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PubMed2002

[Individual sensitivity of jejunal mucosa to small doses of gluten in coeliac disease ].

In coeliac patients the age of development of symptoms, clinical picture of the disease and complications depend on the dose of ingested gluten. The aim of the study was the evaluation of individual sensitivity to small doses of gluten in the group of 60 patients aged 2.65 to 17.92 (mean age 7.49) treated with gluten-free diet for at least 12 months due to coeliac disease diagnosed according to ESPGAN criteria (food allergy to gluten excluded). Gluten challenge with dose of 10 mg/kg body mass/day was controlled with serological tests (IgAEmA, IgAAGA, and IgGAGA antibodies) carried out every 3 to 6 months. Jejunal biopsy was performed before gluten challenge (normal mucosa), and after positive EmA/AGA antibodies tests to confirm diagnosis (flat mucosa). After 35 months of observation 53.7% of all patients presented of jejunal villious atrophy, and positive IgAEmA. In this group 3.7% presented symptoms after 3 months of gluten challenge, 5.5% after 6 months, 3.7% after 9 months, and 3.7% after 12 months. In some coeliac patients ingestion of small amounts of gluten (10 mg/kg/day) can lead to small intestinal villious atrophy.

Adolescent↗
PubMed1976

Cell-mediated immunity to gluten fraction III in adult coeliac disease.

Peripheral blood lymphocytes were obtained from twenty-seven healthy control subjects, twenty-one coeliac patients on a gluten-free diet and fourteen patients on a normal diet. When the cells were cultured in vitro in the presence of 2 and 4 mg of gluten fraction III, there were significant increases in the mean ratios of response for lymphocytes from gluten-free coeliacs compared to healthy controls after 4, 5 and 6 days of culture, but for those on a normal diet significant increases were found only when using 4 mg of gluten on the 4th and 5th days of culture. When three further patients were changed from a normal to a gluten-free diet, the ratios of response for their lymphocytes increased. The results suggest that certain coeliacs may exhibit a weak delayed hypersensitivity reaction to gluten. Its more ready demonstration in patients on a gluten-free diet could be explained on the release of sensitized lymphocytes from the intestinal mucosa into the peripheral circulation after gluten withdrawal.

Antigens↗
PubMed1978

Definitive diagnosis of gluten-sensitive enteropathy. Use of an in vitro organ culture model.

The flat mucosal lesion of the small intestine is not pathognomonic of gluten-sensitive enteropathy (GSE). Frequently, the definitive diagnosis of this condition can only be established after three intestinal biopsies are performed: an initial one to show a flat mucosal lesion, one after a gluten-free diet to show morphological recovery, and one after a gluten challenge to show morphological deterioration. We used an organ culture model of GSE to determine the usefulness of this technique in establishing a diagnosis of GSE on the basis of the initial biopsy. Seventy-five patients with diarrhea, and/or malabsorption were evaluated prospectively; 40 had a flat mucosal lesion of variable degree; of these 26 were ultimately determined to have gluten-sensitive enteropathy by the above criteria. A rise in alkaline phosphatase activity of intestinal tissue from 22 of these 26 patients was inhibited when the tissue was cultured in gluten-containing medium as compared to enzyme activities of cultures in a gluten-free medium (108 +/- 69 versus 206 +/- 96, mean +/- SD, P less than 0.001). Mean enzyme values in the similarly cultured intestinal tissue from 13 of 14 patients ultimately shown not to have GSE were not affected by gluten (224 +/- 94 versus 201 +/- 109, P greater than 0.4). Examination of the data by stepwise discriminant analysis provided a function which correctly classified 35 of the 40 patients (88%). The false-positive and false-negative rate for establishing the diagnosis of GSE was 7% (1 of 14) and 15% (4 of 26), respectively. All patients with normal biopsies were classified correctly. The model can be used to establish prospectively the definitive diagnosis of GSE, obviate the need for additional diagnostic biopsies, and allow for the prompt pursuit of alternative diagnoses when gluten sensitivity is not shown.

Adolescent↗
PubMed1997

Gluten sensitivity in the rectal mucosa of first-degree relatives of celiac disease patients.

