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PubMed2001

Assessment of gliadin in supposedly gluten-free foods prepared and purchased by celiac patients.

BACKGROUND: The present study was designed to evaluate the presence of gliadin in homemade foods prepared by patients with celiac disease and/or their relatives, as well as in processed products consumed by such patients in São Paulo, Brazil, by enzyme immunoassay (EIA) and Western blot (WB) analysis. METHODS: One hundred ninety samples were analyzed: 108 homemade foods prepared in homes of patients with celiac disease, 81 processed products, and 1 positive control of homemade food. All samples were analyzed by EIA based on monoclonal antibodies to heat stable omega-gliadins and related prolamins from wheat, rye, and barley. Samples were also analyzed using the WB technique. RESULTS: Only one (0.9%) of 108 homemade foods contained detectable amounts of gliadin, as determined by EIA. Twelve of 81 processed products contained gliadin by EIA, as follows: 5 of 61 without gluten listed in the ingredients, 2 of 11 malt extracts, 1 of 2 wheat starches, 1 of 2 types of beer, and all 3 positive control products. Gliadin content of these products was between 4 and 10 mg of gliadin/100 g of product, except for the wheat starch sample (28 mg of gliadin/100 g) and all 3 samples with gluten (>4000 mg of gliadin/100 g). The positive control of homemade food contained 152 mg of gliadin/100 g. One hundred three of 190 samples were analyzed by WB, and 21 of these were gliadin positive. A comparison of results obtained by EIA and WB showed no statistical differences between the methods. CONCLUSIONS: The greater part of the foods prepared in homes of patients with celiac disease and most processed products supposed to be gluten-free did not contain gliadin. Therefore, celiac patients adequately prepare gluten-free homemade food and have the expertise to purchase processed gluten-free food in São Paulo, Brazil.

Antibodies, Monoclonal↗
PubMed2005

Antiendomysial antibody detection in biopsy culture allows avoidance of gluten challenge in celiac children.

OBJECTIVE: Antiendomysial antibody (EMA) production has been induced in vitro by the small bowel mucosa of celiac disease (CD) patients in clinical remission cultured in the presence of gliadin peptides. The aim of the present study was to use this in vitro system to determine whether it could be used to predict the clinical or histologic relapse to gluten challenge in CD children on a gluten-free diet (GFD). METHODS: Enrolled were 32 CD children and adolescents on GFD (group 1), and 80 controls (group 2) who underwent in vitro gliadin challenge. Subsequently, 24 group 1 CD children underwent in vivo gluten challenge to confirm the diagnosis. Biopsy cultures, with and without gliadin, morphometric analysis, immunoglobulin (Ig)A and IgG1 EMA detection, both in sera and culture supernatants, were performed. RESULTS: Of the 32 group 1 CD patients, 23 were IgA EMA positive in culture supernatants. The other nine were IgG1 EMA positive. All 24 children who had in vivo gluten challenge showed clinical or histologic relapse. All culture supernatants from disease controls belonging to group 2 were both IgA and IgG1 EMA negative, irrespective of gliadin challenge. CONCLUSIONS: Organ culture with in vitro gliadin challenge is able to reproduce the results of in vivo challenge. This system could reduce the need for gluten challenge in celiac children.

Adolescent↗
PubMed2002

The neurology of gluten sensitivity: separating the wheat from the chaff.

Coeliac disease is the prototypical gluten-sensitive disease. Clinico-pathological features heal on a gluten-free diet and relapse when gluten is reintroduced. An immunopathology is suspected. A number of neurological syndromes may be associated with coeliac disease but it is unclear whether these are directly or indirectly caused by gluten ingestion. It has been proposed that idiopathic ataxias and central nervous system white matter disease are gluten-sensitive syndromes. This is an exciting hypothesis because it offers new therapeutic possibilities including simple exclusion diets. However, interpretation is difficult because occult sub-clinical coeliac disease occurs commonly and background prevalence needs to be accounted for in population-based studies. This review will attempt to summarize the pertinent literature on this fascinating topic.

