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PubMed1994

IgA antibodies to jejunum. Specific immunity directed against target organ of gluten-sensitive enteropathy.

Serum IgA antibodies to jejunum (JAB) were found in 78 (96%) of 81 adults and children with untreated celiac disease. Not only did IgA JAB display a significant higher prevalence than IgA antigliadin antibodies (AGA) (72%) in untreated gluten-sensitive enteropathy, but they also allowed us to identify another three celiacs in addition to those detected by IgA antiendomysial antibodies (EmA). Like IgA EmA, IgA JAB persisted at low titer in seven (14%) of 50 celiacs tested after 12 months of gluten-free diet (GFD) despite the regrowth of jejunal villi, whereas IgA AGA disappeared in all these patients consistently with the normalization of intestinal mucosa. IgA JAB and EmA reappearance was close to 100% in the 13 celiacs studied after six months of gluten challenge, while IgA AGA reached the highest prevalence (about 70%) after one month of gluten ingestion without any increase in the following months. All disease and healthy controls were always negative for the three IgA antibodies. Our results prove that IgA JAB and EmA are the best screening tests for active (untreated and on gluten challenge) celiac disease, whereas IgA AGA should be used for monitoring the response to gluten withdrawal. IgA JAB are an expression of a specific immunity directed against the target organ of gluten-sensitive enteropathy, but, before ascribing them a role in the pathogenesis of celiac disease, it should be ascertained whether their production is a primary event leading to jejunal lesions or whether it is a secondary phenomenon due to antigen release from a previously damaged jejunal mucosa.

Adolescent↗
PubMed1996

Gluten-sensitive enteropathy.

Gluten-sensitive enteropathy is induced by dietary wheat gliadin and related proteins in genetically susceptible individuals. Most evidence suggests that the mucosal lesion represents an immunologically mediated injury triggered by gluten in the context of a particular assortment of major histocompatibility complex genes. The amino acid residues of gliadin and related proteins responsible for toxicity have not been identified; in vitro systems are available, but definitive conclusions must rely on in vivo jejunal challenges. At a conservative estimate, symptomatic gluten-sensitive enteropathy affects approximately 1 in 1000 individuals in Europe; however, it is now becoming clear that a greater proportion of individuals has clinically silent disease, and probably many others have a minor form of the the enteropathy. In most countries, the clinical presentation has changed over the past few years coming closer to the adult type of the disease, and the age of onset of symptoms is shifting upward. Liver, joint, hematologic, dental, and neurologic symptoms are increasingly being recognized. Several diseases are associated the gluten-sensitive enteropathy, such as IgA deficiency, insulin-dependent diabetes mellitus, and a range of other autoimmune diseases. Tests based on the measurement of antigliadin and antiendomysium antibodies have gained success as noninvasive screening tests; however, the ultimate diagnosis still is based on the finding of a severe histologic lesion of the jejunum while the patient is on a gluten-containing diet and on its disappearance once the gluten is excluded from the diet. A lifelong, strict GFD is mandatory for celiac children. Among other long-term problems, an increased risk of intestinal lymphoma has been reported in patients on a normal gluten-containing diet.

Adult↗
PubMed1996

Gluten-sensitive disease with mild enteropathy.

BACKGROUND & AIMS: Celiac disease is a permanent gluten intolerance strongly associated with HLA class II antigens and possibly showing milder changes of mucosal architecture. Ten patients with symptoms suggesting celiac disease and serum antiendomysium antibodies with normal mucosal architecture were studied. METHODS: Immunohistochemical detection of mucosal immune activation and HLA typings were performed. RESULTS: Mucosal immune activation, with normal mucosal architecture and normal gamma/delta+ intraepithelial lymphocytes counts, was found on a gluten-containing diet. In 3 of 6 patients, multiple biopsy specimens showed one sample with severe villous atrophy. Clinical and immunomorphologic features were strictly gluten dependent. The mucosal immune activation was elicited in vitro by gliadin. Only 4 patients had the typical HLA typing of celiac disease. CONCLUSIONS: Gluten-sensitive celiac-like symptoms may occur in patients with serum antiendomysium antibodies, apparently normal intestinal mucosa, and HLA typing not commonly associated with celiac disease. These patients should undergo multiple biopsies, and signs of immunologic activation should be sought accurately; in the presence of mucosal immune activation, a trial with a gluten-free diet should be encouraged to detect gluten dependency. In vitro immunologic response of small intestinal mucosa to gliadin may support the diagnosis of gluten-sensitive enteropathy.

