IBD Watch^®

^{Timely Information for Practicing Physicians}

JANUARY 2007

Surveillance, prevention, and management of dysplasia in ulcerative colitis (UC). Rubin and Turner review the risks of cancer and dysplasia in UC, discussing current prevention recommendations and presenting a sample case to illustrate an approach that involves collaboration between a gastroenterologist and pathologist. In a separate study, Rubin and associates investigated the effect of aminosalicylate use on dysplasia and colorectal cancer (CRC) risk in patients with chronic UC. Twenty-six cases (18 dysplasia, 8 CRC) were matched with 96 controls for age, age at diagnosis of UC, duration of UC, history of primary sclerosing cholangitis, and history of smoking. Conditional logistic regression analysis showed that use of ≥1.2 g/day of aminosalicylate was associated with a 72% reduction in the odds of developing dysplasia or CRC. Finally, Hurlstone and co-workers evaluated the outcomes of patients with UC-related adenoma-like masses (Paris class 0–II and class I lesions), who were treated with endoscopic mucosal resection (EMR). A total of 204 lesions were diagnosed in 169 patients with UC. No significant differences with regard to post-resection complications or interval cancer rates were observed between the UC group and 1675 control patients without UC who had undergone EMR for sporadic adenoma-like lesions. These data indicate that flat dysplastic adenoma-like lesions in UC can be managed safely and effectively with EMR. The authors propose that EMR be included in the management paradigm of patients with UC who develop adenoma-like lesions. (Rubin DT, Turner JR. Clin Gastroenterol Hepatol 2006;4:1309–1313; Rubin DT, et al. Clin Gastroenterol Hepatol 2006;4:1346–1350; Hurlstone DP, et al. Gut 2006; Nov [Epub ahead of print].)

Assessment of rectal mucosa by magnifying colonoscopy (MCS). Risk of UC relapse is difficult to predict by routine colonoscopy. However, colorectal mucosal pit patterns can be assessed by high-resolution MCS. Nishio and colleagues performed MCS in 113 patients with UC in remission to prospectively analyze factors predicting relapse. Pit patterns in the rectal mucosa were classified into four MCS grades according to size, shape, and arrangement. Additionally, mucosal levels of interleukin (IL)-8 were measured and biopsied for histologic disease activity. During 12 months of follow-up, Kaplan-Meier estimates showed that the rate of relapse increased with increasing MCS grade: 0% for grade 1; 21% for grade 2; 43% for grade 3; and 60% for grade 4. MCS grade, histologic grade, and mucosal IL-8 activity were identified as predictors of relapse. These results indicate that MCS may be useful in predicting the probability of relapse in patients with remitted UC. (Nishio Y, et al. Gut 2006;55:1768–1773.)

Expression of I2 antibodies predicts response to fecal diversion. Fecal diversion effectively manages some patients with Crohn’s disease (CD) who have advanced perianal or colorectal disease. Spivak and others correlated clinical features and seroreactivity with microbial and autoantigens in 27 consecutive CD patients undergoing fecal diversion to identify predictors of clinical response. Sera were drawn and tested for anti-I2 (antibodies against Pseudomonas fluorescens), anti-OmpC (antibodies to Escherichia coli outer membrane porin C), ASCA (anti-Saccharomyces cerevisiae antibodies), and pANCA (perinuclear antineutrophil cytoplasmic antibodies) in a blinded fashion. After a median follow-up of 41 months, 17 patients (63%) achieved a clinical response to fecal diversion. No preoperative clinical or surgical factor was predictive of response, but 15 (94%) of 16 patients who were I2-positive achieved a clinical response compared with only 2 (18%) of 11 patients who were I2-negative (P = 0.0001). Seroreactivity to OmpC, ASCA, or pANCA was not associated with clinical response following fecal diversion. These results suggest that the expression of I2 antibodies directed against P fluorescens is associated with clinical response in patients with CD treated with fecal diversion. (Spivak J, et al. Inflamm Bowel Dis 2006;12:1122–1130.)

Neoral^® treatment of steroid-refractory UC. Weber and colleagues evaluated the effectiveness of Neoral, an oral microemulsion preparation of cyclosporine, in 19 consecutive patients with UC flares nonresponsive to intravenous methylprednisolone. Patients were given Neoral, 2.3 mg/kg (range, 1.8 to 2.8 mg/kg) every 12 hours for 20 courses, and received prophylaxis against Pneumocystis carinii. Response was obtained following 17 (85%) of 20 attacks after 3.5 days (range, 1 to 7 days) and remission was achieved following 15 (75%) of 20 attacks after 13 days (range, 2 to 30 days). Fourteen (74%) of the 19 patients remained colectomy free after a median follow-up of 8 months (range, 1 to 41 months). Cyclosporine trough levels and levels 2 hours after Neoral administration in a group of 10 responders were 103 ng/mL (range, 32 to 240 ng/mL) and 761 ng/mL (range, 183 to 1390 ng/mL), respectively. Reported side effects included cytomegalovirus infection (n = 2), mild transient renal impairment (n = 2), esophageal candidiasis (n = 1), and hypertension (n = 1). One bedridden patient with neonatal encephalopathy died. These results suggest that the efficacy and toxicity profile of Neoral is similar to that of intravenous cyclosporine. The authors recommend that trough cyclosporine levels not exceed 100 ng/mL and that the cyclosporine level obtained 2 hours after Neoral administration not exceed 700 ng/mL. (Weber A, et al. Inflamm Bowel Dis 2006;12:1131–1135.)

Report on the vitamin D status of IBD patients. Pappa and associates reviewed vitamin D status in patients with IBD because hypovitaminosis D is known to be high in adults with IBD. However, reports of vitamin D status in children with IBD have been infrequent. In vitro evidence suggests that vitamin D may play a role in the regulation of the immune system of the gut, but the clinical therapeutic potential of vitamin D has not been investigated. In addition, there are no guidelines for monitoring vitamin D status or treating hypovitaminosis D in patients with IBD. Maintaining optimal vitamin D stores may be difficult because of the malabsorption and gastrointestinal losses associated with IBD. (Pappa HM, et al. Inflamm Bowel Dis 2006;12:1162–1174.)

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