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Background and Aim: There has been increased interest in sleep disorders in patients with inflammatory bowel disease (IBD). Studies in North America and Europe reported that the prevalence of restless legs syndrome (RLS) is much higher in patients with Crohn's disease (CD) than in the general population. The aim of this study was to reveal the prevalence and clinical features of RLS in Japanese patients with IBD and investigate the influence of RLS on sleep quality and quality of life (QOL)., Methods: The study included 80 outpatients with IBD who visited Nagasaki University Hospital between December 2012 and July 2014. All patients completed the international RLS study group rating scale, a validated measure of the presence of RLS. Sleep quality was assessed using the Japanese version of the Pittsburgh Sleep Quality Index (PSQI), and health-related QOL was assessed using the Japanese version of the 36-item short form healthy profile (SF-36) version 2., Results: The prevalence of RLS in patients with IBD was 20%, including rates of 21.7% in patients with ulcerative colitis (UC) and 17.6% in patients with CD. Among patients with CD, the proportion of women and serum level of CRP were higher in the RLS group than in the non-RLS group. Among those with UC, there were no differences in clinical characteristics between the RLS and non-RLS groups. Patients in the RLS group slept significantly less well than those in the non-RLS group (PSQI > 5; 62.5 vs. 34.4%, P < 0.05). No significant relationships were observed between QOL indices and the presence of RLS (SF-36 physical score, 46.8 vs. 50.1; mental score, 43.8 vs. 45.7; role/social score, 48.1 vs. 49.2)., Conclusions: RLS occurs frequently in Japanese patients with UC as well as CD. RLS affects sleep quality but not QOL, and it should be considered one of the causes of sleep disturbance in patients with IBD.

Background: Adipocytokines are associated with energy homeostasis and mediate various immune responses and inflammatory processes. Vaspin is a novel adipocytokine that is thought to exhibit anti-inflammatory effects., Aim: We aimed to evaluate serum vaspin levels in inflammatory bowel disease (IBD) and determine its possible associations with the course and to clarify its intestinal localization., Methods: Serum samples were obtained from patients with Crohn's disease (CD; n = 30) and ulcerative colitis (UC; n = 33) and from healthy volunteers (controls; n = 26). Enzyme-linked immunosorbent assays were performed for all patients. Vaspin immunohistochemical staining was performed for intestines affected with IBD., Results: Serum vaspin concentrations were significantly higher in patients with UC than in patients with CD and controls (422.9 ± 361.9 vs. 163.4 ± 116.2 vs. 147.5 ± 89.4 pg/mL, respectively; P < 0.01). There was no difference in the serum vaspin concentrations between the patients with CD and controls. There was also no difference in the serum vaspin concentrations between the patients with active IBD and those with inactive IBD. However, the serum vaspin concentrations of most patients with UC increased after remission induction. Vaspin was expressed in the adipocytes of the mesenteric adipose tissues but not in the epithelial or inflammatory cells of large intestines of the patients with IBD., Conclusions: Serum vaspin concentrations are elevated in patients with UC and increase further after remission induction, suggesting that vaspin may aid the auxiliary diagnosis of UC and may be useful for assessing disease activity in patients.

Background and Aims: Chemokine CXC ligand 13 (CXCL13) and CXC receptor type 5 (CXCR5) are constitutively expressed in tertiary lymphoid follicles where the CXCL13/CXCR5 system regulates B lymphocytes homing. In this study, we sought to examine CXCL13 expression in the H. pylori-infected and -uninfected gastric mucosa and to elucidate the implication in the pathogenesis of HAG in humans., Methods: Using endoscopic biopsies taken from the gastric antrum of 29 subjects infected with Helicobacter pylori and 22 uninfected subjects, mucosal CXCL13 mRNA and protein levels were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively., Results: The CXCL13 expression levels were significantly more elevated in H. pylori-positive patients than uninfected ones. The CXCL13 expression levels correlated with the degree of chronic gastritis and bacterial colonization. Immunohistochemistry and in vitro infection assay showed that CXCL13 was not produced by the gastric epithelium, but the α-smooth muscle antigen expressing mesenchymal cells were the possible source of CXCL13 within H. pylori-infected gastric mucosa. CXCR5 immunostaining was seen in the CD20-positive lymphoid aggregates., Conclusions: The enhanced induction of CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis.