Adult↗
PubMed2006

Coeliac children on a gluten-free diet with or without oats display equal anti-avenin antibody titres.

OBJECTIVE: Recent studies report negligible toxicity of oats in the majority of coeliac disease (CD) patients. It has previously been shown that children with untreated CD have circulating antibodies to oats avenin. In this study we performed serial assessments of anti-avenin antibodies in children under investigation for CD on a gluten-free diet with or without oats. MATERIAL AND METHODS: The study involved 116 children, randomized to a standard gluten-free diet or a gluten-free diet supplemented with oats. Sera were obtained from 86 children, 48 in the standard gluten-free group and 38 in the gluten-free oats group, of which 33 consumed at least 10 g of oats daily. IgA and IgG anti-avenin antibodies were monitored at 0, 3, 6 and 12 months. Nitric oxide metabolites were measured in 7 patients, with deviating antibody results. RESULTS: There was a significant decrease in anti-avenin antibodies in both groups at the end as compared to the beginning of the study, (p<0.001), but no difference was found between the two groups. IgA titres already declined after 3 months. IgG titres, although significantly decreased, remained high in the majority of patients in both groups. Nitric oxide levels were high in four of the analysed samples. CONCLUSIONS: Oats per se, do not seem to produce a humoral immune reaction in children with CD when given in an otherwise gluten-free diet, indicating that the reaction requires gluten challenge. Anti-avenin antibodies were equal in the two study groups, and these findings strengthen the clinical impression that oats can be tolerated by the majority of patients with CD.

Antibodies↗
PubMed2003

Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics.

We previously have described a group of patients with gluten sensitivity presenting with ataxia (gluten ataxia) and suggested that this disease entity may account for a large number of patients with sporadic idiopathic ataxia. We have therefore investigated the prevalence of gluten sensitivity amongst a large cohort of patients with sporadic and familial ataxia and looked at possible genetic predisposition to gluten sensitivity amongst these groups. Two hundred and twenty-four patients with various causes of ataxia from North Trent (59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and 7, and Friedreich's ataxia, 132 sporadic idiopathic and 33 clinically probable cerebellar variant of multiple system atrophy MSA-C) and 44 patients with sporadic idiopathic ataxia from The Institute of Neurology, London, were screened for the presence of antigliadin antibodies. A total of 1200 volunteers were screened as normal controls. The prevalence of antigliadin antibodies in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149 out of 1200 (12%) in the normal controls. The prevalence in the sporadic idiopathic group from London was 14 out of 44 (32%). The difference in prevalence between the idiopathic sporadic groups and the other groups was highly significant (P < 0.0001 and P < 0.003, respectively). The clinical characteristics of 68 patients with gluten ataxia were as follows: the mean age at onset of the ataxia was 48 years (range 14-81 years) with a mean duration of the ataxia of 9.7 years (range 1-40 years). Ocular signs were observed in 84% and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white matter hyperintensities in 19%. Forty-five percent of patients had neurophysiological evidence of a sensorimotor axonal neuropathy. Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of patients. Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia. Antigliadin antibody testing is essential at first presentation of patients with sporadic ataxia.

Adolescent↗
PubMed1998

The diagnosis of gluten sensitivity and coeliac disease--the two are not mutually inclusive.