Ataxia↗
PubMed2005

A major step towards a practical and meaningful gluten analysis.

Coeliac disease is triggered by the cereal protein gluten. Elimination of gluten is the effective therapy. To increase food safety for coeliac patients, gluten has been included in food regulations introducing obligatory labelling. These regulations depend upon effective analytical control. A combined system using cocktail extraction and the R5 enzyme-linked immunosorbent assay has now been described for gluten analysis, which shows good performance. Every effort should be made to keep the diet of coeliac patients as gluten-free as possible.

Celiac Disease↗
PubMed1982

Detection of gluten in human sera by an enzyme immunoassay: comparison of dermatitis herpetiformis and celiac disease patients with normal controls.

We have developed a triple sandwich enzyme immunoassay to detect circulating gluten in human sera. With human sera containing known amounts of added gluten as controls, the assay was sensitive in the range of 0.75 to 75 micrograms of gluten per ml of serum. Forty-one control subjects were compared to 21 patients with dermatitis herpetiformis and 11 patients with celiac disease. The dermatitis herpetiformis and celiac disease patients had significant elevation of serum gluten values over the control subjects. Circulating gluten antigenemia is a previously unrecognized feature which may be important in understanding the pathogenesis of dermatitis herpetiformis and celiac disease.

Adult↗
PubMed2006

Reduction of tissue transglutaminase autoantibody levels by gluten-free diet is associated with changes in subsets of peripheral blood lymphocytes in children with newly diagnosed coeliac disease.

Tissue transglutaminase (tTG) autoantibodies decline after gluten-free diet in patients with coeliac disease. We tested the hypothesis that gluten-free diet-induced change in tTG autoantibody levels affects subsets of peripheral blood lymphocytes. Peripheral blood was obtained from 20 children with biopsy-proven active coeliac disease. Gluten-free diet was initiated and the children examined again after three and six months. tTG autoantibodies were measured in radioligand binding assays and lymphocyte subsets by flow cytometry. IgA-tTG levels at diagnosis, 2204 U/ml (median, range 113-24990), were reduced over six months to 76 U/ml (median, range 1-1261) (P < 0.001). At six months, 12/20 (60%) children had reduced their IgA-tTG levels to < 100 U/ml and these children showed a decrease in B cells (mean change -3.8%, P = 0.014), CD4+ T cells (mean -4.32%, P = 0.011) and CD4+ T cells expressing CD25high (mean change -0.62%, P = 0.036). In contrast, the CD4+CD25(high)CCR4+ T cell population increased during the same period (mean change 11.5%, P = 0.0036). The decline in IgA-tTG levels correlated to the decrease in B cells (r = 0.56, P = 0.01), CD4+ T cells (r = 0.66, P = 0.004) as well as CD4+CD25high T cells (r = 0.59, P = 0.01). A negative correlation was found between the decline in IgA-tTG and CD4+CD25high T cells expressing CD45RO (r = -0.49, P = 0.03) and CCR4 (r = -0.54, P = 0.01). This is the first observational study on the effect of gluten-free diet on concurrent changes of tTG autoantibodies and specific peripheral blood lymphocyte subsets. Our data suggest that flow cytometry may be a useful complement to tTG autoantibodies when studying the effects of gluten-free diet in children with coeliac disease.

Adolescent↗
PubMed1993

Gluten stimulation of coeliac mucosa in vitro induces activation (CD25) of lamina propria CD4+ T cells and macrophages but no crypt-cell hyperplasia.

