Effect of follow-up endoscopy on the outcomes of patients with inflammatory bowel disease.

BACKGROUND: Little is known about the role of follow-up endoscopy in patients with inflammatory bowel disease (IBD). AIM: The present study aimed to evaluate whether repeated endoscopies would be beneficial in improving outcomes of patients with IBD. METHODS: Patients who had been initially confirmed to have IBD at two tertiary hospitals in Korea were regularly followed and included in this study. The clinical impact as assessed by the presence or absence of a change in management after endoscopy and cumulative hospitalization rate was compared between two groups classified according to the presence or absence of indications. RESULTS: A total of 188 patients with IBD were enrolled [69 patients with Crohn's disease (CD) and 119 with ulcerative colitis (UC)]. Of these patients, 130 underwent follow-up endoscopy (48 with CD and 82 with UC). The rate of management change was significantly higher in the group with indications for follow-up endoscopy (p = 0.001 in CD and <0.001 in UC). The presence of any indications for follow-up endoscopy was found to be a significant predictor of hospitalization risk in patients with UC (p = 0.015), but not in those with CD. However, there was no significant difference in cumulative hospitalization hazard with respect to treatment change in patients without any endoscopic indications (p = 0.561 in CD and 0.423 in UC). CONCLUSIONS: Follow-up endoscopy might not have a significant impact on the overall clinical course and outcomes in patients with IBD. However, the presence of endoscopic indications predicts a poor clinical outcome in UC.

Concentration of arginine and optimal time of hypertonic saline in restoration of T-cell dysfunction.

BACKGROUND: Hypertonic saline (HS) restores prostaglandin E(2) (PGE(2))-induced T-cell suppression in the presence of 1100 microM arginine. However, under arginine-free culture conditions, HS dose not restore T-cell proliferation. Therefore, we wanted to determine if HS can restore PGE(2)-induced T-cell suppression in the presence of 80 microM of arginine, the physiologically relevant arginine concentration. We also wanted to determine the concentration of arginine that induces HS restoration of PGE(2)-suppressed T-cell proliferation and whether HS restoration of T-cell dysfunction is dependent on the injection time of HS. MATERIALS AND METHODS: Jurkat cells were cultured in media containing 0, 40, 80, 400, 800, or 1100 microM arginine. In both the PGE(2)-stimulated and HS-treated group, we measured cell proliferation using MTT assay and arginase activity. We also measured cell proliferation relative to HS injection time. RESULTS: In 80 microM arginine, HS did not restore Jurkat cell proliferation that had been suppressed by PGE(2). Increased concentrations of arginine in the media increased MTT cell proliferation. In 800 microM arginine media, HS restored PGE(2)-suppressed Jurkat cell proliferation to normal. HS restored PGE(2)-suppressed Jurkat cell proliferation when it was added at 2 h, similar to at same time and 1 h after PGE(2) stimulation. CONCLUSIONS: In order to restore PGE(2)-suppressed Jurkat cell proliferation, HS requires at least 800 microM arginine. HS restored PGE(2)-suppressed Jurkat cell proliferation even though HS was added at 2 h after PGE(2) stimulation.