Korean J Med.
1999 May;56(5):569-575.
Lactose intolerance in lactase - deficient subjects and patients with inflammatory bowel disease after drinking common doses of milk
- Affiliations
-
- 1Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
- 2Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Abstract
OBJECTIVE
To define whether lactase-deficient subjects are intolerable to even a pack of
milk(200ml) and whether milk intolerance in the patients with IBD is only due to lactose
malabsorption, we performed this study.
METHODS
We evaluated 32 healthy adults and 12 patients with active stage of inflammatory bowel
disease(IBD) who had not received antibiotics therapy within the previous 3 weeks. Thirty-two
healthy adults underwent H2-breath test with 200, 400, 600 and 800ml of milk at 1st, 2nd, 3rd
and 4th day of study, respectively. We measured their end-expiratory hydrogen concentrations
and asked them to record the gastrointestinal symptoms. Twelve patients with IBD were tested
only with 200ml of milk. Lactose malabsorption was defined as the increase of 20ppm over basal
H2 concentration and lactose intolerance as having two or more of the following symptoms;
abdominal pain, diarrhea, borborygmus and flatus.
RESULTS
The prevalence of lactase deficiency was 72%(23 of 32 subjects) at 800ml of
milk(lactose 40g). Among the lactase-deficient subjects, lactose intolerance at 200ml of
milk(lactose 10g) was noticed only in 13%(3 of 23 subjects). In the patients with active stage
of IBD, the frequency of milk intolerance at 200ml of milk was 50%(6 of 12 subjects), which was
higher than in the healthy adults(9%). But the prevalence of lactose malabsorber in the patients
with IBD at 200ml of milk(17%) was not higher than in the healthy adults(16%).
CONCLUSION
Most of lactase-deficient subjects(87%) can ingest one pack of milk without lactose
intolerance. The increased prevalence of lactose intolerance in the patients with IBD at 200ml
of milk is not originated from lactose malabsorption, but probably from incomplete colonic
compensation salvage.