BACKGROUND/AIMS: Rectal gluten challenge is a simple, sensitive, and specific test of mucosal gluten sensitivity. Our aims in this study were to evaluate gluten sensitivity in a group of relatives of celiac patients and to compare these findings with those obtained on small bowel histology, celiac disease-related serology, and HLA typing. METHODS: A 4-h rectal gluten challenge was performed with 6 g of crude gluten in saline solution in 29 first-degree relatives, 20 well-diagnosed celiac patients, and 10 subjects in whom celiac disease had been excluded. The number of intraepithelial lymphocytes in pre- and postchallenge frozen rectal biopsies (pan T-cell immunocytochemistry) was quantified by computerized image analysis. RESULTS: The intraepithelial lymphocyte response after gluten instillation was significantly higher in celiac disease patients (median, 126% increase above the baseline count; 95% confidence interval: 61-213%) compared with control subjects (median, -5%; 95% confidence interval: -29-5%). Using a cut-off of 20% change in intraepithelial lymphocyte count, 14 relatives (48%) showed a celiac-like response. Two of these subjects had partial villous atrophy and increased lymphocyte counts in the small bowel mucosa. One of them also exhibited a positive celiac disease-related serology and the typical celiac human lymphocyte antibody (HLA) DQ2. The remaining 12, and all those relatives with a negative challenge, had normal small bowel mucosa and were negative for antigliadin and endomysial antibodies. The characteristic celiac HLA (DQA1 0501 DQB1 0201 heterodimer) was identified in five relatives with positive challenge (including the patient with more severe mucosal atrophy) but was also present in eight relatives with no evidence of gluten sensitivity in the rectal mucosa. CONCLUSIONS: Our study characterizes a subgroup of relatives of celiac patients who show mucosal evidence of sensitization after local instillation of gluten in the rectum but who have no other features of celiac disease.

Adolescent↗
PubMed2003

Wheat-starch-based gluten-free products in the treatment of newly detected coeliac disease: prospective and randomized study.

BACKGROUND: The safety of wheat-starch-based gluten-free products in the treatment of coeliac disease is debatable. Prospective studies are lacking. AIM: : To compare the clinical, histological and serological response to a wheat-starch-based or natural gluten-free diet in patients with newly detected coeliac disease. METHODS: Fifty-seven consecutive adults with untreated coeliac disease were randomized to a wheat-starch-based or natural gluten-free diet. Clinical response, small bowel mucosal morphology, CD3+, alphabeta+ and gammadelta+ intra-epithelial lymphocytes, mucosal human leucocyte antigen-DR expression and serum endomysial, transglutaminase and gliadin antibodies were investigated before and 12 months after the introduction of the gluten-free diet. Quality of life measurements were performed by standardized questionnaires and the bone mineral density was analysed. RESULTS: In both groups, abdominal symptoms were alleviated equally by a strict diet. There were no differences between the groups in mucosal morphology, the density of intra-epithelial lymphocytes, serum antibodies, bone mineral density or quality of life tests at the end of the study. Four patients on a natural gluten-free diet and two on a wheat-starch-based gluten-free diet had dietary lapses; as a result, inadequate mucosal, serological and clinical recovery was observed. CONCLUSIONS: The dietary response to a wheat-starch-based gluten-free diet was as good as that to a natural gluten-free diet in patients with newly detected coeliac disease.

Adult↗
PubMed2005

Risk of celiac disease autoimmunity and timing of gluten introduction in the diet of infants at increased risk of disease.

