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As an axiom, collagenous colitis is characterised by diarrhoea, lymphocytic inflammation, and a thickened subepithelial collagen layer in the colorectal mucosa.1 Various case presentations in the literature have reported that frequent watery diarrhoea introduces the clinical picture of collagenous colitis and intermittent or continuous diarrhoea can remain.2 On the other hand, numerous cases never suffer from episodes of watery diarrhoea but suffer from chronic constipation. Can we call into question the “incontestable” definition? Bonderup et al investigated the clinical and histological effect of oral budesonide in the treatment of collagenous colitis in 20 patients and concluded that budesonide is a highly effective and well tolerated treatment. The histological inflammation grade in the sigmoid mucosa and the thickness of the collagen layer were significantly reduced. A correlation between the grade of inflammation as well as collagen layer thickness and stool weight was found (Gut 2003;52:248–51).
In our recent study, we investigated 32 patients with histologically identified collagenous colitis. In contrast with the literature, 18 had chronic constipation and only 14 had the well known diarrhoea. We also treated all of them with budesonide (Budenofalk; Dr Falk Pharma) and all patients receiving budesonide had a clinical response: stool frequency and weight. These conflicting results suggest a role for additional factors other than the thickened collagen table. For example, allergy (food allergy), a great mimic, can cause both diarrhoea and constipation. Diseases or symptoms (that is, food protein induced enterocolitis, diarrhoea, or constipation) involving the gastrointestinal system have been attributed to hypersensitivity reactions to food.3–6 Many of these symptoms reflect the concept of “delayed” reactions. This notion presumes that certain clinical symptoms reflect allergies to food which develop over a period of hours or days (or longer) and are caused by immunological mechanisms other than immediate type hypersensitivity. For example, cow’s milk protein allergy should be considered as a cause of chronic refractory constipation in children although the underlying mechanisms still require further investigation. Albeit the aetiology of collagenous colitis is still unknown, the subepithelial band-like collagenous deposit may be produced by fibroblasts after immune stimulation. Our hypothesis was to test whether collagenous colitis might be related to food allergy.
Patient sera were analysed for common food antigens. Our data support the hypothesis that patients with collagenous colitis have laboratory and/or clinical evidence of food allergy: the high frequency of specific antibodies to food antigens and the increased total IgE levels imply a possible connection between collagenous colitis and food allergy and suggest a possible reason for the paradox of diarrhoea-constipation. Corticosteroids are the most effective drugs available for the treatment of allergic diseases and are very useful in treatment because they have potent anti-inflammatory effects.7 Topical corticosteroids work by reducing the effects of histamine and other inflammatory mediators involved in the allergic response and repeated dosing inhibits both the early and late phase allergic reactions, including priming and hyper- responsiveness. These observations suggest further investigations in other groups of patients with collagenous colitis are needed to prove this hypothesis.