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At least 19 recordsLinked to original sources
PubMed1999

Dietary analysis in symptomatic patients with coeliac disease on a gluten-free diet: the role of trace amounts of gluten and non-gluten food intolerances.

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

Adult↗
PubMed1992

Glass transition of gluten. 1: Gluten and gluten-sugar mixtures.

The glass transition in hydrated wheat gluten has been studied using dynamic mechanical thermal analysis, differential scanning calorimetry, pulsed nuclear magnetic resonance and a three point bend test. The results for gluten alone are in good agreement with results obtained by other workers for gluten and glutenin. In contrast to their effect on the Tg of amylopectin, a gluten:sugar ratio of 10:1 (where the sugar is amorphous fructose, sucrose or glucose) has little effect on the glass transition temperature, as a function of water content. A sample containing gluten and fructose in the ratio 2:1 showed plasticization due to the sugar.

Calorimetry, Differential Scanning↗
PubMed1980

Gluten-sensitive enteropathy. Influence of histocompatibility type on gluten sensitivity in vitro.

We previously developed an in vitro organ culture system in which gluten exerts a toxic effect on intestinal mucosa of patients with active gluten-sensitive enteropathy. Gluten generally inhibits the epithelial cell maturation of intestinal biopsy specimens that otherwise occurs if the tissue is cultured for 24-48 h in a gluten-free medium. However, small intestinal mucosa from 15-20% of patients with proven gluten-sensitive enteropathy fails to manifest the expected gluten-induced damage in vitro. In the present study, we explored the relation between in vitro gluten-induced intestinal damage and the presence of HLA-B8. We determined whether the patients' histocompatibility type (HLA-B8 positive or negative) influenced the ability of gluten protein to inhibit epithelial cell maturation of cultured intestinal biopsy specimens from patients with gluten-sensitive enteropathy. Intestinal biopsies from 21 of 24 patients with gluten-sensitive enteropathy and HLA-B8 showed gluten-induced damage in vitro. On the other hand, intestinal biopsies from only 4 of 16 patients with gluten-sensitive enteropathy but without HLA-B8 showed gluten-induced damage in vitro. The difference in the effect of gluten in vitro between these two groups was statistically significant (P < 0.01). The data show a dichotomy between gluten-induced tissue damage in vivo and in vitro in HLA-B8 negative patients, suggesting that HLA-B8 is important for gluten to manifest a cytotoxic influence in organ culture.

Alkaline Phosphatase↗
PubMed1998

Characterization of intestinal morphologic, biochemical, and ultrastructural features in gluten-sensitive Irish Setters during controlled oral gluten challenge exposure after weaning.

OBJECTIVE: To characterize histologic, biochemical, and ultrastructural changes in the intestine of Irish Setters susceptible to gluten-sensitive enteropathy (GSE) during controlled oral challenge exposure with gluten after weaning. ANIMALS: Six gluten-sensitive and 12 healthy Irish Setters and 3 healthy Greyhounds. PROCEDURE: Jejunal biopsy specimens were taken at 4 and 12 months of age from the 6 gluten-sensitive Irish Setters, which had been reared on a gluten-free diet to which a controlled dose of gluten (0.5 g/kg of body weight/d) was added. Control specimens were obtained at 4 (n = 5) and 12 (7) months of age from the healthy Irish Setters, which had been fed a conventional gluten-containing diet, and at 4 months of age from the healthy Greyhounds fed the controlled dose of gluten. The specimens were subjected to histologic and ultrastructural examinations and assay of brush border enzymes. RESULTS: Gluten-sensitive Irish Setters developed abnormalities characteristic of GSE at 4 months. Abnormalities were comparable to changes not seen previously until 12 months in dogs with GSE fed a conventional gluten-containing diet. In addition, microvilli were stunted and irregular, and a few were vesiculated and reduced in number; the glycocalyx was reduced or absent. By 12 months of age, there was improvement in morphologic and biochemical parameters, indicating partial recovery despite continued exposure to gluten. CONCLUSIONS: Relative early onset of intestinal damage, compared with that previously reported, and subsequent partial recovery suggestive of oral tolerance to gluten may be attributable to oral administration of gluten as a purified extract rather than in dietary cereal, but alternative explanations include differences in environment or genetic susceptibility to gluten.