The traditional definition of coeliac disease is inadequate because it includes only patients with abnormal small intestinal morphology. Gluten sensitivity is a systemic disorder whose common factor is an immune response to gluten in the context of the susceptible 'coeliac' HLA haplotype and possibly environmental triggers. Gluten sensitivity embraces traditional coeliac disease as well as subjects with normal small bowel morphology including latent coeliac disease, dermatitis herpetiformis, and symptomatic gluten intolerance. The diagnosis of gluten sensitivity and coeliac disease are not mutually inclusive. Small intestinal biopsy and clinical criteria are essential in diagnosing classical coeliac disease. IgA endomysial antibody is valuable in identifying gluten sensitivity and has particular value as a screening test. Serology should include total IgA levels to exclude selective IgA deficiency, a potential cause of false negative IgA endomysial antibody. A combination of histology, serology and clinical criteria will identify most cases of coeliac disease and gluten sensitivity.

Biopsy↗
PubMed1981

Long-term morphological and immunohistochemical observations on biopsy specimens of small intestine from children with gluten-sensitive enteropathy.

Jejunal biopsy specimens from nine Spanish children with gluten-sensitive enteropathy were studied with morphometric and immunohistochemical techniques in three stages of the diseases: the first biopsy was taken for diagnosis, when the child had a gluten-containing diet, the second after gluten withdrawal, and the third biopsy after gluten-provocation. The findings were compared with those in 10 healthy adults. The villous:crypt ratio and the length of the surface epithelium per stretched millimetre muscularis mucosae were decreased, whereas the number of interepithelial lymphocytes per millimetre surface epithelium was increased when the child had a gluten-containing diet. Although these parameters improved after withdrawal of gluten for at least seven months, they never reached the values of the healthy control group. With the indirect immunoperoxidase technique it was shown that the numbers of IgA-, IgG-, and IgM-containing cells, expressed per "mucosal tissue unit" of 4 micrometer thick and 1 mm wide, were significantly increased during the active phases of the disease. This increase was most striking for the IgM-containing cells. The most sensitive parameters for the histological diagnosis of gluten-sensitive enteropathy are the villous:crypt ratio or the length of the surface epithelium per millimetre muscularis mucosae, the number of interepithelial lymphocytes per millimetre surface epithelium, and the number of IgM-containing cells per millimetre muscularis mucosae.

Celiac Disease↗
PubMed1963

THE NATURE OF THE ANTIPERISTALTIC FACTOR FROM WHEAT GLUTEN.

The ultrafiltrate of an aqueous extract of gluten depressed the peristaltic reflex of the rat isolated jejunum. Further purification increased the activity of the extract 200-fold. Biochemical analysis showed that this purified gluten ultrafiltrate contained over 50% of adenosine. Comparative studies of the effects of adenosine and crude gluten ultrafiltrate were carried out on various biological preparations in vitro and in vivo. Both substances depressed all preparations that contained smooth or cardiac muscle, adenosine being 200- to 1,000-times more active than gluten ultrafiltrate. Large doses of gluten ultrafiltrate were spasmogenic to guinea-pig isolated intestine; this was not found with adenosine. Neither substance had any demonstrable effect on striated muscle or on neuromuscular transmission. Both substances were inactivated by incubation with mammalian small intestinal mucosa and with purified adenosine deaminase. Therefore there seems little doubt that gluten ultrafiltrate owes its antiperistaltic action to its adenosine content.

Antidiarrheals↗
PubMed1982

Effects of gluten on schizophrenics.

Previous studies have suggested that a cereal- and milk-free diet may be beneficial to schizophrenics and that the gluten in regular diets is harmful to schizophrenics. In an effort to replicate these findings, with improved control vehicles, patients on a locked ward were placed on a cereal- and milk-free diet. Thirteen schizophrenics were given gluten-free peanut-flour supplementary cookies and 13 were given virtually identical cookies with gluten added. Tests and rating scales before and after the ten-day study period showed no greater improvement for those receiving the gluten-free cookies than for those receiving the gluten-added cookies. Contrary to expectations, the group receiving gluten-added cookies showed significantly greater improvement of Profile on Mood States measures of tension-anxiety and anger-hostility. Previous findings were not supported. Perhaps a longer time on the diet is required for any beneficial effects to appear.

Adolescent↗
PubMedDate not supplied

Gluten-free diet prevents diabetes in NOD mice.

