Psoriasis and metabolic syndrome (MetS), a common comorbidity of psoriasis, are associated with mild chronic systemic inflammation that increases oxidative stress and causes cell and tissue damage. At the cellular level, chromosomal and DNA damage has been documented, thus confirming their genotoxic effect. The main objective of our study was to show the genotoxic potential of chronic inflammation and determine whether the presence of both pathologies increases chromosomal damage compared to psoriasis alone and to evaluate whether there are correlations between selected parameters and chromosomal aberrations in patients with psoriasis and MetS psoriasis. Clinical examination (PASI score and MetS diagnostics according to National Cholesterol Education Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; NCE/ATPIII criteria), biochemical analysis of blood samples (fasting glucose, total cholesterol, low density and high density lipoproteins; LDL, HDL, non-HDL, and triglycerides;TAG), DNA/RNA oxidative damage, and chromosomal aberration test were performed in 41 participants (20 patients with psoriasis without MetS and 21 with MetS and psoriasis). Our results showed that patients with psoriasis without metabolic syndrome (nonMetS) and psoriasis and MetS had a higher rate of chromosomal aberrations than the healthy population for which the limit of spontaneous, natural aberration was <2%. No significant differences in the aberration rate were found between the groups. However, a higher aberration rate (higher than 10%) and four numerical aberrations were documented only in the MetS group. We found no correlations between the number of chromosomal aberrations and the parameters tested except for the correlation between aberrations and HDL levels in nonMetS patients (rho 0.44; p < 0.02). Interestingly, in the MetS group, a higher number of chromosomal aberrations was documented in non-smokers compared to smokers. Data from our current study revealed an increased number of chromosomal aberrations in patients with psoriasis and MetS compared to the healthy population, especially in psoriasis with MetS, which could increase the genotoxic effect of inflammation and the risk of genomic instability, thus increasing the risk of carcinogenesis.

• Klíčová slova
• chromosomal aberration, metabolic syndrome, psoriasis,
• Publikační typ
• časopisecké články MeSH

OBJECTIVE:: Waist circumference (WC) value reflects abdominal adiposity, but the amount abdominal fat that is associated to cardiometabolic risk factors varies among ethnicities. Determination of metabolic abnormalities has not undergone a WC adaptation process in Venezuela. The aim of the study was (1) to determine the optimal WC cutoff value associated with ≥2 cardiometabolic alterations and (2) incorporating this new WC cutoff, to determine the prevalence of abdominal obesity and cardiometabolic risk factors related in Venezuela. METHODS:: The study was national population-based, cross-sectional, and randomized sample, from 2014 to 2017. To assess performance of WC for identifying cardiometabolic alterations, receiver operating characteristics curves, area under the curve (AUC), sensitivity, specificity, and positive likelihood ratios were calculated. RESULTS:: Three thousand three hundred eighty-seven adults were evaluated with mean age of 41.2 ± 15.8 years. Using the best tradeoff between sensitivity and specificity, WC cutoffs of 90 cm in men (sensitivity = 72.4% and specificity = 66.1%) and 86 cm in women (sensitivity = 76.2% and specificity = 61.4%) were optimal for aggregation of ≥2 cardiometabolic alterations. AUC was 0.75 in men and 0.73 in women using these new cutoffs. Prevalence of abdominal obesity and metabolic syndrome was 59.6% (95 CI; 57.5-61.7) and 47.6% (95 CI; 45.2-50.0), respectively. Cardiometabolic risk factors were associated with being men, higher age, adiposity, and living in northern or western regions. CONCLUSION:: The optimal WC values associated with cardiometabolic alterations were 90 cm in men and 86 cm in women. More than half of the Venezuelan population had abdominal obesity incorporating this new WC cutoff.