Jejunal biopsy specimens from 10 patients with treated coeliac disease and seven non-coeliac controls were challenged in vitro with peptic-tryptic gluten digest. Mucosal T cells were examined in situ by three-colour immunofluorescence staining for expression of the activation marker CD25 (the p55 alpha-chain of interleukin-2 receptor) and the nuclear proliferation marker revealed by monoclonal antibody Ki-67. Intraepithelial T cells expressed CD25 rarely whereas the proportion of activated lamina propria T cells increased (P < 0.002) from median 2.8% (cultured with 20% fetal calf serum alone for 24-48 h) to 10.0% after 24 h with gluten (n = 10; range 1.1-17.4%) and to 10.4% after 48 h (n = 7; range 1.4-17.5%). Such gluten-induced increase of CD25+ T cells was not observed in specimens from non-coeliac control subjects. Crypt-cell hyperplasia and T-cell proliferation (Ki-67+) were observed neither in the coeliac nor in the control mucosae after gluten stimulation. Three-colour staining combining a polyclonal antibody reagent to CD3 and a monoclonal antibody to CD25 with a monoclonal antibody to CD45R0, CD4, CD8, the p75 beta-chain of interleukin-2 receptor, integrin alpha E beta 7, or HLA-DR showed that most of the CD25+ T cells (> 90%) were CD4+CD8-, co-expressed CD45R0 and the p75 beta-chain, and often also the integrin alpha E beta 7 but not HLA-DR. In addition to these activated T cells, a dominating population of CD25+CD3-CD4+ subepithelial pan-HLA-class II+ macrophages (CD68+) with variable expression of the p75 beta-chain was often induced by gluten challenge.

Adult↗
PubMed1994

T cells from the peripheral blood of coeliac disease patients recognize gluten antigens when presented by HLA-DR, -DQ, or -DP molecules.

Coeliac disease (CD) is a T-cell mediated immunological disease of the small intestine which is precipitated in susceptible individuals by ingestion of gluten. We recently reported that gliadin-specific T cells can be found in the small intestinal mucosa of CD patients, and that a preponderance of these T cells was restricted by the CD-associated DQ(alpha 1*0501,beta 1*0201) heterodimer. Here we report studies on whether the same is found for gliadin specific T cells in the peripheral blood of CD patients. T-cell responses towards gluten antigens in vitro were found for both most CD patients and healthy controls. Gluten-specific T-cell clones (TCC) were established from four CD patients. Although a large proportion of these TCC were restricted by DQ molecules, including the CD-associated DQ(alpha 1*0501,beta 1*0201) heterodimer, several were restricted instead by DR or DP molecules. Thus, gluten-derived peptides can be presented to T cells by several different HLA class-II molecules, and the preferential DQ(alpha 1*0501,beta 1*0201) restriction of gluten-specific T cells in the small intestinal mucosa of CD patients is less pronounced than for similar T cells in the peripheral blood.

Antibodies, Monoclonal↗
PubMed1960

The mechanism of the inhibitory effect of gluten fractions on the peristaltic reflex.

The mechanism of the inhibitory effect of gluten fractions on the peristaltic reflex was studied using, first, a filtrate of the autoclaved peptic-tryptic digest of gluten (fraction III A.F.) and, second, the ultrafiltrate of an aqueous extract of gluten (fraction G.U.F.). The fractions did not act as antagonists to naturally-occurring agents such as acetylcholine or substance P, but they did depress the twitch response of the isolated guinea-pig jejunum preparation stimulated coaxially. The output of acetylcholine from cholinergic nerve endings in gut was decreased during rest as well as during electrical stimulation. In large amounts, the gluten fractions depressed acetylcholine synthesis in vitro. It was concluded that the mechanism of inhibition of the peristaltic reflex by gluten fractions was chiefly by decreasing acetylcholine release.

Acetylcholine↗
PubMed2000

Importance of gluten in the induction of endocrine autoantibodies and organ dysfunction in adolescent celiac patients.

