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At least 397 records · Page 22Linked to original sources
PubMed1978

Re-evaluation of the techique of organ culture for studying gluten toxicity in coeliac disease.

In vitro cytotoxicity of four different gluten fractions was tested in organ culture for up to 48 hours using flat intestinal biopsies from children with coeliac disease. The fractions were (1) a peptic-tryptic digest of gliadin containing a moderate amount of alpha-gliadin, (2) a peptic-tryptic digest of gluten (Frazer fraction III) froma strain of wheat with a high content of alpha-gliadin, (3) alpha-gliadin, and (4) alpha-GT-18,000, a tryptic fragment of alpha-gliadin. The latter three fractions were toxic to coeliac patients in vivo. In vitro, however, none of these fractions proved to be cytotoxic. When added to the culture medium they were not capable of inhibiting the regeneration of the surface epithelium as visualised by histology and electron microscopy. The only difference between cultures with and without gluten fractions was that the former produced slightly more mucus when maintained in vitro as observed in the dissecting microscope. Furthermore, for Frazer fraction III the absence of apparent toxicity was confirmed by the behaviour of brush border enzyme activities during culture. Our results are not in accordance with those reported in the literature. We believe that the criteria used at the present time for the assessment of gluten toxicity in vitro should be extended to include the process of enterocyte desquamation.

Celiac Disease↗
PubMed1981

HLA-B8 and cell-mediated immunity to gluten.

The leucocyte migration inhibition (LMI) test was used as an indicator of cell mediated immunity to gluten fraction III in 30 healthy controls and 58 patients with adult coeliac disease and the results related to HLA status and duration of treatment with a gluten-free diet. HLA-B8 controls showed significantly lower leucocyte migration indices, indicating greater immune response, than non-HLA B8 controls. Untreated coeliacs showed no difference from HLA-B8 controls. There was no difference between results from HLA-B8 and non-HLA-B8 coeliacs. Leucocyte migration was even lower in coeliacs early in treatment but rose after treatment for over one year. These results may reflect an immune response gene for gluten in linkage disequilibrium with HLA-B8. The increased immune response to gluten as measured in this test cannot be the sole factor in aetiology of coeliac disease. Furthermore, it is necessary to re-evaluate earlier results of cell-mediated immunity in coeliac disease with reference to HLA status of the controls.

Celiac Disease↗
PubMed1983

Effect of gluten-free diet on splenic hypofunction of adult coeliac disease.

Splenic function has been serially measured by counting pitted red cells in 15 coeliac patients, before and during a gluten-free diet. The basal percentage values of pitted cells decreased significantly during treatment but no correlation was observed between the duration of the gluten-free diet and the percentage of recovery of splenic function over basal values. Out of six coeliacs with pitted cell values consistent with splenic hypofunction, three showed a total recovery after gluten withdrawal. Our data suggest that, contrary to recent reports, hyposplenism in adult coeliac disease is improved by a gluten-free diet, and that environmental factors may be important in determining and maintaining this complication.

Adult↗
PubMed1985

Acute gluten challenge in treated adult coeliac disease: a morphometric and enzymatic study.

Using a Quinton hydraulic biopsy tube, jejunal biopsies were obtained from 10 patients with adult coeliac disease in remission and four healthy volunteers before and after administration of gluten fraction III into the proximal duodenum. The biopsies taken at hourly intervals for four hours, were analysed for changes in brush border enzymes, light microscopic appearances, and villous and crypt population counts. The results indicate that mucosal damage occurs within three to four hours of gluten administration with significant falls in brush border enzyme concentrations and villous population counts. The absence of any change in control biopsies indicates that gluten sensitivity is specific to the mucosa of patients with coeliac disease, the timing of the changes being consistent with a type III immune response or direct toxicity. Some recovery of the brush border enzymes but not the villous population was evident 24 hours after gluten administration while the crypt population showed evidence of a compensatory hyperplastic reaction.

Adult↗
PubMed1987

Cellular hypersensitivity to gluten derived peptides in coeliac disease.

