Screening endoscopy finds high prevalence of Helicobacter pylori and intestinal metaplasia in Korean American with limited access to health care.

BACKGROUND: Gastric cancer (GC) is the leading cause of cancer death among Korean Americans. Prevention and early detection is improved by screening. METHODS: Between September 2013 and March 2015, ethnic Koreans age 40 or older without history or symptoms of GC and without upper endoscopy (UE) during previous 3 years were enrolled. Participants were offered screening with GC risk assessment followed by UE with biopsies. RESULTS: Risk assessment was provided to 146 participants (age 55.6 ± 8.3 years; 52.1% female; 92.5% uninsured), of whom 99 (67.8%) returned for UE. Undergoing UE was independently associated with family history of GC (OR 12.33, 95% CI:1.52-100.17), being a former smoker (6.68,1.42-31.32), and Hp-negative status (0.25,0.11-0.57). Among UE recipients, half (49.5%) had intestinal metaplasia (IM) only (n = 24), Hp only (n = 12), or both (n = 13). No case of GC was found. Adjusted for age, IM was independently associated with male sex (2.89,1.12-7.42), current Hp (2.90,0.99-8.51), unmarried status (single or divorced) (4.23,1.23-14.56). CONCLUSIONS: High prevalence of risk factors associated with gastric carcinogenesis including Hp infection and IM exists in Korean Americans who underwent upper endoscopic screening. Acceptance of GC screening is informed by personal risk factors. These findings support the need to improve access to screening UE among KAs.

Oral tolerance therapy in inflammatory bowel disease.

Oral tolerance is a long-recognized method of inducing immune tolerance or systemic hyporesponsiveness induced by feeding protein. Oral tolerance has been used to prevent and/or treat a variety of T-cell-mediated autoimmune disorders. Feeding colonic extracts prevented colitis in animal model of inflammatory bowel disease (IBD), but the clinical efficacy of oral tolerance in human IBD was unknown. In this issue, the study by Margalit and colleagues suggested that oral administration of autologous colonic extracts to moderately severe Crohn's disease patients might reduce disease activity; however, the study did not employ conventional clinical endpoints. These data provide an important first step to developing "Ag-specific" treatment strategies for IBD in the future. Larger scale studies using variable dosages, modes, and durations of Ag delivery will be required to optimize oral tolerance therapy in IBD.

Anti-interferon-inducible chemokine, CXCL10, reduces colitis by impairing T helper-1 induction and recruitment in mice.

BACKGROUND: Colitis in interleukin (IL)-10 mice is a CD4 T helper 1 (TH1)-mediated disease characterized by intermittent, transmural inflammation reminiscent of human Crohn's disease. In this study, we investigated the hypothesis that production of the CXC chemokine CXCL10 (interferon [IFN]gamma-inducible protein 10) enhances induction of inflammatory responses in draining lymph nodes (LNs) and promotes colonic TH1 cell recruitment. METHODS: Colitis was induced in B6 IL-10 mice. Mice were given anti-CXCL10 mAb in 2-week intervals before and after peak colitis. Colitis severity was graded and cytokine/chemokine levels were analyzed by real-time polymerase chain reaction. Cell yields were quantitated and effector cell recruitment was assessed by recovery of transferred D011.10 TH1 cells shortly (72 h) after transfer. RESULTS: Treatment with anti-CXCL10 during colitis development decreased clinical and histologic disease severity as well as cytokine/chemokine mRNA and accumulation of mononuclear cells in LNs and colon. Treatment of mice with severe colitis reduced colitis scores and cell yields to lesser degrees. Anti-CXCL10 specifically decreased recruitment of transferred TH1 cells into mesenteric LNs (MLNs) and colon of IL-10 mice by 75% (P<0.05). CONCLUSION: These results suggest that CXCL10 plays a dual role in colitis development by enhancing TH1 cell generation in inductive sites and promoting effector cell recruitment to inflamed tissue. Blockade of CXCL10 may be a useful adjunct to remission-inducing therapies in inflammatory bowel disease (IBD) by impairing disease recurrence through selective inhibition of effector cell generation and trafficking in vivo.

Apoptosis and its correlation with proliferative activity in rectal cancer.

BACKGROUND AND OBJECTIVES: Alterations in the normal control of apoptosis and cell proliferation are important factors in multistep colorectal carcinogenesis. The aim of this study was to determine the frequency of apoptosis and cell proliferation in rectal cancers and to examine their relationship to clinicopathological variables and expression of bcl-2 and p53. METHODS: Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining and immunohistochemical staining for Ki-67, bcl-2, and p53 were performed on paraffin-embedded tissue samples of 57 rectal cancers. RESULTS: There was a positive linear correlation between apoptotic index (AI) and proliferative index (PI) (gamma = 0.276, P = 0.038). Both apoptosis and cell proliferation were more frequently found in rectal cancers with lymph node metastasis (P = 0.045 and 0.010, respectively). However, the ratio of AI and PI was not different by nodal status. There was no association between Dukes stage and AI or PI. The frequency of apoptosis was inversely related to the expression of bcl-2, but was not related to the p53 status of rectal cancer. There were no association between cell proliferation and the expression of bcl-2 or p53. CONCLUSIONS: Our results suggest that the susceptibility to apoptosis in rectal cancer is clearly related to the proliferative activity and high turnover rate of tumor cells may contribute to lymph node metastasis.