IBD Watch^®

^{Timely Information for Practicing Physicians}

FEBRUARY 2007

INFLAMMATORY BOWEL DISEASE (IBD)

Gut barrier function. Epithelial barrier function is impaired in Crohn’s disease (CD) and ulcerative colitis (UC). Zeissig and others studied sigmoid colon biopsy samples from patients with mild to moderately active or inactive CD to define the underlying cellular mechanisms. Impedance and conductance analyses showed that patients with active CD had impaired intestinal barrier function characterized by reduced epithelial resistance. Electron microscopy revealed reduced and discontinuous tight junction strands. Occludin and the sealing tight junction proteins claudin 5 and claudin 8 were downregulated while the pore-forming protein claudin 2 was upregulated. Epithelial apoptosis was also significantly increased in patients with active CD. This indicates that tight junction structure is altered and gut barrier dysfunction is pronounced even in mild to moderately active CD. Separately, McGilligan and associates reviewed the relationship between gut permeability and inflammation and suggested hypotheses for the apparent protective mechanism induced by nicotine in cases of UC. (Zeissig S, et al. Gut 2007;56:61–72; McGilligan VE, et al. Inflamm Bowel Dis 2007;13:108–115.)

Herpes zoster incidence. Gupta and associates performed a retrospective cohort study, using data from a General Practice Research Database covering the years 1988–1997, to investigate the risk of herpes zoster in patients with IBD. In this analysis, 7,823 patients with CD and 11,930 patients with UC were matched by age, gender, and primary care practice with 79,563 controls without CD or UC. The incidence of herpes zoster was higher in the patients with CD and UC than in the controls (incidence rate ratios of 1.61 [95% confidence interval (CI), 1.35–1.92] and 1.21 [95% CI, 1.05–1.40], respectively). In addition, receipt of a prescription for a corticosteroid or azathioprine/6-mercaptopurine was associated with the development of herpes zoster among the patients who had CD or UC. These findings demonstrate that patients with IBD, especially those treated with immunosuppressive agents, are at a higher risk for herpes zoster infection than is the general population. (Gupta G, et al. Clin Gastroenterol Hepatol 2006;4:1483–1490.)

IBD is not a risk factor for cardiovascular (CV) disease mortality. Several systemic inflammatory diseases are associated with an increased risk of CV disease. Dorn and Sandler conducted a meta-analysis of studies reporting CV mortality in patients with IBD, published between 1995 and 2006, to investigate whether IBD increases CV mortality. The meta-analysis consisted of 11 studies involving 4,532 patients with CD and 9,533 patients with UC. The results demonstrated that standardized mortality ratios due to CV for CD and UC were not increased (1.0 [95% CI, 0.8–1.1] and 0.9 [95% CI, 0.8–1.0], respectively). The authors suggest that the finding that IBD is not associated with increased CV mortality is indirect evidence against an association between IBD and CV disease. (Dorn SD, Sandler RS. Am J Gastroenterol 2006, Dec 11; Epub ahead of print.)

ULCERATIVE COLITIS

Racial and geographic variations in colectomy rates. Nguyen and colleagues analyzed discharge records from the Nationwide Inpatient Sample database to characterize racial and geographic differences in colectomy rates among patients with UC hospitalized in the United States. A total of 23,389 discharges with UC from 1998 to 2003 were included in this analysis. After adjustment for age, gender, health insurance, comorbidity, and hospital characteristics, the colectomy rate ratios for African Americans and Hispanics compared with whites were 0.46 (95% CI, 0.35–0.60) and 0.74 (95% CI, 0.59–0.93), respectively. Geographic results demonstrated that colectomy rates were threefold higher in hospitals in the West and Midwest than in the Northeast. According to the authors, further studies are needed to elucidate the reasons for these significant variations. (Nguyen GC, et al. Clin Gastroenterol Hepatol 2006;4:1507–1513.)

Curcumin maintenance therapy. Curcumin is a biologically active phytochemical agent present in turmeric that has pharmacologic actions that might benefit patients with UC. Hanai and co-workers conducted a multicenter, double-blind study in which 89 patients with quiescent UC were randomized to receive oral curcumin, 1 g twice daily, or placebo, each in combination with sulfasalazine (SZ) or mesalamine, for 6 months. Two patients relapsed in the curcumin group, compared with eight patients in the placebo group (P = 0.04). Curcumin was associated with improvements in clinical activity index and endoscopic index scores. During 6 months of follow-up, eight more curcumin-treated patients relapsed, compared with six patients in the placebo group. These findings suggest that curcumin may have potential as a maintenance agent in patients with quiescent UC. (Editor’s note: Additional confirmatory and dose-ranging trials are needed before we can adopt this agent into our therapeutic armamentarium—SH.) (Hanai H, et al. Clin Gastroenterol Hepatol 2006;4:1502–1506.)

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