Search

To evaluate the rectal mucosal response to gluten as an indication of gluten sensitivity in patients with primary Sjögren's syndrome (pSS).Rectal challenges with wheat gluten were performed in 20 patients with pSS and 18 healthy control subjects. Fifteen hours after challenge the mucosal production of nitric oxide (NO) was measured.Five patients with pSS had a significant increase in the luminal release of NO after the rectal gluten challenge, indicating gluten sensitivity. All were HLA-DQ2 and/or -DQ8-positive. Two of the patients with increased NO had antibodies against transglutaminase and a duodenal biopsy showed an absolutely flat mucosa consistent with coeliac disease in one of the patients. Before gluten challenge, 15 of the Sjögren's syndrome (SS) patients reported gastrointestinal symptoms, and 8 reported intolerance to various food products. No correlation was found between gluten sensitivity and self-reported food intolerance or gastrointestinal symptoms.Rectal mucosal inflammatory response after gluten challenge is often seen in patients with pSS, signifying gluten sensitivity. However, this reactivity is not necessarily linked to coeliac disease.

Chronic constipation that is unresponsive to laxative treatment is a severe illness, but children unresponsive to laxatives have been successfully treated with an elimination diet. We report the first cases of refractory chronic constipation caused by food hypersensitivity in adults. Four patients with refractory constipation who were unresponsive to high doses of laxatives were put on an oligo-antigenic diet and underwent successive double-blind, placebo-controlled, food challenges (DBPFC). Routine laboratory tests, immunological assays, colonoscopy, esophago-gastroduodenoscopy and rectal and duodenal histology were performed. While on an elimination diet, bowel habits normalized in all patients and a DBPFC challenge triggered the reappearance of constipation. In comparison with another 13 patients with refractory constipation unresponsive to the elimination diet, observed over the same period, the patients with food-hypersensitivity-related constipation had the following characteristics: longer duration of illness (p B /0.03), lower body mass index (p B /0.03), higher frequency of self-reported food intolerance (p B /0.01), higher frequency of nocturnal abdominal pain and anal itching (p B / 0.01). In patients with food hypersensitivity, hemoglobin concentrations and peripheral leukocytes were lower than those in controls (p B /0.03). The duodenal and rectal mucosa histology showed lymphocyte and eosinophil infiltration, and the duodenal villi were flattened in two cases. In adult patients, refractory chronic constipation may be caused by food hypersensitivity and an elimination diet is effective in these subjects.

Adult lactose intolerance, which affects the majority of the population in the world, has been associated with a single nucleotide polymorphism, C-13910T, located upstream of the lactase gene.Adult patients undergoing lactose tolerance tests with lactose challenge and plasma glucose measurements were included in the study comprising 44 Swedes and 7 non-Swedish individuals. A real-time PCR method was established for the genotyping.Out of 51 patients 48 had concordant results on genotyping and lactose tolerance tests, e.g. -13910T/T and -13910C/T genotypes had high glucose elevations. All patients with the heterozygous genotype, -13910C/T, had high glucose elevations, and no gene-dose relationship was observed when comparing maximal glucose increases for cases with -13910C/T and -13910T/T genotypes.Genotyping could replace lactose challenge as a first-stage screening test in adults of European descent, but should be used together with tolerance tests in children and patients where secondary lactose intolerance is suspected.