OBJECTIVE: It is well known that a high number of celiac patients may develop autoantibodies against endocrine glands, but it has not yet been clarified if this increased autoimmune response and the impaired organ function that can develop may be related to the presence or absence of gluten in the diet. The aim of the present study was to evaluate the effect of gluten on the autoimmunity and function of the endocrine glands in adolescent celiac patients. METHODS: To clarify this aspect we investigated 44 patients (28 females), aged 11-20 yr (15.21+/-2.7 yr): 25 (mean age, 15.1+/-2.2 yr) on a gluten-free diet (treated patients) and 19 (mean age 15.4+/-2.9 yr) with a diet containing gluten (untreated patients). Forty adolescent subjects, aged 14-19 yr (mean age, 14.9+/-2.7 yr), of whom 20 were females, were studied as controls. Antibodies against the thyroid, adrenal, and pancreas were evaluated. Thyroid-stimulating hormone FT3, FT4, T3, T4, dehydroepiandrosterone sulphate, 17-OH progesterone, and cortisol, analyzed basally and 60 min after intravenous ACTH stimulation, were assayed to evaluate thyroid and adrenal function. The fasting glycemia level was used to evaluate the endocrine pancreas function. An ultrasonogram of the thyroid gland was performed on all patients. HLA class II typing for DR3 and DQB1 was performed in 32 of 44 patients. RESULTS: Seven of 44 (15.9%) patients were positive for antibodies against peroxidase. Six of 44 (13.6%) were positive for antibodies against thyreoglobulin and four of them also showed positive antibodies against peroxidase. Therefore, in nine of 44 at least one antibody directed against thyroid tissue was positive. Seven of 44 (15.9%) were positive for antibodies against islet cell, one of 44 (2.3%) positive for antibodies against glutamic acid decarboxilase, one of 44 (2.3%) positive for antibodies against insulin, and none for antibodies against islet cell- 512bdc. In 15 of 44 (34%) at least one antibody against an endocrine tissue was positive. The genotype DR3 was found in 21 of 32 (65.6%) celiac patients (10 in the untreated and 11 in the treated group, respectively) and the genotype DQB1*02 (DQ2) was found in 30 of 32 (93.8%) patients (16 in the treated and 14 in the untreated group, respectively). DHA-S values were significantly lower in the untreated (30.5+/-28.5 microg/dl) than in the treated group (61.3+/-59.4 microg/dl, p < 0.05), and both showing significantly (p < 0.01) lower levels with respect to the controls (161+/-52 microg/dl). One patient showed diabetes, another one clinical hypothyroidism (thyroid-stimulating hormone > 6), and two patients showed preclinical hypothyroidism. Interestingly, at least one antibody was positive in 10 of 19 untreated patients (52.6%) but only in five of 25 treated patients (20%), with a significantly different distribution (p < 0.001) between the two groups and without differences in the HLA genotype. The ultrasonographic evaluation of the thyroid resulted in a pathological score in six patients of the 44 examined (13.6%), suggesting the presence of thyropathy. CONCLUSIONS: The main results of this study are the high incidence of thyroid and pancreatic antibodies, and the possible role of gluten in the induction of the antibodies as well as, in few cases, the consequent organ dysfunction.

Adolescent↗
PubMed2001

Efficacy of gluten-free diet alone on recovery from iron deficiency anemia in adult celiac patients.

OBJECTIVE: Iron deficiency anemia has been reported as the most frequent extraintestinal symptom in adult celiac disease. Prospective studies on the effect of gluten-free diet on recovery from iron deficiency anemia are lacking. The aim of this study was to verify in adult patients with celiac disease the efficacy of and the time course of recovery from iron deficiency anemia by a gluten-free diet alone. METHODS: We studied 190 consecutive adult patients with iron deficiency anemia, screened for celiac disease by duodenal biopsies. New diagnosed celiac patients were invited to follow a gluten-free diet alone without iron supplementation. After 6 months of diet, duodenal biopsies were performed and hematological tests were repeated at 6, 12, and 24 months. RESULTS: Celiac disease was diagnosed in 26 (24 women, 2 men; 13.7%) adult patients. After 6 months of gluten-free diet 14 of 18 (77.8%) female patients recovered from anemia, but only 5 of 18 (27.8%) reversed from iron deficiency. At 12-month control all but one patient (94.4%) recovered from anemia and 9 patients (50%) from iron deficiency. After 24 months of diet, only the patient who did not recover from anemia at 12-month control was still anemic, whereas 10 patients (55.5%) reversed from iron deficiency. A significant inverse correlation (r = -0.7141, p = 0.0003) between increase of Hb concentrations and decrease of individual histological scores of duodenitis was observed. CONCLUSIONS: A screening for celiac disease should be carried out in adult patients with iron deficiency anemia. Recovery from anemia occurs between 6 and 12 months on a gluten-free diet alone as a consequence of normalization of histological alterations of the intestinal mucosa.