Alkaline Phosphatase↗
PubMed2001

Gluten challenge in borderline gluten-sensitive enteropathy.

OBJECTIVES: In patients with signs and symptoms of malabsorption, suggestive of gluten-sensitive enteropathy, small intestinal biopsies sometimes only reveal infiltration of lymphocytes into the mucosal epithelium. This infiltrative lesion (Marsh I) is not a definite proof for gluten-sensitive enteropathy. However, in the present study, we aimed to show that a subgroup of these patients could ultimately be identified as being gluten sensitive. METHODS: A total of 38 patients with a Marsh I lesion were subjected to a gluten challenge comprising 30 g of gluten added daily to a normal gluten-containing diet for 8 wk. Before and after the challenge, small intestinal biopsies were taken, and symptoms and signs of malabsorption were scored. RESULTS: In 12 patients we demonstrated a significant change in mucosal histopathology, i.e., subtotal villous atrophy (Marsh IIIB, n = 1), partial villous atrophy (Marsh 3A, n = 6) or infiltrative-crypthyperplastic lesions (Marsh II, n = 5). In the other 26 patients, the small intestinal mucosa remained unchanged. After initiation of a gluten-free diet, follow-up small intestinal biopsies in 12 patients who initially had progressive mucosal pathology after gluten challenge showed normalization of mucosal pathology in seven cases, regression to a Marsh I lesion in four, and to a Marsh II lesion in one. Symptom relief was seen in all 12 patients. Ten of 26 patients without histological response to the gluten challenge were motivated to adhere to a gluten-free diet. Follow-up biopsies revealed unchanged Marsh I lesions in eight patients and normalization (Marsh 0) in two patients. Three patients had follow-up biopsies while on a normal diet. All had unchanged Marsh I lesions. CONCLUSIONS: In the present study we demonstrated that a gluten challenge might be useful in identifying patients as being sensitive to gluten if initial small intestinal biopsies reveal only minor abnormalities.

Adolescent↗
PubMed1976

Gluten-sensitive enteropathy. Inhibition by cortisol of the effect of gluten protein in vitro.

Cortisol partially prevents the harmful effect of gluten on the jejunal mucosa of patients with gluten-sensitive enteropathy. To investigate further the pathogenesis of this disorder, we analyzed the effect of cortisol in cultures of jejunal specimens obtained by biopsy. Cultures were done with and without gluten or cortisol. Morphology and alkaline phosphatase activity were assessed before and after 24 hours. Biopsies from untreated patients cultured with gluten showed low enzyme values and cuboidal epithelial cells before and after culture. Biopsies cultured in a gluten-free medium showed a threefold increase in enzyme values (P less than 0.01) and morphologic improvement with change to columnar epithelial cells. Cultures with gluten plus cortisol showed rises in alkaline phosphatase and morphologic improvement indistinguishable from cultures without gluten. Cortisol and gluten had no effect on cultures from appropriate controls. Cortisol thus prevents the harmful effects of gluten on biopsies from patients with gluten-sensitive enteropathy in vitro.

Adolescent↗
PubMed2003

Evaluation of residual immunoreactivity in red and white wines clarified with gluten or gluten derivatives.