OBJECTIVE: Chronic constipation in children can be linked to cow''s milk intolerance (CMI) but the existence of a food intolerance-dependent proctitis is still debated. The aim of this study was to evaluate the histologic data in patients with food intolerance-related constipation. MATERIAL AND METHODS: Fifty-two consecutive patients (22 M, median age 4 years) with chronic constipation unresponsive to common treatment were enrolled. All patients were put on a cow''s milk-free diet for 4 weeks and those uncured on this diet underwent a subsequent 4-week period of oligoantigenic diet. In the patients cured on elimination diet, a subsequent double-blind food challenge was performed to confirm the diagnosis of food intolerance. At entry to the study, routine hemato-chemical and immunologic assays, rectoscopy, and histologic study of the rectal mucosa were performed. In the patients cured on elimination diet, rectal histology was repeated when they were cured. RESULTS: Twenty-four patients were found to be suffering from CMI and 6 from multiple food intolerance. These patients had a normal stool frequency on elimination diet, while constipation reappeared on food challenge. The condition of the remaining 22 patients did not improve on elimination diet. The patients with food intolerance showed a significantly higher frequency of erosions of the mucosa, number of intraepithelial lymphocytes and eosinophils, and number of eosinophils in the lamina propria. Study of the rectal mucus gel layer showed that the food-intolerant patients had a significantly lower thickness than the other subjects studied. In the food intolerant patients, histologic abnormalities disappeared on elimination diet, when the patients were well. CONCLUSIONS: Food intolerance-related constipation is characterized by proctitis with eosinophil infiltrate of the rectal mucosa. A reduced mucus gel layer can be considered a contributory factor in the pathogenesis of the constipation.

Lactose intolerance with adult-onset is due to the inadequate enzymatic activity of lactasephlorizin hydrolase (LPH). It is frequently seen in patients with Crohn disease, but the mechanism remains to be elucidated. Two DNA genotypes, C/C(-13910) and G/G(-22018), located upstream from the LCT locus, the gene encoding for LPH, were recently identified as representing genetic markers for lactose intolerance. We utilized these two DNA genotypes to study their role in inflammatory bowel disease.We investigated the prevalence of these two DNA variants using specific restriction enzyme digest assays in 166 patients with Crohn disease, in 120 healthy first-degree relatives of Crohn disease patients, in 63 patients with ulcerative colitis and in 187 healthy individuals.The analysis revealed a frequency of 21.4% of the 2 genotypes for adult-type hypolactasia in our studied German cohort of healthy individuals, which is higher than previously reported (15%) based on the hydrogen (H2) breath test. This might indicate a higher sensitivity of genotyping, but it has to be confirmed in larger cohorts. No significant difference was detectable in the frequency of the C/C(-13910) and G/G(-22018) genotypes in patients with Crohn disease (C/C(-13910): 21.7%; G/G(-22018): 22.3%) compared to first-degree relatives (C/C(-13910): 21.7%; G/G(-22018): 20.8%), patients with ulcerative colitis (C/C(-13910): 20.3%; G/G(-22018): 20.3%) and healthy individuals (C/C(-13910): 21.4%; G/G(-22018): 21.4%).The C/C(-13910) and G/G(-22018) genotype of adult-type hypolactasia is not associated with susceptibility to the pathogenesis of Crohn disease and ulcerative colitis.

It is known that patients with peptic ulcer disease (PUD) often have an unhealthy lifestyle that results in increased mortality because of smoking-related diseases. No thorough study has been done to see what changes, if any, the patient makes to lifestyle after eradication of Helicobacter pylori.One-hundred-and-eighty-three patients were enrolled in an open-endoscopy setting; 58% had PUD and 42% gastritis and/or duodenitis (G/D). They filled out a lifestyle questionnaire before the start of anti-Helicobacter therapy and again 1 year later.The prevalence of food intolerance decreased from 71% to 44% among patients with PUD (P0.0001) and from 76% to 63% among patients with G/D (P = 0.09). Tolerance improved for coffee, orange juice, fried foods, spicy foods and fruits. There was no significant change in smoking or alcohol consumption after eradication. Coffee and tea consumption was unchanged. Milk consumption decreased from 4.2 dL/day to 3.3 (P = 0.01). The number of meals decreased from 3.5/day to 3.4 (P = 0.005) and snacking from 1.3 snacks/day to 1.1 (P = 0.02). Consumption of fruit increased from 4.0 to 4.3 times/week (P = 0.04), but the frequency of meat, fish, vegetables, spicy foods, salty foods, sweets and cakes did not change. The time spent on each meal was unchanged. There was no change in the time spent exercising. There were few significant differences between PUD and G/D patients.Food was better tolerated, but there were no major changes in lifestyle after eradication of H. pylori. Patients therefore do not abuse the privilege of a more tolerant digestion by indulging in a more unhealthy lifestyle.