BACKGROUND: Epidemiological as well as animal studies have shown that environmental factors such as nutrition contribute to the development of diabetes. In this study we investigated whether the early introduction of a gluten-free diet can influence the onset and/or incidence of diabetes, as well as insulitis and the number of gut mucosal lymphocytes, in non-obese diabetic (NOD) mice. METHODS: Gluten-free and standard Altromin diets (with the same milk protein and vitamin content) were given to breeding pairs of NOD mice as well as to the first generation of NOD female mice, which were then observed for 320 days. RESULTS: A substantially lower diabetes incidence (chi(2)=15.8, p=0.00007) was observed in NOD mice on the gluten-free diet (15%, n=27) compared to mice on the standard diet (64%, n=28). In addition, mice on the gluten-free diet developed diabetes significantly later (244+/-24 days SEM) compared to those on the standard diet (197+/-8 days, p=0.03). No differences in the number of CD3(+), TCR-gammadelta(+), IgA(+), and IgM(+) cells in the small intestine were observed. CONCLUSION: We showed that gluten-free diet both delayed and to a large extent prevented diabetes in NOD mice that have never been exposed to gluten.

Animal Feed↗
PubMed2004

Gluten- and casein-free diets for autistic spectrum disorder.

BACKGROUND: It has been suggested that peptides from gluten and casein may have a role in the origins of autism and that the physiology and psychology of autism might be explained by excessive opioid activity linked to these peptides. Research has reported abnormal levels of peptides in the urine and cerebrospinal fluid of persons with autism. If this is the case, diets free of gluten and /or casein should reduce the symptoms associated with autism. OBJECTIVES: To determine the efficacy of gluten- and/or casein- free diets as an intervention to improve behaviour, cognitive and social functioning in individuals with autism. SEARCH STRATEGY: Electronic searching of abstracts from the Cochrane Library (Issue 3, 2003), PsycINFO (1971- May 2003), EMBASE (1974- May 2003), CINAHL (1982- May 2003), MEDLINE (1986- May 2003), ERIC (1965-2003), LILACS (to 2003) and the specialist register of the Cochrane Complementary Medicine Field (January 2004). Review bibliographies were also examined to identify potential trials. SELECTION CRITERIA: All randomised controlled trials involving programmes which eliminated gluten, casein or both gluten and casein from the diets of individuals diagnosed with autistic spectrum disorder. DATA COLLECTION AND ANALYSIS: Abstracts of studies identified in searches of electronic databases were read and assessed to determine whether they might meet the inclusion criteria. The authors independently selected the relevant studies from the reports identified in this way. As only one trial fitted the inclusion criteria, no meta-analysis is currently possible and data are presented in narrative form. MAIN RESULTS: The one trial included reported results on four outcomes. Unsurprisingly in such a small-scale study, the results for three of these outcomes (cognitive skills, linguistic ability and motor ability) had wide confidence intervals that spanned the line of nil effect. However, the fourth outcome, reduction in autistic traits, reported a significant beneficial treatment effect for the combined gluten- and casein- free diet. REVIEWERS' CONCLUSIONS: This is an important area of investigation and large scale, good quality randomised controlled trials are needed.

Autistic Disorder↗
PubMed1977

The immunoglobulin-bearing cells in the lamina propria and the clinical response to a gluten-free diet in dermatitis herpetiformis.

In 17 patients with DH, multiple duodenal and jejunal biopsies were performed. In all patients the small-intestinal biopsy-specimens showed histopathological changes compatible with coeliac disease. Fourteen of the patients maintained a gluten-free diet (GFD) for more than 8 months. The small-intestinal lesions improved in all patients investigated during the GFD. The dosage of Dapsone needed to control the sin lesions could be reduced by more than 50% in 4 patients and the Dapsone could be stopped in 5 other patients on GFD. The immunoglobulin-bearing cells in the lamina propria were counted in 8 patients not on a gluten-free diet, in 6 patients on gluten-free diet, and in 8 healthy controls. The numbers of IgA-, IgM- and IgG-bearing cells were increased in most of the DH patients who were not on a gluten-free diet. The number of IgM-bearing cells in the DH patients who were on a gluten-free diet was the same as that in the control group. This may indicate a mainly IgM response in the lamina propria induced by gluten.

