Microsoft word - ibd watch march 2006 final.doc

IBD Watch™ Editorial Board: Stephen Hanauer, MD, (Chair);
Sunanda Kane, MD; Gary Lichtenstein; MD; Daniel Present, MD; Bruce Sands, MD, MS Timely Information for Practicing Physicians
www.ibdwatch.com
MARCH 2006

Risk factors for ileal pouch disease. Shen and coworkers reviewed the demographic and clinical data of 240 consecutive patients
who had undergone ileal pouch–anal anastomosis (IPAA) after restorative proctocolectomy for ulcerative colitis (UC). Patients were
classified as having pouchitis (n = 61), irritable pouch syndrome (n = 50), healthy pouches (n = 49), cuffitis (n = 41), or Crohn's
disease (CD) of the pouch (n = 39). Logistic regression analysis identified the following risk factors: (1) for pouchitis: IPAA for
dysplasia, no history of smoking, no history of anti-anxiety agents, and prior use of nonsteroidal anti-inflammatory drugs (NSAIDs);
(2) for CD of the pouch: lengthy duration since the IPAA and current history of smoking; (3) for cuffitis: arthralgias and younger age;
and (4) for irritable pouch syndrome: current use of anti-depressants or anti-anxiety agents. The risk factors for these inflammatory
and noninflammatory pouch conditions differ, suggesting different etiologies. The identification of these risk factors may help to
improve the treatment of ileal pouch complications following IPAA. (Shen B, et al. Clin Gastroenterol Hepatol. 2006;4:81–89.)
Editors’ Note: Of importance is the fact that only 49 (20%) of 240 patients had “healthy pouches” from this very experienced center.

Serum immune response in children as a predictor of disease progression. Childhood-onset CD has an aggressive
phenotype. Dubinsky and colleagues prospectively examined the association of immune responses directed against microbial
antigens to disease behavior in a population of 196 pediatric patients with CD. Sera were tested for anti-I2 antibodies, outer
membrane protein C (anti-OmpC) antibodies, anti-CBir1 flagellin antibodies, and anti-Saccharomyces-cerevisiae antibodies
(ASCA). These patients were followed for a median of 18 months. The risk for progression of CD to internal penetrating and/or
stricturing disease was highest among pediatric CD patients who were positive for all four immune responses (P = 0.03). In addition,
both anti-OmpC and anti-I2 immune responses were associated with internal penetrating and/or stricturing disease (P <0.0006 and
P <0.003, respectively). These results demonstrated that immune responses to microbial antigens were associated with the
aggressive disease phenotypes seen in children with CD. Further studies are warranted to confirm these findings. (Dubinsky MC, et
al. Am J Gastroenterol. 2006;101:360–367.)
Infliximab use is not associated with an increased risk of neoplasia. Biancone and others performed a multicenter, matched-
pair study in which the incidence of neoplasia among 404 patients with CD treated with infliximab (cases) was compared with that of
404 patients with CD who had never received infliximab (controls). The cases and controls were matched for age, gender, site of
CD, age at diagnosis, immunosuppressant use, and length of follow-up. From April 1999 to October 2004, nine patients in the
infliximab group and seven patients in the control group developed neoplasia. The median age at diagnosis of neoplasia was similar
between the two groups (50 vs 45 years; P = 0.5). In addition, no difference in survival was observed between the two groups (P =
0.9). The neoplasias that developed in the infliximab-treated patients were breast cancer (n = 3), anal carcinoma (n = 2),
cholangiocarcinoma (n = 1), laryngeal cancer (n = 1), leukemia (n = 1), and skin cancer (n = 1). The neoplasias that developed in
the control group were intestinal adenocarcinoma (n = 3), basalioma (n = 1), breast cancer (n = 1), non-Hodgkin's lymphoma (n =
1), and spinalioma (n = 1). The results of this matched-pair study showed that the frequency of a new diagnosis of neoplasia in
patients with CD treated with infliximab was comparable to that of patients with CD who had never received infliximab. (Biancone L,
et al. Gut. 2006;55:228–233.)

The effect of iron therapy for anemia on quality of life (QOL). Wells and coworkers studied a cohort of 50 patients with
inflammatory bowel disease (IBD) to examine the association of changes in blood hemoglobin (Hb) levels with changes in QOL and
cognitive function independent of changes in disease activity. Among the cohort of 50 patients with IBD were 21 patients with low
Hb levels treated with iron replacement therapy. The patients treated with iron had lower Hb levels and higher disease activity
scores at baseline than did untreated patients. A hierarchical regression model analysis demonstrated that changes in disease
activity and changes in Hb level accounted for 13% and 18% of the variance in change of the SF-36 QOL instrument, respectively,
as well as 12% and 17% of the variance in change of an IBD questionnaire. Increases in Hb concentration were found to improve
QOL scores, and there was no evidence that iron therapy caused a worsening of disease activity. Thus, the findings of this small
pilot study suggest that treatment of IBD-associated anemia with iron may improve QOL. (Wells CW, et al. Inflamm Bowel Dis.
2006;12:123–130.)
Budesonide treatment. Chopra and others reviewed the medical records of 225 patients with IBD who were prescribed oral
budesonide therapy between November 2001 and October 2002. Patients received budesonide for ileocolonic CD (group 1; n =
108), CD elsewhere (group 2; n = 62), and other conditions (group 3; n = 55). A favorable outcome was achieved in 61% of patients
in group 1 while only 24% of patients in group 2 demonstrated a response. In group 3, only patients with microscopic colitis (n = 28)
and pouchitis (n = 13) and demonstrated response rates >50%. This study indicates that budesonide is effective treatment for
ileocolic CD and microscopic colitis. Patients with pouchitis may also benefit from budesonide therapy; further studies are needed to
confirm these results. (Chopra A, et al. Inflamm Bowel Dis. 2006;12:29–32.)
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