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Because women with IL-10 (-1082) AA genotype have 3.38-fold increased risk of developing PE according to GG genotype (95% CI 1.21-9.4, P = 0.01), we suggest that IL-10 (-1082) variant A allele is associated with an increased risk of preeclampsia, which is independent from its metabolic effects.

Background: Vitiligo is a progressive depigmenting disorder characterized by the loss of functional melanocytes from the epidermis. The etiopathogenesis of vitiligo is still unclear. Vitamin D has both stimulatory and protective effects on melanocytes and acts through its nuclear vitamin D receptor (VDR) on target cells. Aim: The aim of this study was to investigate the association between VDR gene polymorphisms and susceptibility to vitiligo. Methods: 98 patients with vitiligo and 216 age- and sex-matched controls recruited from dermatology outpatients attending the same department were included in the study. Genomic DNA was extracted from peripheral blood leukocytes using a DNA isolation kit. The VDR polymorphisms of BsmI, ApaI, TaqI, FokI and Cdx2 were investigated by rapid capillary PCR with melting curve analysis. Differences in genotype distributions and allele frequencies in vitiligo cases versus controls were compared for statistical significance using χ² test. Results: Subjects with TaqI polymorphism had a 2.23-fold increased risk of developing vitiligo. Furthermore, a haplotype analysis showed that BsmI/ApaI/TaqI/FokI/Cdx2 GCCCG wassignificantly overrepresented in the vitiligo patients in comparison with controls (p = 0.031). Conclusion: This study showed that VDR TaqI gene polymorphism and the haplotype BsmI/ApaI/ TaqI/FokI/Cdx2 GCCCG may be considered as novel risk factors in vitiligo.

Increased serum visfatin, fetuin-A, and PTX3 levels, and the presence of positive correlation between visfatin, fetuin-A, and PASI score, probably reflect the inflammatory state and IR seen in psoriasis.

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An increase in the metabolically active serum phospholipid fraction is reflected in elevated neoplastic tissue phospholipid. This produces altered proportions between lipid fractions in tumorous areas and may result in changes in the intact nature of the cellular membrane, spread, and malignant proliferation.

Our results suggest that TNFalpha and IL-10 promoter polymorphism might be a risk factor for AD. The combined effects of TNFalpha-308, IL-6 -174 and IL-10 -1082 variant alleles may be more decisive to induce functional differences and modify the risk for AD.