BACKGROUND: Waist circumference (WC) value reflects abdominal adiposity, but the amount abdominal fat that is associated to cardiometabolic risk factors varies among ethnicities. Determination of metabolic abnormalities has not undergone a WC adaptation process in Venezuela. AIMS: The aim of the study was (1) to determine the optimal WC cutoff value associated with ≥2 cardiometabolic alterations and (2) incorporating this new WC cutoff, to determine the prevalence of abdominal obesity and cardiometabolic risk factors related in Venezuela. METHODS: The study was national population-based, cross-sectional, and randomized sample, from 2014 to 2017. To assess performance of WC for identifying cardiometabolic alterations, receiver operating characteristics curves, area under the curve (AUC), sensitivity, specificity, and positive likelihood ratios were calculated. RESULTS: Three thousand three hundred eighty-seven adults were evaluated with mean age of 41.2 ± 15.8 years. Using the best tradeoff between sensitivity and specificity, WC cutoffs of 90 cm in men (sensitivity = 72.4% and specificity = 66.1%) and 86 cm in women (sensitivity = 76.2% and specificity = 61.4%) were optimal for aggregation of ≥2 cardiometabolic alterations. AUC was 0.75 in men and 0.73 in women using these new cutoffs. Prevalence of abdominal obesity and metabolic syndrome was 59.6% (95 CI; 57.5-61.7) and 47.6% (95 CI; 45.2-50.0), respectively. Cardiometabolic risk factors were associated with being men, higher age, adiposity, and living in northern or western regions. CONCLUSION: The optimal WC values associated with cardiometabolic alterations were 90 cm in men and 86 cm in women. More than half of the Venezuelan population had abdominal obesity incorporating this new WC cutoff.

• Klíčová slova
• Abdominal obesity, Adiposity, Metabolic syndrome, Venezuela, Waist circumference,
• Publikační typ
• časopisecké články MeSH

BACKGROUND: Assessing the relationship between lung cancer and metabolic conditions is challenging because of the confounding effect of tobacco. Mendelian randomization (MR), or the use of genetic instrumental variables to assess causality, may help to identify the metabolic drivers of lung cancer. METHODS AND FINDINGS: We identified genetic instruments for potential metabolic risk factors and evaluated these in relation to risk using 29,266 lung cancer cases (including 11,273 adenocarcinomas, 7,426 squamous cell and 2,664 small cell cases) and 56,450 controls. The MR risk analysis suggested a causal effect of body mass index (BMI) on lung cancer risk for two of the three major histological subtypes, with evidence of a risk increase for squamous cell carcinoma (odds ratio (OR) [95% confidence interval (CI)] = 1.20 [1.01-1.43] and for small cell lung cancer (OR [95%CI] = 1.52 [1.15-2.00]) for each standard deviation (SD) increase in BMI [4.6 kg/m2]), but not for adenocarcinoma (OR [95%CI] = 0.93 [0.79-1.08]) (Pheterogeneity = 4.3x10-3). Additional analysis using a genetic instrument for BMI showed that each SD increase in BMI increased cigarette consumption by 1.27 cigarettes per day (P = 2.1x10-3), providing novel evidence that a genetic susceptibility to obesity influences smoking patterns. There was also evidence that low-density lipoprotein cholesterol was inversely associated with lung cancer overall risk (OR [95%CI] = 0.90 [0.84-0.97] per SD of 38 mg/dl), while fasting insulin was positively associated (OR [95%CI] = 1.63 [1.25-2.13] per SD of 44.4 pmol/l). Sensitivity analyses including a weighted-median approach and MR-Egger test did not detect other pleiotropic effects biasing the main results. CONCLUSIONS: Our results are consistent with a causal role of fasting insulin and low-density lipoprotein cholesterol in lung cancer etiology, as well as for BMI in squamous cell and small cell carcinoma. The latter relation may be mediated by a previously unrecognized effect of obesity on smoking behavior.

• MeSH
• fenotyp MeSH
• index tělesné hmotnosti MeSH
• inzulin krev   MeSH
• inzulinová rezistence MeSH
• jednonukleotidový polymorfismus MeSH
• lidé MeSH
• lipidy krev   MeSH
• mendelovská randomizace * MeSH
• nádory plic krev   komplikace   metabolismus   patologie   MeSH
• obezita krev   komplikace   MeSH
• omezení příjmu potravy MeSH
• pravděpodobnostní funkce MeSH
• rizikové faktory MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• inzulin MeSH
• lipidy MeSH