Adult↗
PubMed1979

Incidence of coeliac disease and transient gluten intolerance in children in a Swedish urban community.

The incidence of coeliac disease in children in the city of Malmö, South Sweden, was 1 : 982 during 1966 to 1975. The diagnostic criteria were: flat intestinal mucosa on gluten-containing diet, free of symptoms, and improvement in mucosal morphology on gluten-free diet, and morphological and/or evident clinical relapse (three times) on gluten challenge. 6 (12%) of 49 children with initially a flat mucosa still had a normal mucosa on a gluten-containing diet for two years or longer, having so-called transient gluten intolerance.

Celiac Disease↗
PubMed1990

The impact of gluten on haematological status, dietary intakes of haemopoietic nutrients and vitamin B12 and folic acid absorption in children with coeliac disease.

The haematological status, as well as the fractional absorptions of folic acid-and of vitamin B12 (FAFol and FAB12) were studied longitudinally in 20 coelic children aged 1.2-16.6 yr (mean 7.5 yr) during periods of gluten-free and gluten containing diets. The absorption methods were specially adapted to use in children, and age-related reference limits were established. Also, dietary intakes of iron, folate and B12 were registered. The haemoglobin concentrations did not show any significant differences in relation to shifts in diet. A few had mild anaemia while the haemoglobin concentrations in the other patients remained within normal range. The iron status, as judged from mean corpuscular volume (MCV), serum (S)-iron, S-transferrin and saturation %, appeared to be generally insufficient. However, the only significant change related to shifts in diet was an increase of S-iron during the first period of gluten-free diet. Dietary intakes of iron proved to be insufficient, regardless of the type of diet. Plasma (P)-B12 concentrations demonstrated a wide range of values above the lower normal limit, whereas the level in a single patient was within the "intermediate range" of B12 insufficiency (150-200 pmol/l). The folate status (erythrocyte-folate) showed significant variations related to dietary changes. However, few patients were folate depleted. FAFol and FAB12 demonstrated rapidly occurring, and significant decreases and increases in relation to gluten challenge and gluten-free diet, respectively. Bacterial overgrowth of the small intestinal tract was not found to be a plausible cause of the B12 malabsorption in the case of 5 patients observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1976

Criteria for diagnosis of temporary gluten intolerance.

Strict criteria for the diagnosis of temporary gluten intolerance are formulated in the light of the case of an 8-week-old infant with severe diarrhoea and failure to thrive, who recovered on an elimination diet that was gluten-free. 8 weeks later an oral challenge with 2.5 g twice daily of powdered gluten for one day produced diarrhoea, weight loss, and impaired xylose absorption. Gluten was successfully reintroduced into the diet 9 months later without incident. Jejunal histology remains normal after 26 months of a daily diet that contains 5 to 10 g gluten.

Glutens↗
PubMed1984

Dermatitis herpetiformis: jejunal findings and skin response to gluten free diet.