Adult↗
PubMed2005

Gluten: a two-edged sword. Immunopathogenesis of celiac disease.

Celiac disease (CD) is a small intestinal disorder caused by adaptive and innate immune responses triggered by the gluten proteins present in wheat. In the intestine, gluten is partially degraded and modified, which results in gluten peptides that bind with high affinity to HLA-DQ2 or HLA-DQ8 and trigger an inflammatory T cell response. Simultaneously, gluten exposure leads to increased production of IL15, which induces the expression of NKG2D on intraepithelial lymphocytes and its ligand MICA on epithelial cells, leading to epithelial cell destruction. The gluten-specific T cell response results in the production of antibodies against tissue transglutaminase and these are specific indicators of disease. CD is one of the most common inherited diseases, the HLA-DQ locus being the major contributing genetic factor. However, as the inheritance does not follow a Mendelian segregation pattern, multiple other genes, each with relative weak effect, contribute to disease development. An important role for environmental factors, however, can not be ignored as the concordance rate in monozygous twins is considerably less than 100%. The identification of these environmental factors and susceptibility genes may allow a better understanding of disease etiology and provide diagnostic and prognostic markers. The current treatment for CD consists of a life-long gluten-free diet. Although long thought to be impossible, recent results suggest that the development of nontoxic wheat varieties may be feasible, which would aid disease prevention and provide an alternative food source for patients.

Autoantibodies↗
PubMed1988

Occupational asthma from reactivity to an alkaline hydrolysis derivative of gluten.

A 29-year-old female subject had been working for 13 years in a company producing biscuits. She was exposed intermittently to an alkaline hydrolysis wheat gluten derivative (AHGD) that was incorporated into marshmallows. Five years before being referred, she started reporting rhinoconjunctivitis and asthmatic symptoms immediately after handling AHGD. When she was first assessed, she had avoided contact with AHGD for 1 year, and she was asymptomatic. Normal spirometry and bronchial responsiveness to histamine (provocative concentration causing a 20% fall in FEV1, 22 mg/ml) were obtained. There was a positive allergy skin test to ragweed pollen and to AHGD at 0.01 mg/ml. Skin tests with individual extracts of cereals, including wheat, were negative. Inhalation challenge with AHGD for 15 seconds caused immediate rhinoconjunctivitis and bronchoconstriction (maximum fall of 40% in FEV1 30 minutes after the exposure) with complete recovery 2 hours later. There was no reaction thereafter, and the provocative concentration of histamine causing a 20% fall in FEV1 was not significantly changed (13.1 mg/ml) 9 hours after the challenge. Inhalation challenge with wheat flour containing native gluten for 30 minutes did not cause any symptoms or significant change in FEV1. IgE RAST counts were greater with the AHGD than with gluten and the whole wheat extract; the opposite was generally found with sera from individuals with baker's asthma and wheat food allergy. With the serum of the affected worker, AHGD completely inhibited the corresponding RAST, but gluten did not. With wheat food allergy, AHGD was relatively inactive inhibition of the wheat and gluten RAST, but gluten was effective.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Dietary gluten and learning to attend to redundant stimuli in rats.

The purpose of the present study was to assess the effect of a high-gluten diet against a gluten-free diet on learning stimulus-response relationships in rats. In the first phase of training rats learned to associate a stimulus light with responding on a particular response lever. In the second phase, the same rats were exposed to new, but redundant stimuli to guide responding (a tone and houselight). Probe trials, involving only new stimuli, revealed that rats fed a gluten-free diet displayed a "blocking" effect. That is, gluten-free rats did not learn to associate these new stimuli with particular responses. In contrast, high-gluten rats very quickly learned to use these redundant stimuli to guide responding. Subsequent phases of training demonstrated, however, that this group difference could be removed. The present findings are discussed in the context of the possible links between dietary gluten and schizophrenia.