Gluten or hydrolyzed gluten could be a suitable alternative to animal proteins in the wine clarification process, but their residues could represent a risk for individuals suffering from coeliac disease or allergic to cereal proteins. The aim of this study was to investigate the presence of gluten in wines treated with gluten or its hydrolysate in the clarification process and to assess its antigenicity in commercial products. The presence of residual immunoreactive gluten was evaluated by electrophoresis (SDS-PAGE) and immunoblotting. Data obtained in several red and white wine samples showed that no residue was detectable in any of the red wines. In white wines, gluten reduced the protein content less completely, but most samples showed no immunoreactivity after the wine had been treated with gluten or its derivatives, either alone or combined with bentonite, silica gel or tannins. The use of gluten derivatives coupled with bentonite was the most effective method of removing immunoreactive protein in white wines. In conclusion, the use of gluten derivatives in wine clarification seems to exclude a risk for subjects susceptible to coeliac disease or gluten allergy. However, it is recommended that wine producers continuously monitor the clarification process in order to protect the most sensitive individuals.

Antigens↗
PubMed2000

Time course of nitric oxide synthase generation after gluten exposure in the rectal mucosa of gluten-sensitive patients.

BACKGROUND: Nitric oxide is thought to play an important role in modulating chronic inflammatory responses as well as in immune-mediated inflammation. We reproduced a gluten-mediated mucosal response in the rectum of celiac and control subjects in order to determine the role of inducible and constitutive nitric oxide synthases in the pathogenesis of this process. MATERIAL: Nine patients with confirmed celiac disease and five healthy controls underwent a long-term rectal gluten challenge (48 h) after an enema of 6 g of crude gluten, and constitutive and inducible nitric oxide synthase activity were determined in rectal biopsies. The histological localization of inducible nitric oxide synthase was determined by immunohistochemistry. RESULTS: Activity of both isoforms of nitric oxide synthase in control subjects did not change significantly after gluten instillation. In celiac patients, constitutive nitric oxide synthase on rectal mucosa also showed no significant changes after challenge with gluten. Inducible nitric oxide synthase isoform exhibited a modest increase 4 h after gluten instillation in celiac patients (mean increase 35% compared with baseline levels) but, 8 h after challenge, generation of iNO synthase was significantly higher: 54% more than pre-challenge production (P < 0.05) and higher than control values (P < 0.05). Inducible nitric oxide synthase staining was mostly localized in mononuclear cells of the epithelium and the lamina propria. After gluten instillation, the enhanced staining was mainly localized in subepithelial areas of the lamina propria. CONCLUSION: Our data suggest a role for nitric oxide, generated by inducible nitric oxide synthase, in the process of rectal mucosa injury by local gluten instillation in sensitized patients. We could not, however, determine if the role of nitric oxide in the ensuing injury of this gluten-induced immune inflammation model is a protective one, or merely a by-product generated by the activation of the inflammatory cells.

Adult↗
PubMed1998

Insulin-like growth factor axis of gluten-sensitive dogs during a gluten challenge.

Eight gluten-sensitive Irish setters underwent a gluten challenge to investigate changes in the insulin-like growth factor (IGF) axis. In the first study, they were challenged with an acute intraduodenal administration of tryptic-peptic gluten digest and then maintained on dietary gluten for three months. In the second study, the challenge came solely from dietary gluten fed for three months. After the acute intraduodenal administration of gluten, serum IGF-I levels decreased significantly by 21.8 per cent, (P = 0.01) on day 3 after challenge and then returned to normal. There was also a decrease (52.5 per cent, P < 0.03) in the levels of serum IGF-binding protein-3 (IGFBP-3) until day 14 after challenge but they had returned to normal by day 28. In two dogs IGFBP-3 levels decreased through specific serum protease activity. There were no changes in serum IGF-I or IGFBP levels during the second study after the dietary gluten challenge alone, or in four non-gluten-sensitive beagles studied as controls during the acute intraduodenal/dietary gluten challenge.

Animals↗
PubMed1983

Gluten-free diet in patients with dermatitis herpetiformis. Effect on the occurrence of antibodies to reticulin and gluten.