CONTEXT: While gluten ingestion is responsible for the signs and symptoms of celiac disease, it is not known what factors are associated with initial appearance of the disease. OBJECTIVE: To examine whether the timing of gluten exposure in the infant diet was associated with the development of celiac disease autoimmunity (CDA). DESIGN, SETTING, AND PATIENTS: Prospective observational study conducted in Denver, Colo, from 1994-2004 of 1560 children at increased risk for celiac disease or type 1 diabetes, as defined by possession of either HLA-DR3 or DR4 alleles, or having a first-degree relative with type 1 diabetes. The mean follow-up was 4.8 years. MAIN OUTCOME MEASURE: Risk of CDA defined as being positive for tissue transglutaminase (tTG) autoantibody on 2 or more consecutive visits or being positive for tTG once and having a positive small bowel biopsy for celiac disease, by timing of introduction of gluten-containing foods into the diet. RESULTS: Fifty-one children developed CDA. Findings adjusted for HLA-DR3 status indicated that children exposed to foods containing wheat, barley, or rye (gluten-containing foods) in the first 3 months of life (3 [6%] CDA positive vs 40 [3%] CDA negative) had a 5-fold increased risk of CDA compared with children exposed to gluten-containing foods at 4 to 6 months (12 [23%] CDA positive vs 574 [38%] CDA negative) (hazard ratio [HR], 5.17; 95% confidence interval [CI], 1.44-18.57). Children not exposed to gluten until the seventh month or later (36 [71%] CDA positive vs 895 [59%] CDA negative) had a marginally increased risk of CDA compared with those exposed at 4 to 6 months (HR, 1.87; 95% CI, 0.97-3.60). After restricting our case group to only the 25 CDA-positive children who had biopsy-diagnosed celiac disease, initial exposure to wheat, barley, or rye in the first 3 months (3 [12%] CDA positive vs 40 [3%] CDA negative) or in the seventh month or later (19 [76%] CDA positive vs 912 [59%] CDA negative) significantly increased risk of CDA compared with exposure at 4 to 6 months (3 [12%] CDA positive vs 583 [38%] CDA negative) (HR, 22.97; 95% CI, 4.55-115.93; P = .001; and HR, 3.98; 95% CI, 1.18-13.46; P = .04, respectively). CONCLUSION: Timing of introduction of gluten into the infant diet is associated with the appearance of CDA in children at increased risk for the disease.

Autoantibodies↗
PubMed1992

[Hot weather damage of wheat gluten: determination of the intermediate lysine degradation in chicks using isotope techniques (14C-U-L-lysine oxidation].

The aim of our experiments was to identify a restricted lysine bioavailability after heating of wheat gluten by estimating a reduced metabolic 14C-lysine degradation. In two trials, male broiler chickens were fed with six diets based on wheat and wheat gluten (gluten untreated or heated), but differing in lysine content according to lysine supplementation. In trial 1 animals were fed restrictively, in trial 2 they were fed ad libitum. For estimation of metabolic lysine degradation all animals received an additional i.v. injection of 14C-U-L-lysine 3 weeks posthatching, followed by hourly collection of 14CO2 up to 3 h after injection. There were no differences between groups receiving untreated or heated gluten concerning weight gain and N-balance if the lysine supplementation was medium or high. When applying a lysine supply close to the requirement level or above the requirement the lysine degradation to 14CO2 (% of the dose) and the specific radioactivity of CO2 in animals receiving heated gluten was significantly lower compared to the corresponding group with untreated gluten. It can be concluded that reduced bioavailability of lysine due to heat treatment of gluten might be indicated by means of weight gain or N-balance only at lysine supply levels below the requirement. In contrast, measurements of lysine degradation by means of 14CO2-excretion after i.v. lysine injection indicate the heat-damaging effect, especially at lysine levels close to the requirement.

Animal Feed↗
PubMed1987

Effect of gluten supplementation in healthy siblings of children with celiac disease.

The clinical, functional, and histopathological effects of 18 g additional gluten intake daily for 4 wk was studied in 13 healthy siblings of Spanish children with celiac disease, including two pairs of discordant monozygotic twins. Five of the 13 children were HLA-DR identical to the celiac sibling, 5 shared only one HLA-DR antigen with the celiac sibling, and 3 had completely different HLA-DR antigens than their respective celiac brothers or sisters. Clinical evaluation and functional tests (routine blood, xylose absorption, and fecal fat excretion studies) were performed before, during, and after gluten challenge. A jejunal biopsy specimen was taken at the end of the 4-wk period of gluten supplementation. No clinical abnormalities were found during the period of the study and there was no significant decrease of xylose absorption. Fecal fat excretion studies gave normal results, both before and after gluten challenge. The high gluten diet did not lead to histopathologic abnormalities in any of the jejunal biopsy specimens, which showed a normal range of crypt to villus ratio and surface-cell height. The present results do not support the view that excessive gluten intake is toxic for individuals who are genetically predisposed but do not have overt celiac disease. The findings also suggest that other factors besides HLA-DR antigens and gluten intake are important for expression of the disease.

Biopsy↗
PubMed1991

Self-management of dietary compliance in coeliac disease by means of ELISA "home test" to detect gluten.

