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P007. Rates of lactose malabsorption amongst Irish Caucasian inflammatory bowel disease patients

S. O'Connor1, C. O'Morain2, P. Pavli3

1The Townsville hospital, Gastroenterology, Townsville, Australia; 2Adelaide & Meath Hospital, Gastroenterology, Dublin, Ireland; 3The Canberra Hospital, Gastroenterology, Canberra, Australia

Background: Lactose malabsorption (LM) is the reduced absorption of lactose or its monosaccharide components, glucose and galactose. Our objective was to examine the prevalence of lactose malabsorption amongst various subgroups of Irish Caucasian inflammatory bowel disease patients with controls matched for age, sex and ethnicity.

Methods: Patients were recruited from inflammatory bowel disease outpatient clinics and as inpatients at the Adelaide and Meath hospital in Dublin, Ireland. All patients had an established diagnosis from previous endoscopy and histological examination of mucosal biopsies as well as various radiological investigations. Disease activity at the time of testing was determined by the Crohn's disease activity index (CDAI) [1] for CD and for UC was determined by Truelove and Witt's criteria [2]. All patient breath tests were done between May 2005 and September 2005. Controls were recruited retrospectively from a list of previously breath tested individuals who were known to have no signs of IBD or any other gastrointestinal pathology. Subjects were breath tested using a Quintron Hydra Microlyser. A baseline reading was taken before giving the subjects a 25 g load of lactose in the form of 450 mL of cow's milk. Readings were then taken every 30 minutes for the next 3hours with a total of 7 readings. A rise from baseline of greater than 20 parts per million (ppm) was considered positive [3–5].

Results: From those patients with ulcerative coltis (UC) 13.6% (95% Confidence interval [CI]; 3.9–34.1%) were shown to be lactose malabsorbers. In those patients with Crohn's disease (CD) 29.7% (95% CI; 17.4–45.9%) were shown to be lactose malabsorbers (LM). In the controls the rate of lactose malabsorption was 8.2% (95% CI; 4.2–15.0%). The rate of lactose malabsorption in the CD group was shown to be significantly higher than the control group (p = 0.002). When the parameter of disease activity was examined it was found that patients with active CD (CDAI >150) were more likely to be lactose malabsorbers. Of the 11 CD patients who had a positive breath test 8 or 72.7% had active disease (p = 0.03).

Conclusions: The prevalence of LM in CD is higher than in controls and UC patients and is likely to reflect the presence of transient hypolactasia due to inflammation in active disease. An increased small bowel motility or small bowel bacterial overgrowth may also be contributing to a positive breath test.

1. Best WR, Becktel JM, Singleton JW (1979), Rederived values of the eight co-efficients of the Crohn's Disease Activity Index (CDAI). Gastrenterology, 843–846.

2. Truelove SC, Witts LJ (1955), Cortisone in ulcerative colitis: final report on a therapeutic trial. Br Med J 1041–1048.

3. Shaw AD, Davies GJ (1999), Lactose Intolerance: Problems in diagnosis and treatment. J Clin Gastroenterol 208–16.

4. Von Tirpitz C, Kohn C, Steinkamp M, Geerling I, Maier V, Moller P, Adler G, Reinshagen M (2002), Lactose intolerance in active Crohn's disease. Clinical value of duodenal lactase analysis. J Clin Gastroenterol 49–53.

5. DiPalma JA, Eves MM (1999), Breath testing in health and disease: Lactose maldigestion, bacterial overgrowth, intestinal transit time and Helicobacter pylori infection. Prac Gastroenterol 72–78.