In a prospective study of 51 patients with dermatitis herpetiformis (DH), the occurrence of antibodies against reticulin and gluten was investigated and the influences of gluten-free, gluten-restricted, and normal diets on the persistence of these antibodies were compared. After a period extending from 11 to 47 months, none of the patients who were eating a gluten-free diet had reticulin or gluten antibodies. The patients eating a normal diet had the same incidence of reticulin autoantibodies at the end of the study as at its beginning, and gluten antibodies developed in some additional patients during the follow-up period. Thus, we have shown that the elimination of gluten from the diet of patients with DH has an important influence on the occurrence of antibodies to both reticulin and gluten.

Adult↗
PubMed1993

Effects of dietary gluten elimination in patients with recurrent minor aphthous stomatitis and no detectable gluten enteropathy.

Fifty patients with a history of minor recurrent aphthous stomatitis were entered into a 6-month double-blind controlled trial of a gluten-free diet. After hematologic and biochemical investigations and jejunal biopsy, one half of the group was given a gluten-free diet; the other half served as controls and received a gluten-free diet supplemented by gluten given blind (control diet). Twenty-three patients completed the trial, 11 patients on a gluten-free diet, 12 on the control diet. Four of the 11 on the gluten-free diet and 7 of the 12 on the control diet reported significant benefit in terms of minor recurrent aphthous stomatitis, but there was no statistical difference between the responses. The results fail to support studies that report widespread benefit in aphthae of gluten withdrawal and suggest simply a marked placebo response in the condition.

Adolescent↗
PubMed2000

TCR Vbeta expression in the small bowel of patients with dermatitis herpetiformis and gluten sensitive enteropathy. Limited expression in dermatitis herpetiformis and treated asymptomatic gluten sensitive enteropathy.

Dermatitis herpetiformis (DH) is a blistering skin disease characterized by cutaneous deposits of IgA and an associated, most often asymptomatic, gluten sensitive enteropathy (GSE). Gluten sensitive enteropathy is also seen in patients that do not have skin disease or cutaneous IgA deposits, but do have significant gastrointestinal (GI) complaints. Patients with DH and with GSE without skin disease have similar small bowel morphologic changes and HLA associations and both the skin disease and the GI symptoms can be controlled by a gluten free diet. It is not known what factors allow almost all patients with DH to continue to eat gluten and not develop symptomatic gastrointestinal disease. We have examined the expression of the Vbeta T-cell receptor (TCR) in the small bowel of patients with DH (n=11) and of patients with both symptomatic (n=10) and asymptomatic (n=7) GSE without skin disease to determine if differences in the pattern of TCR Vbeta expression are associated with differences in the clinical manifestations of these diseases. TCR Vbeta expression was analyzed using RT-PCR from small bowel biopsies. Patients with DH and those with GSE without skin disease that were on a gluten free diet and asymptomatic were found to express 6.6 and 5.6 out of 20 Vbeta families respectively, with no single family preference. Examination of peripheral blood lymphocytes from these patients did not reveal any restriction of TCR Vbeta family expression. In contrast, patients with symptomatic GSE expressed 12.6 Vbeta families (P< 0.05), with no consistent preferential expression of any single Vbeta family between patients. Patients with DH, who are continuing to ingest wheat, show a more restricted pattern of TCR Vbeta utilization, similar to that of treated patients with GSE without skin disease, and significantly different from GSE without skin disease patients eating gluten. These findings suggest that the restricted nature of the TCR Vbeta expression may play a role in the different clinical manifestations of dermatitis herpetiformis and isolated gluten sensitive enteropathy.

Adolescent↗
PubMed2003

How gluten-free is gluten-free, and what does this mean to coeliac patients?

A gluten-free diet is the cornerstone treatment of coeliac disease. Until now, it is not known conclusively whether trace amounts of gluten might be allowed in the diet, as suggested by Codex Alimentarius. Gluten-free foods intended for dietary use can now be analysed reliably for residual gluten by the new R5 enzyme-linked immunosorbent assay (ELISA) system. Some major problems of gluten analysis (sensitivity, specificity, reproducibility) can be solved by the new method. Therefore, the information given by the new test system is relevant and superior to earlier methods. Further clinical studies using small dose challenges and dietary records including gluten analysis are necessary until a more meaningful discussion on standards for gluten-free foods can be started.