Wheat gluten derived antigens have been tested for their ability to inhibit the migration of leucocytes from healthy subjects and patients with coeliac disease. Three preparations of a water soluble fraction (Frazer's fraction III, FIII) of partial peptic tryptic digests of wheat gluten had different effects in a direct (one stage) assay. Subfractions B and B2 caused migration inhibition of leucocytes from patients with treated coeliac disease but not of leucocytes from healthy volunteers or patients with Crohn's disease or ulcerative colitis. This migration inhibition seems to be specific for gluten fractions because maize zein fraction B, beta-lactoglobulin and ovalbumin did not cause it. The sensitivity of coeliac leucocytes to fraction B is not related to factors present in coeliac serum as the migration of leucocytes from healthy individuals preincubated with coeliac sera was not inhibited. Puromycin diminished inhibition by fraction B, which was active at 1.2 micrograms/ml in an indirect (two stage) migration inhibition assay; this is consistent with a process involving elaboration of lymphokine(s). More highly purified fractions of B2, P1-P4 were prepared by reverse phase high performance liquid chromatography (HPLC) and showed differing potency in direct and indirect assays, with P4 being the most active fraction. Inhibition of migration by gluten derived peptides appears to result from the release of lymphokine by leucocytes specifically from coeliac patients.

Antigens↗
PubMed1982

Studies of intestinal lymphoid tissue. IV--The predictive value of raised mitotic indices among jejunal epithelial lymphocytes in the diagnosis of gluten-sensitive enteropathy.

It has been established that considerable blast-transformation and mitotic activity occurs among epithelial lymphocytes of untreated coeliac mucosa. This paper is concerned solely with the proliferative activity of epithelial lymphocytes (expressed as percentage "mitotic index") in the prospective diagnosis of coeliac disease, in comparison with other conditions such as lymphoma. Crohn's disease and immunodeficiency which are often associated with malabsorption and flattening of jejunal mucosa. The results demonstrate that a high mitotic index (greater than 0.2%) clearly distinguishes, and hence predicts, gluten-associated enteropathies (including dermatitis herpetiformis and malignant histiocytosis) from others in which gluten plays no aetiological role and where the mitotic index differs insignificantly from normal control mucosae (much less than 0.2%). Furthermore, it has been demonstrated that the mitotic index is raised in so-called "non-responsive coeliacs," thus suggesting that such patients may also be gluten-sensitive despite their subsequent failure to respond morphologically to dietary gluten restriction.

Adolescent↗
PubMedDate not supplied

Failure of added dietary gluten to induce small intestinal histopathological changes in patients with watery diarrhea and lymphocytic colitis.

Lymphocytic colitis is a form of microscopic colitis usually characterized by watery diarrhea and often associated with biopsy-defined celiac disease. Two patients with lymphocytic colitis and normal small intestinal biopsies who were administered 40 g of added dietary gluten for four consecutive weeks are presented. Small intestinal biopsies from multiple sites in the proximal small bowel were done after three and four weeks to determine whether pathological changes in latent celiac disease could be induced in these patients with a high gluten-containing diet. In addition, colorectal biopsies were done to determine whether the colitis was sensitive to oral gluten. No alterations in the small intestinal biopsies were detected in either patient and no changes occurred in colitis severity. Although microscopic forms of colitis have been linked to celiac disease, this study indicates that lymphocytic colitis is a heterogeneous clinicopathological disorder that, in some patients, is independent of any gluten-induced intestinal pathological changes.

Biopsy↗
PubMed2001

In vivo gluten challenge in celiac disease.

In vivo gluten challenge has been used since the early 1950s to study the role of cereal fractions in celiac disease. While early studies relied on crude indicators of celiac toxicity, the advent of jejunal biopsy and sophisticated immunohistochemical techniques has allowed accurate studies to be performed. Studies to determine the nature of the cereal component that is toxic to patients with celiac disease have concentrated on wheat because of its nutritional importance. A number of in vitro studies indicated the presence of one or more celiac-activating epitopes with the N-terminus of the A-gliadin molecule. In vivo challenge with three synthetic peptides subsequently indicated the toxicity of a peptide corresponding to amino acids 31 to 49 of A-gliadin. In vivo gluten challenge is the gold standard for the assessment of celiac toxicity; however, jejunal biopsy is a relatively invasive procedure, thus, other methods have been investigated. Direct infusion of the rectum with gluten has been shown to result in an increase in mucosal intraepithelial lymphocytes, occurring only in celiac patients. This method has been used to study the celiac toxicity of gliadin subfractions. The in vitro technique of small intestinal biopsy organ culture is also a useful tool and appears to give the same results as in vivo challenge. The importance of tiny amounts of gliadin in the diet, such as that which occurs in wheat starch, has been studied by in vivo challenge; this technique has clarified the position of oats in the gluten-free diet. Several studies suggest that this cereal may be included in the diet of most adult celiac patients. Studies of the transport of gliadin across the enterocyte following ingestion or challenge suggest that gliadin may be metabolized by a different pathway in celiac disease. This could result in an abnormal presentation to the immune system, triggering a pathogenic rather than a tolerogenic response.