Background Abdominal complaints after ingestion of cereals are not uncommon. We assessed how reliable such a history is as a marker for the presence of overt coeliac disease, and whether we should also take into account latent coeliac disease and cereal allergy. Methods The study group comprised 93 consecutive adults from health centres spontaneously reporting abdominal symptoms after consumption of cereals. Small bowel mucosal morphology, CD3+, alphabeta+ and gammadelta+ intraepithelial lymphocytes (IELs), HLA DQ alleles and serum IgA-class endomysial (EmA), tissue transglutaminase (tTg) and gliadin (AGA) antibodies were determined. Skin prick and patch tests and serum radioallergosorbent tests for cereals were carried out. Thirty non-coeliac adults served as biopsy controls. Results Eight (9%) patients had coeliac disease and one mild partial villous atrophy. Altogether 17 had an increased density of gamma delta+ IELs without atrophy. However, only seven (8%) showed evidence of latent coeliac disease, i.e. both an increase in gammadelta+ IELs and the presence of coeliac disease-type HLA. One or more of the allergy tests for cereals was positive in 19; 9 adopted a gluten-free diet and abdominal symptoms were alleviated in all. In non-coeliac patients, serum EmA and tTg tests were negative in all, whereas AGA was seen in 40%. Conclusions Intolerance to cereals is not a specific sign of overt or latent coeliac disease. All experimental dietary interventions before proper diagnosis of coeliac disease are therefore to be discouraged. Allergy to cereals, on the other hand, should be considered even in adults.

Whereas many people with coeliac disease (CD) are asymptomatic when consuming a gluten-free diet (GFD), a proportion continues to experience symptoms. The reasons for this are unclear.Thirty-nine adult members of The Coeliac Society of New South Wales, all of whom had persistent gastrointestinal symptoms despite adhering to a GFD, were evaluated. Dietary analysis indicated that 22 (56%) were consuming a GFD as defined by the WHO/FAO Codex Alimentarius (Codex-GFD), in which foods containing up to 0.3% of protein from gluten-containing grains can be labelled as 'gluten free'. The remaining 17 were following a no detectable gluten diet (NDG)-GFD, as defined by Food Standards Australia. All subjects were required to follow a NDG-GFD during the study. Those in whom symptoms persisted after changing from a Codex-GFD and those who entered the study already on a NDG-GFD began an elimination diet followed by open and double-blind challenges to identify specific non-gluten food or food chemical intolerances.Of 22 patients who switched to a NDG-GFD symptoms resolved in 5 (23%) and were reduced in 10 others (45%). Thirty-one subjects commenced the elimination diet. Symptomatic improvement was experienced in 24 (77%). Subsequent food or food chemical challenges resulted in a mean of five positive challenges per individual. Diarrhoea was the most commonly provoked symptom, followed by headache, nausea, and flatulence. Symptoms were especially provoked by amine, salicylate and soy.The consumption of trace amounts of gluten, traditionally allowed in a Codex-GFD, may be responsible for the continuing symptoms seen in some patients with CD. Further investigation for non-gluten food intolerances should follow if symptoms persist after adherence to a NDG-GFD.

Recent advances in the field of neuroimmunology have provided clear demonstrations of i) the neuromodulation of immune function, and ii) the involvement of the immune system in responses induced by psychologic stress in animals and in man. This has led to speculation about the role of the immune system in psychosocial disease. The irritable bowel syndrome (IBS) is characterized by chronic gastrointestinal dysfunction, which may reflect in altered motility, epithelial function, or sensory perception in the gut. IBS is heterogeneous not only in terms of its clinical presentation but also in terms of its pathogenesis, and factors ranging from psychoneurotic behavior and emotional stress, to dietary fiber deficiency, food intolerance, and enteric infection have been implicated. There is evidence of an increase in the inflammatory cells present in the gut of some IBS patients and in an emerging literature that demonstrates the immunomodulation of the motor system of the gut. These findings invite speculation that the immune system may play a role in the pathogenesis and pathophysiology of at least a subpopulation of IBS patients.