Purpose: In the field of colorectal cancer and adenoma, Kudo's classification of pit pattern with magnifying chromocolonoscopy using crystal violet (CV) staining is now accepted. Magnifying endoscopy using narrow band imaging has been used for the diagnosis of gastric carcinoma; the characteristic findings of microvascular patterns have been demonstrated. However, there was limited information on magnified endoscopic findings with CV staining for gastric neoplasms in terms of their pit patterns., Methods: Magnifying chromoendoscopy with CV was performed in 175 patients with early gastric cancer and 18 with gastric adenoma, prior to treatment. Surface patterns of gastric tumors were classified into five types: (1) long tubular pit pattern, (2) irregular size pit pattern, (3) small round pit pattern, (4) destroyed pit pattern, and (5) non-structural pattern., Results: Long tubular pit pattern was most common in gastric adenoma. Well differentiated adenocarcinoma and papillary adenocarcinoma tended to show different size of pit pattern or destroyed pit pattern. Small round pit pattern was most commonly seen in moderately differentiated adenocarcinoma. Non-structural pattern was most frequently observed in poorly differentiated adenocarcinoma and signet ring cell carcinoma (P < 0.0001)., Conclusion: For gastric neoplasms, magnifying endoscopy may help predict histopathological type.

Purpose: To determine whether simvastatin is able to inhibit inflammation in trinitrobenzene sulfonic acid (TNBS)-induced or oxazalone (OXA)-induced colitis., Results: In the prophylactic protocol, simvastatin dose-dependently suppressed the decrease in body weight and inflammatory grade of TNBS-treated mice. In contrast, in the therapeutic protocol, no significant difference in body weight reduction was observed between simvastatin-treated and control mice. IFN-gamma release from LP cells was significantly suppressed in mice receiving high-dose simvastatin in the prophylactic protocol. In contrast to TNBS colitis, even high-dose prophylactic simvastatin had no suppressive effects on either weight reduction or the inflammatory grade in OXA colitis., Conclusion: Our results indicate that simvastatin negatively regulates inflammation in TNBS-induced colitis, but not in OXA-induced colitis. In TNBS-induced colitis, simvastatin suppressed the Th1-polarized immune response. Our findings suggest that simvastatin has potential effects as a therapeutic agent in human inflammatory bowel disease, particularly Crohn's disease.

To determine whether human CD4(+)CD25(+) cells express glucocorticoid-induced tumor necrosis factor receptor (GITR) and transforming growth factor-beta (TGF-beta) and the difference in CD4(+)CD25(+) cells between patients with inflammatory bowel diseases and healthy subjects, peripheral blood lymphocytes were obtained from patients with ulcerative colitis (UC; n = 50), Crohn's disease (CD; n = 49), and healthy volunteers (control; n = 50) and flow cytometric analysis was performed. In control subjects, the expression of GITR on CD4(+)CD25(+) cells (41.8 +/- 10.5%) was significantly higher than on CD4(+)CD25(-) cells (11.1 +/- 7.4%). Similarly, TGF-beta expression on CD4(+)CD25(+) cells (5.3 +/- 4.6%) was higher than on CD4(+)CD25(-) cells (1.2 +/- 1.4%). There were no significant differences among UC, CD, and control in CD4(+)CD25(+)/CD4(+) ratio. However, there was a significant difference in the CD4(+)CD25(+) TGF-beta+/CD4(+)CD25(+) ratio between active UC and inactive UC (2.7 +/- 2.6 and 7.2 +/- 3.9%, respectively). The results suggest that TGF-beta is involved in the induction or sustained remission of UC.

Visceral hypersensitivity, intestinal dysmotility, and stress play major roles in irritable bowel syndrome. However, the significance of visceral hypersensitivity in stress-induced changes of colorectal motor function is not conclusive. A rat model of chronic visceral hypersensitivity was induced by mechanical colorectal irritation during postnatal development. Defecation and colonic transit time were not different between the visceral hypersensitivity and the control groups at baseline. Stress and a 5-hydroxytryptamine (5-HT) agonist both resulted in a significant increase in defecation in the visceral hypersensitivity group compared with the controls. Prior administration of granisetron, a 5-HT3 receptor antagonist, inhibited stress-induced changes in defecation in the visceral hypersensitivity group as well as the controls. Stress-induced acceleration of colonic transit was not significantly different between the two groups. Our results indicate that chronic visceral hypersensitivity can modulate the effect of stress on defecation via a serotonergic pathway and suggest that visceral hypersensitivity may be related to the susceptibility of the defecative response to stressful events in patients with irritable bowel syndrome.