Celiac Disease↗
PubMed1993

Time-course of adhesion molecule expression in rectal mucosa of gluten-sensitive subjects after gluten challenge.

Adhesive interactions between endothelium and circulating cells, such as monocytes, neutrophils and lymphocytes, are crucial for localizing the inflammatory response. We investigated the inflammatory response of rectal mucosa to local gluten challenge as a dynamic model of antigen-induced tissue injury, during which the expression of adhesion molecules on leucocytes and endothelial cells could be sequentially observed. Expression of ELAM-1, ICAM-1 and VCAM-1 was monitored in 10 treated and eight untreated patients with gluten sensitivity (coeliac disease), and in five disease controls for up to 4 h (short challenge), while a further seven treated coeliacs were monitored for up to 24 h (long challenge) following rectal gluten challenge. In the former, the expression of VCAM-1 and ELAM-1 was significantly raised 4 h after gluten challenge compared with controls. VCAM-1 and ELAM-1 expression was also increased in mucosae of treated patients, but to a lesser extent. VCAM-1 expression continued to increase for up to 24 h after gluten, while ELAM-1 had begun to wane by 4 h, reaching basal levels by 24 h. In contrast, the expression of ICAM-1 did not change in any of the disease groups studied. These findings relate to significant increases in lymphocytes (CD3+ cells) after 8 h, and neutrophils (CD15+ cells) after 4 h in the lamina propria. This approach has permitted novel studies of the inflammatory response to a defined antigen in sensitized (gluten-sensitive) human patients.

Celiac Disease↗
PubMed1983

Studies of intestinal lymphoid tissue. VI--Proliferative response of small intestinal epithelial lymphocytes distinguishes gluten- from non-gluten-induced enteropathy.

Several diseases of the small intestine, including gluten-sensitivity, present with malabsorption and a "flat" mucosa. Determination of the mitotic index of epithelial lymphocytes provides a simple, objective method of assessing, and thus of predicting, whether a flat mucosa is due to gluten-sensitivity (index greater than 0.2%), or not (index less than 0.2%). The use of this index in circumstances especially likely to cause diagnostic confusion--for example, intestinal lymphoma; Crohn's jejunitis of immunodeficiency--is illustrated in this paper. Of seven cases, five (two primary lymphoma, three immunodeficiency) had been treated with a gluten-free diet without benefit; a mitotic index performed on the initial biopsy in each of these patients could have predicted from the outset that none was gluten-sensitive. Of the remaining two cases, determination of the mitotic index on the biopsy initially obtained from a man with severe hypogammaglobulinaemia would have indicated that he was also gluten-sensitive. Empirical use of a gluten-free diet was avoided in the other patient (with flat small intestinal mucosa and low mitotic index) in whom the diagnosis was ultimately shown to be due to Crohn's disease of jejunum.

Adolescent↗
PubMed1983

The lectin properties of gluten as the basis of the pathomechanism of gluten-sensitive enteropathy.

The pathogenesis of gluten-sensitive enteropathy is as yet unknown. According to one theory gluten may act as a lectin with toxic properties for the intestinal cells. We can now confirm this theory by laser nephelometric measurements and demonstrate the oligomannosyl specificity of this lectin-like protein gluten. Furthermore, we demonstrate the highly more intensive binding capacity of gluten for the glycoproteins of the immature crypt cells of the intestinal brush border compared to those from the mature villous zone. It is discussed that gluten-sensitive enteropathy is caused by a genetically determined defect-glycosylation of intestinal glycoproteins with the synthesis of more mannosylated glycoproteins.

Celiac Disease↗