Acoustic Stimulation↗
PubMedDate not supplied

Gluten-sensitive enteropathy in Irish setter dogs: characterisation of jejunal microvillar membrane proteins by two-dimensional electrophoresis.

This study investigated whether gluten-sensitive enteropathy (GSE) in Irish setter dogs was associated with underlying structural abnormalities of microvillar membrane proteins. Jejunal biopsies taken from eight-month-old GSE-affected dogs reared on a normal, gluten-containing diet exhibited partial villous atrophy and contained more intra-epithelial lymphocytes than controls. The morphological abnormalities were reversed by feeding a gluten-free diet for five months and the changes were accompanied by an increase in the mucosal activity of the microvillar hydrolases, particularly aminopeptidase N and dipeptidyl aminopeptidase IV, which reverted to pre-treatment levels after a gluten challenge. Two-dimensional electrophoresis of microvillar membrane proteins isolated from GSE-affected dogs revealed an essentially normal protein map that was comparable to controls. The exception was an intense 85 kDa protein spot that diminished when the affected dogs were fed a gluten-free diet and re-intensified after a gluten challenge.

Alkaline Phosphatase↗
PubMed2004

Biodegradability of wheat gluten based bioplastics.

A large variety of wheat gluten based bioplastics, which were plasticized with glycerol, were subjected to biodegradation. The materials covered the total range available for the biochemical control parameter Fi, which expresses the percentage of aggregated proteins. This quantity can be related to the density of covalent crosslinks in the wheat gluten network, which are induced by technological treatments. The biodegradability tests were performed in liquid medium (modified Sturm test) and in farmland soil. All gluten materials were fully degraded after 36 days in aerobic fermentation and within 50 days in farmland soil. No significant differences were observed between the samples. The mineralization half-life time of 3.8 days in the modified Sturm test situated gluten materials among fast degrading polymers. The tests of microbial inhibition experiments revealed no toxic effects of the modified gluten or of its metabolites. Thus, the protein bulk of wheat gluten materials is non-toxic and fully biodegradable, whatever the technological process applied.

Biocompatible Materials↗
PubMed2002

Soybean hulls, wheat middlings, and corn gluten feed as supplements for cattle on forage-based diets.

Soybean hulls, wheat midds, and corn gluten feed are viable alternative supplements for forage-fed cattle. All three result from the processing of major Unites States agricultural crops, so large supplies are available. Their value is better for ruminant animals than for monogastrics because they contain digestible fiber components. These byproducts are widely available throughout the Unites States and will generally be more economical than traditional feed grains or commercial feeds when used appropriately as supplements to forage-based diets. Knowledge about the composition of base forage must be used in planning supplementation strategies because base forages vary in protein and mineral content [9]. Soybean hulls alone may be a good selection in situations in which forages are adequate or high in protein. In situations where forage is marginal or deficient in protein, wheat midds, corn gluten feed, or a mix of soybean hulls and corn gluten feed might be most desirable. All three feeds can be variable in nutrient composition, so they should be analyzed to ensure a balanced nutrient level in diets. Soybean hulls are especially variable in crude protein content and should always be analyzed when forages are marginal or deficient in protein. Despite the fact that published energy levels are substantially lower, research has shown that soybean hulls and wheat midds have a value comparable to corn and soybean meal in forage-based diets. Corn gluten feed has also been comparable to corn and soybean meal in most reports but is closer in value to its published energy levels. In general, results with soybean hulls have been surprisingly good and consistent, whereas responses to wheat midds and corn gluten feed supplementation have been more variable and sometimes disappointing. Feeding rates for soybean hulls can range from low to extremely high depending on forage availability and desired performance. Wheat midds should be limited in most situations to 50% of the expected dry matter intake because of their rapidly digested starch content. Corn gluten feed should be limited to approximately 50% of expected dry matter intake because of its high sulfur content. Several research groups are currently evaluating self-feeding programs for these byproducts, and while the potential for health and production problems exist, results have been encouraging in most cases. Self-feeding would reduce the labor costs of hand feeding and could provide backgrounders with a program to expand cattle numbers on a limited land base.

Animal Feed↗