Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GLUTEN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources

Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study.

OBJECTIVES: Many afflictions have been associated with celiac disease, but chance associations may exists. The aim of this study was to establish, by means of a multicenter prospective study, the prevalence of thyroid impairment among adult patients with newly diagnosed celiac disease and to evaluate the effect of a 1-yr gluten withdrawal on thyroid function. METHODS: A total of 241 consecutive untreated patients and 212 controls were enrolled. In 128 subjects a thorough assessment, including intestinal biopsy, was repeated within 1 yr of dietary treatment. Thyroid function was assayed by measuring the levels of TSH, free T3, free T4, thyroperoxidase, and thyroid microsome antibodies. RESULTS: Thyroid disease was 3-fold higher in patients than in controls (p < 0.0005). Hypothyroidism, diagnosed in 31 patients (12.9%) and nine controls (4.2%), was subclinical in 29 patients and of nonautoimmune origin in 21. There was no difference regarding hyperthyroidism, whereas autoimmune thyroid disease with euthyroidism was present in 39 patients (16.2%) and eight controls (3.8%). In most patients who strictly followed a 1-yr gluten withdrawal (as confirmed by intestinal mucosa recovery), there was a normalization of subclinical hypothyroidism. Twenty-five percent of patients with euthyroid autoimmune disease shifted toward either a subclinical hyperthyroidism or subclinical hypothyroidism; in these subjects, dietary compliance was poor. In addition, 5.5% of patients whose thyroid function was normal while untreated developed some degree of thyroid dysfunction 1 yr later. CONCLUSIONS: The greater frequency of thyroid disease among celiac disease patients justifies a thyroid functional assessment. In distinct cases, gluten withdrawal may single-handedly reverse the abnormality.

Adult↗

High rate of gastrointestinal symptoms in celiac patients living on a gluten-free diet: controlled study.

OBJECTIVES: The aim of this study was to determine the occurrence of GI symptoms in adults with celiac disease (CD) treated with a gluten-free diet for several years. METHODS: We studied a cohort of adults with CD (n = 51; 59% women) aged 45-64 yr and proved to be in remission after 8-12 yr of treatment. They were examined by the GI Symptom Rating Scale, which comprises five syndromes: indigestion, diarrhea, constipation, abdominal pain, and reflux. A general population sample (n = 182; 57% women) of same age served as controls. RESULTS: Subjects with CD reported significantly more GI symptoms than the general population sample, as assessed by the GI Symptom Rating Scale total score (p < 0.01). This was particularly true for women with CD who scored worse than female controls for all syndromes on the GI Symptom Rating Scale. By contrast, the men with CD reported no more symptoms than male controls. The women with CD showed generally more complaints than the men with CD did, notably within indigestion, constipation, and abdominal pain, corresponding to a 2-fold higher rate of GI symptoms (60% vs 29%; p < 0.04). CONCLUSIONS: Adult CD patients on a gluten-free diet for several years experienced significantly more GI symptoms than the general population sample. This may have some of its origin in the composition of a gluten-free diet. The symptoms were more pronounced in the women. This may raise questions of an association with their subjective health status, which has been shown to be lower than in men with CD.

Age Distribution↗

Gliadin antibodies identify gluten-sensitive oral ulceration in the absence of villous atrophy.

This study demonstrates gluten-sensitive recurrent oral ulceration (ROU) in the absence of gastrointestinal abnormalities which is associated with a humoral response to wheat protein. Ten patients with severe ROU were investigated; all had normal small intestinal biopsies. Four patients had raised levels of antibodies to alpha gliadin, a wheat protein fraction; in three of these four, the ulceration remitted on treatment with a gluten-free diet (G.F.D.) and relapsed on gluten challenge. None of the remaining six patients had raised alpha gliadin antibody (AGA) levels and none responded to G.F.D. Thus raised AGA levels can be used to identify patients with ROU who are likely to respond to a GFD.

Adult↗

Wheat gluten as a pathogenic factor in schizophrenia.

Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten.

Adult↗

Postpubertal gluten challenge in coeliac disease.

Altogether 38 postpubertal children with coeliac disease were rebiopsied. Mucosal abnormality in nine (24%) of them indicated poor adherence to the diet. Gluten challenge with a diet containing a normal amount of gluten was performed in those 29 patients with a normal mucosa. During challenge, rebiopsy was done when reticulin antibodies turned positive (mean 0.6 years, range 0.2-2.0) or at the end of the two year study. Histologically a clear relapse into coeliac disease was seen in all 23 patients who were positive for reticulin antibodies. At this time gliadin antibodies were positive in all but two. Sixteen (70%) of those who relapsed were completely asymptomatic. Three girls and one boy did not relapse within two years, indicating the possible recovery from coeliac disease to be 11%. All four had undergone gluten challenge earlier in childhood, after initial diagnosis and mucosal recovery, and this had resulted in mucosal relapse. To establish definite postpubertal recovery from coeliac disease in cases with normal mucosa at two years from challenge, further follow up studies of reticulin antibodies and later rebiopsy are needed. The reticulin antibody test seems to be suitable for prediction of mucosal relapse in coeliac disease.

Adolescent↗

Immune response to gluten in adult coeliac disease.

Cultures of mesenteric node lymphocytes obtained from two adult coeliac disease patients were stimulated by gluten fraction III. No stimulation was observed in cultures of axillary node lymphocytes from one of these patients, of mesenteric node lymphocytes from the two patients with other diseases or of peripheral blood lymphocytes from adult coeliacs and normal subjects. Peripheral blood lymphocytes of two of the six adult coeliac patients responded poorly to phytohaemagglutin alone, but this was probably owing to technical factors. In a further six adult coeliacs skin tests to gluten fraction III were negative. It is suggested that delayed hypersensitivity to gluten is likely to have a secondary pathogenic role in adult coeliac disease.

