Small-bowel capsule endoscopy in patients with gastrointestinal food allergy.

BACKGROUND: Food allergy may present with a plethora of gastrointestinal and extraintestinal symptoms such as abdominal pain, diarrhea, cardiocirculatory symptoms, cutaneous reactions, or rhinitis. Macropathological lesions like lymphofollicular hyperplasia and erosive or ulcerative lesions have seldom been described in gastroscopy and colonoscopy previously. METHODS: Fifteen patients presenting with unspecific abdominal symptoms in which food allergy was detected in due course were included. During the examination process, those patients showed various indications for small-bowel capsule endoscopy, such as weight loss and anemia. RESULTS: Fourteen (93.3%) of the 15 small-bowel capsule endoscopies could be assessed, showing nonerosive lesions such as erythema, swelling, and lymphoid hyperplasia in 8 patients (57.1%) and erosive lesions such as aphthoid lesions, erosions, and petechiae in 4 patients (28.6%) with food allergy. CONCLUSION: In 15 patients with confirmed food allergy and after exclusion of other diseases, 12 (85.7%) showed various unspecific nonerosive or erosive mucosal lesions within the small bowel, resulting, however, partially in grave consequences such as anemia. Lymphoid hyperplasia was the most prominent finding in 7 patients (50%), albeit infectious disease had been excluded. Anemia improved within 1 year after adequate antiallergic treatment.

Analysis of immediate ex vivo release of nitric oxide from human colonic mucosa in gastrointestinally mediated allergy, inflammatory bowel disease and controls.

Nitric oxide (NO) is a local mediator in inflammation and allergy. The aim of this study was to investigate whether live incubated colorectal mucosal tissue shows a direct NO response ex vivo to nonspecific and specific immunological stimuli and whether there are disease-specific differences between allergic and chronic inflammatory bowel disease (IBD). We took biopsies (n=188) from 17 patients with confirmed gastrointestinally mediated food allergy, six patients with inflammatory bowel disease, and six control patients. To detect NO we employed an NO probe (WPI GmbH, Berlin, Germany) that upon stimulation with nonspecific toxins (ethanol, acetic acid, lipopolysaccharides), histamine (10(-8)-10(-4)M), and immune-specific stimuli (anti-IgE, anti-IgG, known food allergens) directly determined NO production during mucosal oxygenation. Non-immune stimulation of the colorectal mucosa with calcium ionophore (A23187), acetic acid, and ethanol induced a significant NO release in all groups and all biopsies. Whereas, immune-specific stimulation with allergens or anti-human IgE or -IgG antibodies did not produce significant release of NO in controls or IBD. Incubation with anti-human IgE antibodies or allergens produced a ninefold increase in histamine release in gastrointestinally mediated allergy (p<0.001), but anti-human IgE antibodies induced NO release in only 18% of the allergy patients. Histamine release in response to allergens or anti-human IgE antibodies did not correlate with NO release (r(2)=0.11, p=0.28). These data show that nonspecific calcium-dependent and toxic mechanisms induce NO release in response to a nonspecific inflammatory signal. In contrast, mechanisms underlying immune-specific stimuli do not induce NO production immediately.