Adult↗
PubMed1998

Gluten stimulation induces an in vitro expansion of peripheral blood T gamma delta cells from HLA-DQ2-positive subjects of families of patients with celiac disease.

The intestinal gluten sensitivity formally known as celiac disease (CD) is characterized by an evident involvement of local immune response and it is associated with the expression of HLA-DQ2 allele. The major role in the disease seems to be played by the T lymphocyte population bearing gamma delta T cell receptor (T gamma delta cells) which are increased both in peripheral blood and intestinal mucosae of celiac patients. In this paper data on the effects of in vitro gluten stimulation on lymphocytes expressing the T gamma delta phenotype are reported. Gluten seems to be able to induce the expansion of the T gamma delta cell population both in CD patients and their HLA-DQ2-positive asymptomatic relatives, in spite of the absence of clinical evidence of the disease. In addition, the evaluation of gluten-induced cytokine production shows that interleukin-4 could be implied in the early phases of pathogenesis of CD.

Adolescent↗
PubMed1993

Coeliac disease and gluten-free diet: a following-up study of fifteen young adults.

Fifteen patients with coeliac disease diagnosed in infancy and early childhood between 1959 and 1971 were included in the study. The primary diagnosis was made on the basis of typical symptoms and signs, stool examination for fat, xylose test and clinical and laboratory improvement after introduction of gluten-free diet. All patients were challenged with gluten for a minimum of 4 weeks to 4 years before a peroral proximal jejunal biopsy was performed between 1973 and 1976. The biopsy specimen showed changes consistent with coeliac disease in all patients. Gluten-free diet induced again clinical recovery and was recommended as a life-long diet. The patients were reinvestigated after 15-18 years (mean 17 years) and 13 biopsies were evaluated. Five of these biopsy specimens showed variable histopathological changes. Only 5 patients were still on a strict gluten-free diet. There was no correlation between the presence of gastro-intestinal symptoms and abnormal biopsies. All patients had haematological tests within the normal range. Anti-gliadin IgA levels above the upper normal limit were found in 2 out of 3 patients with grade IV histopathological changes in the mucosa, and in 1 of the patients on a normal diet who refused to have a biopsy performed. The patients' knowledge of their disease was evaluated, and suitable follow-up programs for coeliac patients are discussed.

Biopsy↗
PubMed1988

Levels of circulating IgA immune complexes after gluten-rich diet in patients with IgA nephropathy.

Measurement of IgA circulating immune complexes (IgA-CIC) in sera from patients with IgA nephropathy after a gluten-poor diet, an unrestricted diet and a gluten-rich diet is described. High levels of IgA-CIC in sera were detected in patients after these diets. However, the levels of IgA-CIC in sera 2 weeks after the gluten-rich diet were not significantly increased compared with those after the other diets. It is suggested that, for a short duration, the gluten-rich diet might not increase the levels of IgA-CIC in sera from Japanese patients with IgA nephropathy.

Adolescent↗
PubMed2005

Gluten-free diet may alleviate depressive and behavioural symptoms in adolescents with coeliac disease: a prospective follow-up case-series study.

