Background/AimsStudies concerning red cell distribution width (RDW) for use in the assessment of inflammatory bowel disease (IBD) activity are limited. We investigated whether RDW is a marker of active disease in patients with IBD.MethodsIn total, 61 patients with ulcerative colitis (UC) and 56 patients with Crohn's disease (CD) were enrolled in the study group, and 44 age- and-sex-matched healthy volunteers were included as the control group. A CD activity index >150 in patients with CD indicated active disease. Patients with moderate and severe disease based on the Truelove-Witts criteria were considered to have active UC. In addition to RDW, serum C-reactive protein levels, erythrocyte sedimentation rates, and platelet counts were measured.ResultsTwenty-nine (51.7%) patients with CD and 35 (57.4%) patients with UC had active disease. The RDW was significantly higher in patients with CD and UC than in controls (p<0.001 and p<0.001, respectively). A subgroup analysis indicated that for a RDW cut-off of 14%, the sensitivity for detecting active CD was 79%, and the specicity was 93% (area under curve [AUC], 0.935; p<0.001). RDW was the most sensitive and specific marker for active CD. However, it was not valid for UC, as the ESR at a cutoff of 15.5 mm/hr showed a sensitivity of 83% and a specicity of 76% (AUC, 0.817; p<0.001), whereas the RDW at a cutoff of 14% showed 17% sensitivity and 84% specicity for detecting active UC.ConclusionsRDW was elevated in IBD in comparison with healthy controls and increased markedly in active disease. RDW may be a sensitive and specific marker for determining active CD, whereas ESR is an important marker of active UC.

The response rate of IBD patients receiving HBV vaccinations were significantly lower compared to controls. The response rate of those receiving immunosuppressive therapy and with active disease was much too low. Vaccination should be given during remission and at immunosuppression-free times.

SummarySirtuins are members of the silent information regulator 2 (Sir2) family, a group of Class III histone/protein deacetylases. There are 7 different sirtuins in mammals (SIRT1-7), of which SIRT1 is the best known and most studied. SIRT1 is responsible for the regulation of protein activation by means of deacetylating a variety of proteins that play important roles in the pathophysiology of metabolic diseases. Recently, it has been shown that SIRT1 plays key roles in the regulation of lipid and glucose homeostasis, control of insulin secretion and sensitivity, antiinflammatory effects, control of oxidative stress and the improvements in endothelial function that result due to increased mitochondrial biogenesis and β-oxidation capacity.Nonalcoholic fatty liver disease (NAFLD) is currently the most common liver disease, and it has been accepted as the hepatic component of metabolic syndrome. Recent studies have shown that SIRT expression in the liver is significantly decreased in an NAFLD model of rats fed a high-fat diet, and moderate SIRT1 overexpression protects mice from developing NAFLD. In addition to resveratrol, a natural SIRT1 activator, small-molecule pharmacologic SIRT1 activators have positive effects on metabolic diseases. These effects are particularly promising in the case of diabetes mellitus, for which phase studies are currently being performed. With this information, we hypothesized that the pharmacologic activation of SIRT1, which has been implicated in the pathogenesis of NAFLD, will be a potential therapeutic target for treating NAFLD. In this paper, we review the metabolic effects of SIRT1 and its association with the pathophysiology of NAFLD.

Sirtuins (SIRTs) are members of the silent information regulator-2 family and act as nicotinamide adenine dinucleotide (NAD+)-dependent histone/protein deacetylases. The de-acetylation of proteins and histones results in an up- or down-regulation of gene transcription and protein function. In recent years, the regulatory action of the deacetylation activity of SIRT1 has been shown to have a positive impact on the pathophysiological mechanisms of nonalcoholic fatty liver disease (NAFLD). Among the effects of SIRT1 are: its healing activity on insulin sensitivity, thereby ameliorating glycemic regulation; its mimetic activity on calorie restriction; its antihyperlipidemic activity on lipid homeostasis via the liver, adipose tissues and skeletal muscles; its anti-inflammatory activities; its protective effects against cardiovascular events and endothelial dysfunction; its positive influence on autophagy, apoptosis and cancer; and finally, its anti-aging activity. The current approach for the treatment of NAFLD involves the treatment of etiological factors and recommendation of life-style changes including more physical activity and a low-calorie diet. However, there is no specific medical treatments for NAFLD. The therapeutic potential of SIRT1 activity in the treatment of NAFLD discovered in humans has been presented in this article. In this review, the potential effects of SIRT1 activation on NAFLD-related pathophysiological mechanisms and on the treatment of NAFLD are discussed.

In this study, we aimed to evaluate the endothelial functions in patients with nonalcoholic fatty liver disease (NAFLD). In this observational case-control study, a total of 51 patients with NAFLD in study group and a total of 21 with age- and sex-equivalent individuals in control group were enrolled. In both patients and control groups, levels of asymmetric dimethylarginine (ADMA), systemic endothelial function (brachial artery flow-mediated dilation) (FMD) and carotid artery intima-media thickness (C-IMT) were measured. FMD and C-IMT were evaluated by vascular ultrasound. Plasma levels of ADMA were measured by ELISA. C-IMT was significantly higher in patients with NAFLD group than control group (0.67 ± 0.09 vs. 0.52 ± 0.11 mm, P < 0.001). The average C-IMT measurements were found in groups of control, simple steatosis, and NAFLD with (borderline and definite) NASH as 0.52 ± 0.11, 0.63 ± 0.07, and 0.68 ± 0.1 mm, respectively. The differences between groups were significant (P < 0.001). Measurement of brachial artery FMD was significantly lower in patients with NAFLD group compared to control group (7.3 ± 4.8 vs. 12.5 ± 7.1 %, P < 0.001). FMD measurements in groups of control, the simple steatosis, and NAFLD with NASH as 12.5 ± 7.1, 9.64 ± 6.63, and 7.03 ± 4.57 %, respectively, and the differences were statistically significant (P < 0.001). The increase in C-IMT and decrease in FMD was independent from metabolic syndrome and it was also more evident in patients with simple steatosis and NASH compared to control group. There was no significant difference between the control and NAFLD groups in terms of plasma ADMA levels (0.61 ± 0.11 vs. 0.69 ± 0.37 μmol/L, P = 0.209). Our data suggested that NAFLD is associated with endothelial dysfunction and increased earlier in patients with atherosclerosis compared to control subjects.