To improve compliance with a gluten-free diet in coeliac disease a simple prototype test kit was developed to detect gluten in foods for use at home. The test is based on monoclonal antibodies to heat-stable gluten proteins which crossreact appropriately with barley and rye proteins. It is suitable for use with a wide range of raw or cooked foods. The food is extracted with dilute hydrochloric acid and 1 drop of the extract transferred to an antibody-coated tube; enzyme-labelled gluten detection antibody is added and after 3 min the tube is washed and colour developer is added. The reaction is stopped after 2 min, stabilising the blue colour. The home kit was compared with a quantitative laboratory kit, and the qualitative agreement was very good. The kit could distinguish foods with trace gluten contents (acceptable for a "gluten-free" diet) from those with a slightly higher but unacceptable gluten content. In a trial of the prototype kit by 47 coeliac disease patients of diverse ages and educational backgrounds, 93% of tests correctly identified foods as acceptable or unacceptable.

Adolescent↗
PubMed1995

Lack of proliferative response by gluten-specific T cells in the blood and gut of patients with dermatitis herpetiformis.

The majority of patients with Dermatitis Herpetiformis (DH) have a gluten-sensitive enteropathy which may be triggered by a T cell-mediated immune response to gluten. Using a proliferative assay, the responses to gluten fraction III, recall antigens and mitogens of peripheral blood mononuclear cells (PBMC) and gut T cell lines (TCL) isolated from patients with Dermatitis Herpetiformis (DH) and normal controls were studied. In most cases, neither PBMC nor gut T cell lines (which were predominantly CD3+, CD4+, TCR alpha beta +) from either controls or patients proliferated in response to gluten fraction III alone. However, the addition of 10 U/ml IL-2 to PBMC cultures containing gluten fraction III resulted in a marked increase in proliferation in 9/19 DH patients and 7/11 controls compared to IL-2 alone. Furthermore, gluten-induced upregulation of IL-2 receptor (CD25) expression was demonstrated on PBMC from 4/4 patients with DH and 2/3 controls after 7 days' culture with antigen. A similar effect by exogenous IL-2, or the same concentration of IL-4, was observed in 8/11 (P = 0.02) and 5/6 respectively DH, and 3/4 normal gut T cell lines. No difference was observed in the response of DH and control PBMC to Tetanus toxin, Candida albicans and PPD; both normal and DH gut T cell lines were unresponsive to these antigens. However, the addition of IL-2 increased the response to Candida albicans by DH gut T cell lines. Moreover, the response of DH gut T cell lines to PHA (P < 0.001), Concanavalin A and anti-CD3 were markedly reduced compared to PBMC from the same patients. These findings suggest that gluten-specific T cells present in the blood and gut of normal and DH individuals are activated by but do not proliferate in response to specific antigen.

Candida albicans↗
PubMed1981

Effect of gluten-free diet on an immunological assay for coeliac disease.

The leucocyte migration inhibition factor (LIF) test for the presence of lymphocytes sensitised to gluten was evaluated over the past 4 years in patients with coeliac disease and correlated with the presence of gluten in the patients' diet. 149 LIF tests were done in 66 coeliac patients, 35 of whom were on a normal diet. However, 7 of 8 clinically and histologically diagnosed cases of coeliac disease who were LIF negative when first tested on a normal diet became LIF positive when placed on a gluten-free diet, so that 94% of patients with coeliac disease were LIF positive. On a prolonged gluten-free diet about 50% of LIF-positive cases became negative. The response to the LIF test seems to be related to gluten intake, with higher LIF values when the patient is taking gluten, and lower values when gluten is eliminated from the diet.

Celiac Disease↗
PubMedDate not supplied

Swelling behavior and structural characteristics of wheat gluten polypeptide films.