BACKGROUND: Coeliac disease in adolescents has been associated with an increased prevalence of depressive and disruptive behavioural disorders, particularly in the phase before diet treatment. We studied the possible effects of a gluten-free diet on psychiatric symptoms, on hormonal status (prolactin, thyroidal function) and on large neutral amino acid serum concentrations in adolescents with coeliac disease commencing a gluten-free diet. METHODS: Nine adolescents with celiac disease, aged 12 to 16 years, were assessed using the semi-structured K-SADS-Present and Lifetime Diagnostic interview and several symptom scales. Seven of them were followed at 1 to 2, 3, and 6 months on a gluten-free diet. RESULTS: Adolescent coeliac disease patients with depression had significantly lower pre-diet tryptophan/ competing amino-acid (CAA) ratios and free tryptophan concentrations, and significantly higher biopsy morning prolactin levels compared to those without depression. A significant decrease in psychiatric symptoms was found at 3 months on a gluten-free diet compared to patients' baseline condition, coinciding with significantly decreased coeliac disease activity and prolactin levels and with a significant increase in serum concentrations of CAAs. CONCLUSION: Although our results of the amino acid analysis and prolactin levels in adolescents are only preliminary, they give support to previous findings on patients with coeliac disease, suggesting that serotonergic dysfunction due to impaired availability of tryptophan may play a role in vulnerability to depressive and behavioural disorders also among adolescents with untreated coeliac disease.

Adolescent↗
PubMed1992

Scanning electron microscopy of the small intestine during gluten-challenge in celiac disease.

The celiac disease syndrome is characterized by structural and ultrastructural alterations of the small intestine mucosa. According to criteria by European Society of Paediatric Gastroenterology and Nutrition, the conclusive diagnosis of celiac disease in children depends on the demonstration of histological relapse of the mucosa after reintroduction of gluten in the diet, as this syndrome is a permanent condition of gluten intolerance. Under these diseased conditions, the structure of the intestinal villi has been studied by light microscopy; morphological alterations were revealed only when the gluten challenge induced a clinical relapse. Scanning electron microscopy analyses of the intestinal mucosa in celiac diseased patients showed a strikingly uniform destruction of the villi with changes in their dimensions and arrangement. At high magnification the enterocytes were irregular in size and shape with a decrease and disruption of the glycocalyx. Reductions in length and density of microvilli were also clearly identified. Although these scanning electron microscopy findings could not demonstrate a relationship between the degrees of mucosal atrophy and the duration of the gluten challenge, they nevertheless revealed early stages of fine villous alterations that cannot be detected by the presently employed low resolution light microscopic techniques.

Autopsy↗
PubMed1993

Rectal epithelial gamma/delta T-lymphocyte responses to local gluten challenge in coeliac disease.

The proportion of intra-epithelial lymphocytes (IEL) that utilize the gamma/delta form of the T-cell receptor (TCR) is increased in coeliac disease, but their function remains unexplained. The response of intra-epithelial lymphocytes to rectal gluten challenge in coeliac and control subjects was studied after a rectal challenge of 2 g of Frazer's fraction III. A marked rise in CD3+ IEL occurred after challenge in the coeliac patients, peaking at 6 h and returning to normal by 48 h, with no significant changes in the gamma/delta TCR+ IEL. The IEL did not significantly change after gluten challenge in the controls. Acute gluten challenge induces infiltration of the rectal mucosa by T cells in coeliac patients, which is not accompanied acutely by increased numbers of gamma/delta TCR+ IEL. This study supports the hypothesis that alpha/beta TCR+ T cells may be of importance in the early response of coeliac patients to local gluten challenge.

Adult↗
PubMed1989

Corn gluten meal and blood meal mixture for dairy cows in midlactation.

Twelve midlactation Holstein cows were assigned to a switchback design with 4-wk periods to compare a corn gluten meal and blood meal mixture with soybean meal as supplemental protein sources. All experimental diets contained 60% ammoniated corn silage, on a dry basis, and a corn and oats (2:1) basal concentrate mixture. Diets were: urea control (12.5% CP); soybean meal (16.1% CP); low protein (14.3% CP) corn gluten and blood meal mixture; and high protein (16.8% CP) corn gluten and blood meal mixture. Cows fed the control diet consumed less DM, and produced less milk containing a lower percentage of protein than cows fed other diets. Protein efficiency and milk fat percentage were higher for cows fed the control diet than for cows fed the natural protein diets. Fat-corrected milk and fat yields did not differ among diets. The high protein diets (16.1 and 16.8% CP) decreased protein efficiency and increased SNF percentage. Milk yield per unit of DM intake was higher when cows fed the lower degradable protein source (corn gluten-blood meal) than when they were fed soybean meal. The low degradable protein mixture produced a similar lactation response to soybean meal at both the high and low concentrations of total dietary protein. This study indicates that the dietary protein and undegradable protein concentration needed by midlactation Holstein fed complete mixed diets may be lower than generally recommended.

