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Association of lactose sensitivity with inflammatory bowel disease – demonstrated by analysis of genetic polymorphism, breath gases and symptoms
Author(s) -
Eadala P.,
Matthews S. B.,
Waud J. P.,
Green J. T.,
Campbell A. K.
Publication year - 2011
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2011.04799.x
Subject(s) - medicine , inflammatory bowel disease , gastroenterology , lactose , polymorphism (computer science) , inflammatory bowel diseases , disease , genotype , genetics , food science , gene , biology
Aliment Pharmacol Ther 2011; 34: 735–746 Summary Background Sensitivity to lactose has been reported in Crohn’s disease, but its true role in inflammatory bowel disease (IBD) is unclear. The genetic marker CC 13910 , on chromosome2, with measurement of breath hydrogen and methane, and gut and systemic symptoms, are now the most comprehensive tests for evaluating sensitivity to lactose. Aim To investigate, for the first time, the prevalence of lactose sensitivity in IBD, using the most comprehensive tests for diagnosing this condition. Methods Prevalence of CC 13910 genotype was investigated using RT‐PCR in 165 patients (Crohn’s disease = 70, ulcerative colitis = 95), and 30 healthy volunteers. Genotype was correlated with breath hydrogen and methane up to 6 h after 50 g of oral lactose, all symptoms being recorded for up to 48 h. Critically, Crohn’s disease and ulcerative colitis patients were selected with no record of lactose sensitivity, in remission at the time of the test. Results Lactose sensitivity occurred in a much higher proportion of patients, (approximately 70%), with IBD than previously thought. Seventeen per cent had raised methane, without raised breath hydrogen; those with ulcerative colitis exhibiting most symptoms. All CC patients were lactose sensitive. There was no correlation between genetic phenotype and IBD. As substantial numbers of IBD patients were CT or TT, and were lactose sensitive, this polymorphism cannot explain full down‐regulation of the lactase gene. Conclusions Our results have implications for the clinical management of IBD. The high breath methane raised the possibility of a pathogenic role for methanogenic archaebacteria (Archaea) in IBD. This needs to be investigated.