siMS Score: Simple Method for Quantifying Metabolic Syndrome.

OBJECTIVE:To evaluate siMS score and siMS risk score, novel continuous metabolic syndrome scores as methods for quantification of metabolic status and risk. MATERIALS AND METHODS:Developed siMS score was calculated using formula: siMS score = 2*Waist/Height + Gly/5.6 + Tg/1.7 + TAsystolic/130-HDL/1.02 or 1.28 (for male or female subjects, respectively). siMS risk score was calculated using formula: siMS risk score = siMS score * age/45 or 50 (for male or female subjects, respectively) * family history of cardio/cerebro-vascular events (event = 1.2, no event = 1). A sample of 528 obese and non-obese participants was used to validate siMS score and siMS risk score. Scores calculated as sum of z-scores (each component of metabolic syndrome regressed with age and gender) and sum of scores derived from principal component analysis (PCA) were used for evaluation of siMS score. Variants were made by replacing glucose with HOMA in calculations. Framingham score was used for evaluation of siMS risk score. RESULTS:Correlation between siMS score with sum of z-scores and weighted sum of factors of PCA was high (r = 0.866 and r = 0.822, respectively). Correlation between siMS risk score and log transformed Framingham score was medium to high for age groups 18+,30+ and 35+ (0.835, 0.707 and 0.667, respectively). CONCLUSIONS:siMS score and siMS risk score showed high correlation with more complex scores. Demonstrated accuracy together with superior simplicity and the ability to evaluate and follow-up individual patients makes siMS and siMS risk scores very convenient for use in clinical practice and research as well

Five patients with calculated siMS scores and siMS risk scores within time.

<p>Five patients with calculated siMS scores and siMS risk scores within time.</p

Correlation between siMS risk score and Framingham score.

<p>Correlation between siMS risk score and Framingham score.</p

Correlations between siMS score and other metabolic syndrome scores.

<p>Correlations between siMS score and other metabolic syndrome scores.</p

Clinical Indicators of Bone Deterioration in Alcoholic Liver Cirrhosis and Chronic Alcohol Abuse: Looking beyond Bone Fracture Occurrence

Although previous studies indicated that chronic alcohol abuse (CAA) and alcoholic liver cirrhosis (ALC) are associated with increased bone fragility, understanding bone fragility determinants is still modest in these individuals. We used a comprehensive individualized clinical fracture risk assessment approach (vertebral osteodensitometry, femoral osteodensitometry and geometry, and serum bone turnover biomarkers) to compare adult male patients with ALC who have not previously had femoral or vertebral fractures (n = 39), patients with CAA (without liver cirrhosis, n = 78) who have not previously had femoral or vertebral fractures and healthy age- and sex-matched controls (n = 43). Our data suggested that intertrochanteric bone mineral density was significantly lower in ALC and CAA patients than in controls. Also, the trabecular bone score was considerably lower in ALC patients compared with CAA and control individuals. The most significant inter-group differences in femoral geometry were noted on the femoral shaft. Patients with ALC and CAA have a higher 10-year risk of major osteoporotic fractures compared to the controls. Analysis of bone turnover biomarkers showed increased osteoprotegerin and beta-C-terminal telopeptide serum concentrations and decreased insulin growth factor-1 concentrations in patients with ALC compared to CAA and control groups. Our data revealed that bone alterations are present in patients with ALC and CAA even if they did not sustain a nontraumatic bone fracture, but it is also indicative that current bone-assessing clinical methods are not entirely reliable. Thus, future studies should focus on developing a reliable integrative clinical tool that can be used to accurately predict and prevent bone fracture occurrences in patients with ALC and CAA

MDR1 gene polymorphisms are associated with ulcerative colitis in a cohort of Serbian patients with inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a chronic disease of unknown etiology in which genetic factors contribute to development of disease. Single nucleotide polymorphisms (SNPs) in multidrug resistance 1 (MDR1) gene encoding transporter P-glycoprotein have been associated with IBD, but their role in disease susceptibility remains unclear. Therefore, the aim of this study was to investigate the association of three MDR1 polymorphisms, C1236T (rs1128503), G2677T/A (rs2032582) and C3435T (rs1045642), with Serbian IBD patients.A total of 206 IBD patients, 107 Crohn's disease (CD) and 99 ulcerative colitis (UC), and 255 healthy controls were included in the study. All subjects were genotyped using TaqMan SNP genotyping assays. Comparisons between the groups were performed using the Pearson Chi-square test. False discovery rate according to Benjamini-Hochberg procedure was applied to adjust for multiple comparisons.Carriers of T allele of all three MDR1 SNPs were more common in UC patients compared to healthy controls, suggesting predisposing role of T allele of these SNPs in UC pathogenesis. Consistently, TT genotype of C1236T and TTT haplotype were also found more frequently in UC patients. On the other hand, C allele and CC genotype of C1236T and C3435T, as well as G allele and GG genotype of G2677T/A were more frequent in healthy subjects, implying protective role of these variants in UC. Likewise, CGC haplotype and CGC/CGC diplotype were more frequent in controls. Contrary to UC, no statistical difference was observed between CD patients and controls in any of the SNPs analyzed.MDR1 gene variants and haplotypes were associated with UC in Serbian IBD patients, further supporting their potential role in susceptibility to UC

Hepcidin Is a Reliable Marker of Iron Deficiency Anemia in Newly Diagnosed Patients with Inflammatory Bowel Disease

Background and Aim. Differentiating iron deficiency anemia (IDA) from anemia of chronic disease (ACD) in patients with inflammatory bowel disease (IBD) represents a clinical challenge. Hepcidin is a polypeptide synthetized in the liver, and iron levels or inflammation mostly regulate hepcidin production. Our aim was to determine serum hepcidin levels in patients with inflammatory bowel disease (IBD) as well to investigate whether hepcidin levels correlate with disease activity. Material and Methods. A case-control study was preformed among newly diagnosed IBD patients and same number age- and sex-matched healthy controls. All patients underwent a total ileocolonoscopy. Complete blood count was obtained in addition to inflammatory markers (CRP, erythrocyte sedimentation rate-ESR). Serum levels of hepcidin were determined with commercially available enzyme-linked immunosorbent assay (DRG Instruments Marburg, Germany). Serum iron, TIBC, and UIBC were assessed with an electrochemiluminesence immunoassay, and soluble transferrin receptor (sTfR) was assessed using an immunoturbidimetric method. Mayo score and CDAI, respectively, were calculated for each patient. Statistical analyses were performed using the SPSS software version 20.0 for Windows. Results. There was a high statistically significant difference between IBD patients and controls in levels of hepcidin (P0.05). However, we have found a statistically significant negative correlation of sTfR and TIBC with hepcidin (P<0.01). Conclusion. Results of our study suggest that hepcidin is a reliable marker of IDA in patients with IBD, and it could be used in routine clinical practice when determining adequate therapy in these patients

Allele and genotype frequencies of <i>MDR1</i> SNPs in controls, CD and UC groups.

<p>Allele and genotype frequencies of <i>MDR1</i> SNPs in controls, CD and UC groups.</p

Main clinical characteristics of CD and UC patients.

<p>Main clinical characteristics of CD and UC patients.</p