Wheat gluten films were subjected to controlled thermomechanical treatments to increase the percentage of aggregated sodium dodecyl sulfate (SDS)-insoluble gluten protein, the aggregation reaction being disulfide bonding. The rheological properties of the films were measured under immersion in water, where wheat gluten films are stable and show only slight swelling. The equilibrium swelling of the gluten films in water decreased with the increase of the percentage of SDS-insoluble protein aggregates, and the frequency the independent shear modulus increased sharply with increasing percentage of SDS-insoluble aggregates. Both findings confirm that disulfide bonding between gluten proteins is the predominant cross-linking reaction in the system. A relationship between shear modulus and aggregated protein compatible with a power law (of exponent 3) suggests the existence of a protein network at a molecular scale. However, the classical Flory-Rehner model failed to describe the relationship between the plateau modulus and the gluten volume fraction (a very drastic increase, compatible with a power law of an exponent of about 14). This result shows that gluten cannot be described as an entangled polymer network. The interpretation of both relationships is a network of mesoscale particles which in turn have a fractal inner structure (with a fractal dimension close to 3).

Glutens↗
PubMed2003

Impact of xylanases with different substrate selectivity on gluten-starch separation of wheat flour.

The influence on wheat flour gluten-starch separation of a xylanase from Aspergillus aculeatus (XAA) with hydrolysis selectivity toward water extractable arabinoxylan (WE-AX) and that is not inhibited by wheat flour xylanase inhibitors was compared to that of a xylanase from Bacillus subtilis (XBS) with hydrolysis selectivity toward water unextractable arabinoxylan (WU-AX) and that is inhibited by such inhibitors. XAA improved gluten agglomeration through degradation of WE-AX and concomitant reduction in viscosity, which in the laboratory scale batter procedure with a set of vibrating sieves (400, 250, and 125 microm), increased protein recoveries on the 400 microm sieve. In contrast, XBS had a negative effect as it decreased gluten protein recovery on this sieve, probably as a result of the viscosity increase that accompanied WU-AX solubilization. Hence, it was active even if most likely a considerable part of its activity was prevented by xylanase inhibitors. A combination of XAA and XBS at a low dosage yielded a distribution of gluten proteins on the different sieves comparable to that of the control. At a high combined dosage, the gluten agglomeration was better than that with XAA alone, indicating that both WE-AX and WU-AX have a negative impact on gluten agglomeration. Finally, experiments with endoxylanase addition at different moments during the separation process suggest that the status of the arabinoxylan population during dough mixing is far less critical for its impact on gluten agglomeration than that during the batter phase.

Aspergillus↗
PubMed1997

Increased proinflammatory cytokine gene expression in the colonic mucosa of coeliac disease patients in the early period after gluten challenge.

Activation of T cells in the intestinal mucosa in response to gluten exposure is thought to play a key role in the pathogenesis of coeliac disease. Moreover, the response of the rectal mucosa to gluten challenge has been considered a useful predictor of gluten sensitivity in coeliac disease. In the present study, we assessed early changes in the expression of proinflammatory cytokine genes and the T cell receptor (TCR) Vbeta repertoire in the rectal mucosa of coeliac disease patients following experimental gluten challenge. Cytokine gene expression was assessed in rectal mucosal biopsies from coeliac disease subjects and controls before and after rectal gluten challenge using quantitative reverse transcription polymerase chain reaction analysis, and the TCR Vbeta repertoire was characterized using a multiprobe RNase protection assay. Marked up-regulation of expression of the C-X-C chemokine IL-8, the proinflammatory cytokine IL-1beta, and the C-C chemokine monocyte chemotactic protein-1 occurred within 24 h of rectal gluten challenge in coeliac disease subjects, but not in controls. Furthermore, these changes occurred in the absence of parallel changes in the expressed repertoire of TCR Vbeta genes in the rectal mucosa. Thus, an increased expression of proinflammatory cytokine genes precedes the expansion of antigen-specific T cell populations in the early period following experimental exposure of the rectal mucosa of coeliac disease patients to gluten. These findings provide new insights into pathways that may be involved in the activation or reactivation of coeliac disease.

Administration, Rectal↗
PubMed2000

The glycaemic index of a range of gluten-free foods.

AIMS: The number of people with both diabetes and coeliac disease is increasing. This study examined the effect of gluten-free, as opposed to gluten-replete carbohydrate containing foods, on post-prandial blood glucose concentrations. METHODS: The glycaemic index of six commonly used gluten-free carbohydrates are reported and compared with published figures for similar non-gluten-free products. RESULTS: The results indicate that the glycaemic index of gluten-free and gluten containing foods are similar. CONCLUSIONS: The inclusion of gluten-free foods in the diet of diabetic individuals with coeliac disease should not compromise glycaemic control.