(2000). Food Intolerance and Gallstones: Erratum and Update of a Meta-Analysis. Scandinavian Journal of Gastroenterology: Vol. 35, No. 1, pp. 110-111.

A representative sample of an adult population, earlier examined by gastroscopic biopsy, was subjected to correlation and regression analyses to quantitate the influences of different factors on the development of three dyspeptic complaints. In this study a large part of the complaints were incriminated by the subjects to poor tolerance of certain foods and/or beverages. According to the results of formal analysis, the state of the corpus and antral mucosa and the presence of Helicobacter pylori play only an accompanying role in some regression models.

Serum samples from 458 consecutive adult patients with intestinal symptoms and/or suspected food intolerance were examined for IgG and IgA antibody activities to gluten, egg, and cow's milk antigens by an enzyme-linked immunosorbent assay (ELISA). Increased IgA and/or IgG activities to gluten were seen in 61 patients: 35 had coeliac disease (CD) as suggested by jejunal villous atrophy and subsequent histologic and/or clinical improvement on a gluten-free diet; 4 were previously diagnosed CD patients with clinically suspected dietary failure; 2 had dermatitis herpetiformis with a CD-like intestinal morphology; and 3 had possible gluten intolerance without villous atrophy. The rest had other disorders that might have affected the permeability of the gastrointestinal mucosa or the hepatic IgA catabolism. When the IgA activity to gluten was increased, neither the IgA/IgG activities to nongluten antigens nor the ratio of nongluten to gluten antibodies could discriminate between CD patients and those without CD. However, the median IgA activity to gluten was significantly higher in the CD group. The probability for CD thus increased from 33% in patients with IgA activity to gluten between 0.4 and 0.8 OD units to 90% in those with such activity above 2.4 OD units. Nevertheless, seven untreated CD patients had IgG and IgA activities to gluten within the normal range. ELISA determinations of serum antibodies to gluten antigens are a valuable adjunct in the diagnosis of adult CD, but a negative test does not exclude this disorder.

Although suggested, it has never been convincingly documented that food sensitivity is of pathogenetic importance in chronic inflammatory bowel disease. However, many patients may relate their gastrointestinal symptoms to specific food items ingested and may restrict their diet accordingly.A questionnaire was sent to all patients with chronic inflammatory bowel disease who attended the outpatient clinic, Medical Dept., Roskilde County Hospital in Køge, Denmark, in the year 1993. The patients were asked whether they had problems with any particular food item and, if so, to describe the symptoms experienced from it. A control group of 70 healthy persons were included.Among 189 patients, 132 (70%) responded. One hundred and thirty had completed the questionnaire, 52 males and 78 females aged 13-89 years (median, 43 years). Fifty-three (41%) had Crohn's disease (CD), 69 (53%) ulcerative colitis (UC), and 8 (6%) unclassified colitis. Forty-one patients (31 CD, 10 UC) were-operated on; 51 (19 CD, 32 UC) had disease activity. Sixty-five per cent of the patients and 14% of the controls reported being intolerant to one or more food items (P0.0001). The intolerance covered a wide range of food products. The commonest symptoms among patients were diarrhoea, abdominal pain, and meteorism and among controls, regurgitation. Food intolerance was equally common in CD (66%) and UC (64%) and was not related to previous operation, disease activity or disease location.Most patients with chronic inflammatory bowel intolerance disease feel intolerant to different food items and may restrict their diet accordingly. The frequency and pattern of food intolerance did not differ between patients with CD and UC. The food intolerance was probably unspecific rather than of pathogenetic importance.

Fifteen patients with suspected food intolerance were investigated. Ten patients showed a positive reaction to double-blind intragastric food challenge. Mast cell degranulation induced by in vitro challenge with foods or food antigens on mucosal specimens corresponded well with the results of intragastric food challenge. There was agreement in 13 positive and 18 negative tests; there was disagreement in 5 tests. Thus only one in vitro challenge failed to produce mast cell degranulation when the intragastric challenge gave a clinical reaction, and four mucosal specimens showed mast cell degranulations despite no clinical reaction. The results of radio-allergosorbent and skin tests afforded little information as to whether the patient would react to the intragastric food challenge.