Fifty seven children with dermatitis herpetiformis, 18 from Finland and 39 from Hungary, were studied. Diagnostic criteria included the finding of granular IgA deposits in the skin of all patients. The mean age at onset of the rash was 7 X 2 years and favoured sites were the elbows, knees, and buttocks. Symptoms suggesting small intestinal disease were rare but in 35 (61%) of the children subtotal villous atrophy and in 16 (28%) partial villous atrophy were found on jejunal biopsy. Eighteen children underwent a second biopsy after a mean of 21 months on a gluten free diet; villous height was found to be increased and the intraepithelial lymphocyte count decreased in all these patients. Gluten challenge caused a reversal in the two children who underwent a third biopsy. The effect of the gluten free diet on the rash was examined in Finnish children by observing the daily requirements of dapsone, a drug used to control the rash at the beginning of the diet. Eight (67%) of the 12 children were able to stop taking dapsone after a mean of 11 months on the diet and all three patients treated with diet alone became asymptomatic after three to 6 months on the diet. These results confirm that most children with dermatitis herpetiformis have jejunal villous atrophy, though they rarely have gastrointestinal symptoms. The central role of gluten in childhood dermatitis herpetiformis is evidenced by the fact that a gluten free diet helps the damaged jejunal mucosa to recover and controls the rash even in those children who do not have an abnormal jejunal biopsy.

Adolescent↗
PubMed1991

Intestinal permeability after single dose gluten challenge in coeliac disease.

The changes of intestinal permeability before and after a gluten load were studied. The study group comprised 27 patients with coeliac disease (mean age 12.3 years) and 19 healthy controls matched by sex and age. Intestinal permeability was studied by measuring the urinary excretion of two sugars, lactulose and L-rhamnose, before and six hours after the ingestion of five palatable biscuits made with 50 g of gluten powder. The patients with coeliac disease had been on a gluten free diet during the previous two years. After the gluten load lactulose and L-rhamnose urinary excretion changed significantly in patients, and a significant increase in the lactulose: L-rhamnose ratio was also observed. No significant changes were observed in the controls. In view of the modification of the three biopsies diagnostic protocol made by the European Society for Paediatric Gastroenterology and Nutrition, permeability tests associated with single gluten challenges may be an added contribution to the accuracy of the diagnosis in childhood.

Adolescent↗
PubMed1997

Influence of infant feeding and gluten intake on coeliac disease.

OBJECTIVES: To study the impact of infant feeding habits and actual gluten intake on gluten induced enteropathy. METHODS: A case-referent design, controlling for the HLA alleles conferring increased genetic risk, was used. All 164 siblings of 97 probands were investigated. Eighty five of the siblings, carrying the genes DQA1*0501-DQB1*02 conferring susceptibility for the disease, were investigated by interview, food recording, and taking a small intestinal biopsy sample. Eight cases of silent coeliac disease were found and these were compared with the 73 siblings in whom the diagnosis was excluded. RESULTS: No statistically significant differences were found between cases and referents in terms of duration of breast feeding, age at introduction of cows' milk products, frequency of breast feeding after gluten introduction, and gluten consumption. CONCLUSIONS: The studies factors may be of less importance for the development of gluten induced enteropathy.

Adolescent↗
PubMed1972

Lymphocytic infiltration of epithelium in diagnosis of gluten-sensitive enteropathy.

The macroscopic appearance of the mucosa of the small intestine and the lymphocytic infiltration of the epithelium were studied in 27 patients with dermatitis herpetiformis and in 11 control subjects. The mucosa was abnormal in appearance in 13 of the patients and normal in 14 patients and in all the controls. In 25 (93%) of the patients the intraepithelial lymphocyte count was significantly raised compared with the controls. The increased lymphocytic infiltration of the epithelium in the patients probably represented an underlying immunological reaction of the small intestine to gluten, since the infiltration lessened in five out of six patients after a year on a gluten-free diet and in all of four patients after three years on a gluten-free diet.Increased lymphocytic infiltration of the epithelium of the small intestine seems a surer sign of gluten sensitivity than the macroscopic appearance of the mucosa, and a diagnosis of gluten-sensitive enteropathy may no longer be excluded when the mucosa appears normal. Further evidence of the significance of increased lymphocytic infiltration is that patients with normal-looking mucosa but with raised intraepithelial lymphocyte counts often had low serum folate levels.

Biopsy↗