Blood Glucose↗
PubMed2003

Increase in nitric oxide urinary products during gluten challenge in children with coeliac disease.

BACKGROUND: Coeliac disease is a gluten-sensitive enteropathy where pro-inflammatory cytokines and excess nitric oxide (NO) production can contribute to mucosal damage. NO urinary products are elevated in coeliac children on a gluten diet, but it is not known how rapidly this increase develops after gluten exposure. METHODS: Oral gluten challenge was performed in 25 children whose families kept a daily record of gluten intake and symptoms. Blood was analysed monthly for antigliadin (AGA) and endomysium antibodies (EMA). Urine was analysed every second week for NO products, i.e. the sum of nitrite and nitrate was measured with a colorimetric method. We performed a third biopsy when clinical symptoms indicated a relapse. Median age at the post-challenge biopsy was 3.8 (2.7-8.8) years. RESULTS: Signs of morphological or serological relapse were seen in all children. Mean daily gluten intake was 0.10 (range 0.02-0.26) g/kg bodyweight. Median NO level was doubled and significantly higher after 4 weeks of challenge but not after 2 weeks. EMA, but not AGA levels, correlated positively with NO. Intraepithelial lymphocyte count was significantly higher in the post-challenge biopsy, but did not correlate with the NO levels. CONCLUSIONS: NO products in urine increased during gluten challenge. EMA levels reflected severity of mucosal damage, and NO products reflected the inflammatory response, which was doubled after 4 weeks of challenge. The NO analysis is simple and non-traumatic for the child. It can be performed repeatedly during investigation of children with suspected coeliac disease.

Celiac Disease↗
PubMed2003

Urinary NOx:creatinine ratios during gluten challenge in children with celiac disease.

OBJECTIVES: Celiac disease is a gluten-induced small bowel enteropathy. Inflammation is known to be associated with enhanced nitric oxide (NO) production. An increase in urinary nitrate and nitrite (NOx) reflects increased NO production. The urinary NOx:creatinine ratio can be used as an indicator of the endogenous NO production. The aim of the study was to determine whether the urinary NOx:creatinine ratio of celiac disease patients increases during gluten challenge. METHODS: The authors studied 20 patients with unconfirmed celiac disease who had been following a gluten-free diet for at least 1 year. These patients underwent an 80-day gluten challenge. Urinary samples were obtained before and 10, 20, 40, and 80 days after starting the gluten challenge. The Griess reagent method was used for measuring urinary NOx. RESULTS: Gluten challenge confirmed the diagnosis of celiac disease in 15 of 20 patients. The NOx:creatinine ratios (mmol:mmol) of the biopsy-confirmed celiac disease patients were significantly higher than those of the unconfirmed celiac disease patients (0.67 vs. 0.17 on day 10; 0.78 vs. 0.15 on day 20; 0.85 vs. 0.25 on day 40; and 0.85 vs. 0.17 on day 80). CONCLUSIONS: Gluten challenge resulted in an increased urinary NOx:creatinine ratio in patients with biopsy-confirmed celiac disease. The NOx:creatinine ratio could be useful for the serial evaluation of disease activity.

Celiac Disease↗
PubMed1990

Macrophage procoagulant activity as an assay of cellular hypersensitivity to gluten peptides in coeliac disease.

Gluten and casein digests were tested for their ability to induce a cellular immune response on peripheral blood mononuclear cells (PBM) obtained from coeliac patients as well as healthy volunteers and disease control patients using the macrophage procoagulant assay. PBM from coeliac patients who had been on a gluten-free diet for less than 2 years responded strongly to gluten peptides, while coeliac patients at diagnosis or who had maintained a strict gluten-free diet for longer than 5 years showed weaker responses. PBM from healthy volunteers did not respond to gluten or casein peptides, whereas those from patients with Crohn's disease displayed weak reactivity to gluten and casein peptides. Our study using the macrophage procoagulant assay confirms previous findings that lymphoid cells from patients with coeliac disease exhibit a specific cellular immune response to gluten. This assay represents an alternative measure for cell-mediated immunity and is technically much simpler than the previously described leucocyte migration inhibition assay. Macrophage procoagulant activity is measured using a simple plasma recalcification time assay or spectrophotometrically using commercially available chromogenic substrates.

Adult↗