2, wildtype ApaI and mutant TaqI alleles were significantly associated with rosacea. These results indicate a possible role of vitamin D and VDR pathways in the pathogenesis of rosacea, although causality could not be assessed.