Amino Acids↗
PubMed1979

Effect of low protein diets on free amino acids in plasma of young men: effect of wheat gluten diet.

Studies were made on alterations in plasma amino acids in young men fed a diet containing graded levels of wheat gluten. After one week on a standard diet containing 200 mgN/kg of mixed protein (animal protein content 45%), 38 young men were given a wheat gluten diet containing 170, 100, 60, 30, 15 or zero mgN/kg for 2 weeks. Blood samples measuring plasma free amino acids were taken before breakfast at the end of the periods on a standard diet and an experimental diet. In subjects on diets containing 170 to 30 mgN/kg the plasma concentrations of threonine, valine, methionine, leucine, tyrosine, phenylalanine, serine, histidine and arginine fell significantly with decrease in protein intake, but the concentration of alanine increased significantly. On the other hand, in subjects on diets containing 15 or zero mgN/kg, the plasma concentrations of the essential amino acids did not decrease, but increased to slightly more than in subjects on a diet containing 30 mgN/kg, and the alanine and glycine concentrations increased steadily. Values for plasma lysine varied from 146 +/- 22 to 194 +/- 31 mumoles/liter with gluten intakes of 170 to zero mgN/kg, but were comparable with that of 186 +/- 33 mumules/liter in subjects on a standard diet, showing that the plasma lysine concentration did not clearly reflect the dietary concentration of lysine in young men on a wheat gluten diet.

Adult↗
PubMed1996

Dietary wheat gluten alleviates the elevation of serum transaminase activities in D-galactosamine-injected rats.

The effects of dietary protein on the elevation of activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in D-galactosamine-injected rats were investigated. The rats fed with experimental diets containing test protein sources for 2 weeks were injected with D-galactosamine (0.8 g.kg-1 body weight). The activities of AST and ALT in serum were assayed after 20 h. According to the results, these enzyme activities in the rats fed 40% casein diet were higher than those of 5, 10, or 20% casein groups. In the 40% gluten group, these enzyme activities were lower than in the 40% casein group. This difference was not considered to be caused by the deficit of L-lysine and L-threonine in gluten. The extent of the reduction of UTP and UDP-glucose in liver by D-galactosamine was almost the same in the 40% gluten and 40% casein groups. These results suggest that levels and quality of dietary protein affect the susceptibility of animals to the hepatotoxin D-galactosamine and dietary gluten was found to alleviate the elevation of serum transaminases in rats by the drug.

Alanine Transaminase↗
PubMed2007

Malignancy and mortality in a population-based cohort of patients with coeliac disease or "gluten sensitivity".

AIM: To determine the risk of malignancy and mortality in patients with a positive endomysial or anti-gliadin antibody test in Northern Ireland. METHODS: A population-based retrospective cohort study design was used. Laboratory test results used in the diagnosis of coeliac disease were obtained from the Regional Immunology Laboratory, cancer statistics from the Northern Ireland Cancer Registry and mortality statistics from the General Registrar Office, Northern Ireland. Age standardized incidence ratios of malignant neoplasms and standardized mortality ratios of all-cause and cause-specific mortality were calculated. RESULTS: A total of 13 338 people had an endomysial antibody and/or an anti-gliadin antibody test in Northern Ireland between 1993 and 1996. There were 490 patients who tested positive for endomysial antibodies and they were assumed to have coeliac disease. There were 1133 patients who tested positive for anti-gliadin antibodies and they were defined as gluten sensitive. Malignant neoplasms were not significantly associated with coeliac disease; however, all-cause mortality was significantly increased following diagnosis. The standardized incidence and mortality ratios for non-Hodgkin's lymphoma were increased in coeliac disease patients but did not reach statistical significance. Lung and breast cancer incidence were significantly lower and all-cause mortality, mortality from malignant neoplasms, non-Hodgkin's lymphoma and digestive system disorders were significantly higher in gluten sensitive patients compared to the Northern Ireland population. CONCLUSION: Patients with coeliac disease or gluten sensitivity had higher mortality rates than the Northern Ireland population. This association persists more than one year after diagnosis in patients testing positive for anti-gliadin antibodies. Breast cancer is significantly reduced in the cohort of patients with gluten sensitivity.

Adolescent↗