Adult↗

Measuring the response of the jejunal mucosa in adult coeliac disease to treatment with a gluten-free diet.

A previously described technique for measuring changes in the architecture of the small intestinal mucosa was used to measure the long-term response in six patients with adult coeliac disease to treatment with a gluten-free diet. All had flat or flat-with-mosaic jejunal mucosae before treatment and were subsequently believed to keep strictly to a gluten-free diet. They were followed for between four and 14 months from the start of treatment. The ratio of the area of surface epithelium to that of crypt epithelium (;area ratio') invariably increased following gluten withdrawal, but did not begin to do so until after several weeks of treatment. No patient attained complete histological normality within the limited period of observation, which was never more than 14 months. In one of the three patients followed for a year or more the area ratio increased to within the control range, and in two of these three the ratio was about 10 times the pretreatment ratio. There was a highly significant linear correlation between area ratio and time on the diet (r = 0.775, p < 0.005). The surface cell height measurements for these patients, by contrast, rose steeply and almost invariably during the first few weeks of treatment, but after that they fluctuated without further significant change. It is suggested that the two methods of measurement were complementary to each other, surface cell height being useful while the patient was in hospital on a rigidly strict diet, and the area ratio after return home, when minor dietary lapses were almost invariable.

Celiac Disease↗

Reintroduction of gluten in adults and children with treated coeliac disease.

Twenty-eight patients, thought to have coeliac disease and on gluten free diets, were put on a normal diet to confirm their diagnoses. Nineteen had been diagnosed in adult life (ACD) and nine in childhood (CCD). Patients were assessed on jejunal, morphological, and symptomatic parameters. Eighteen patients with ACD relapsed within seven weeks. Nine patients with CCD relapsed at variable times but five took longer than seven weeks, the longest period beint 10 months. Seven patients had no symptoms despite morphological deterioration during challenge and one patient, with ACD, did not relapse and was HLA B8 negative. This patient with ACD had subtotal villous atrophy on two jejunal biopsies and later showed morphological improvement on a gluten free diet. There was no correlation between the relapse time and time spent on a gluten free diet.

Adolescent↗

Serum cholesterol precursor sterols in coeliac disease: effects of gluten free diet and cholestyramine.

Enhanced biliary secretion and high faecal excretion of cholesterol are associated with increased cholesterol synthesis in coeliac disease. We have further investigated cholesterol synthesis in coeliac disease by determining the concentrations of faecal steroids and cholesterol precursors in serum, with and without a gluten free diet and while taking cholestyramine. The levels of unesterified methyl sterols and free and esterified lathosterol, but not those of squalene and desmosterol, were increased in proportion to the level of cholesterol synthesis, as measured with the sterol balance technique. Serum esterified methyl sterol concentrations were also slightly higher but, unlike free methyl sterols or lathosterol, they were not significantly correlated with cholesterol synthesis. The gluten free diet decreased the level of cholesterol synthesis, and the levels of lathosterol and free methyl sterols. There was less decrease in the concentration of esterified methyl sterols, and an insignificant decrease in the concentrations of squalene and desmosterol. Cholestyramine lowered the serum cholesterol concentration and increased that of serum free methyl sterols less in the patients than in the controls, and the increase was proportionate to increase of cholesterol elimination (or synthesis). The increase of serum free methyl sterols per unit of the increase of cholesterol elimination (or synthesis) was three times higher in the bile acid malabsorption caused by cholestyramine than in the cholesterol malabsorption caused by gluten enteropathy. On the other hand, the decrease in the level of serum cholesterol relative to the increase in cholesterol elimination (or synthesis) was higher in cholesterol malabsorption due to coeliac disease than in cholestyramine induced bile acid malabsorption. Effective secretion of newly synthesised and/or absorbed cholesterol directly into the bile could be a factor in the marked decrease of the serum cholesterol concentration in coeliac disease.

Celiac Disease↗

Reflux oesophagitis in adult coeliac disease: beneficial effect of a gluten free diet.

BACKGROUND: Coeliac disease patients show a number of gastrointestinal motor abnormalities, including a decrease in lower oesophageal sphincter pressure. The prevalence of endoscopic oesophagitis in these subjects however is unknown. AIM: To evaluate whether untreated adult coeliac patients had an increased prevalence of reflux oesophagitis and, if so, to assess whether a gluten free diet exerted any beneficial effect on gastro-oesophageal reflux disease (GORD) symptoms. PATIENTS AND METHODS: We retrospectively studied 205 coeliac patients (females/males 153/52, median age 32 years) who underwent endoscopy for duodenal biopsy and 400 non-coeliac subjects (females/males 244/156, median age 37 years) referred for endoscopy for upper gastrointestinal symptoms. Each patient was given a questionnaire for evaluation of GORD symptoms prior to and 4-12 months after endoscopy. Coeliac patients were given a gluten free diet. Oesophagitis patients of both groups, following an eight week course of omeprazole, were re-evaluated for GORD symptoms at four month intervals up to one year. Significance of differences was assessed by Fisher's exact test. RESULTS: Oesophagitis was present in 39/205 (19%, 95% confidence interval (CI) 13.8-25.0%) coeliac patients and in 32/400 (8%, 95% CI 5.5-11.1%) dyspeptic subjects. At the one year follow up, GORD symptoms relapsed in 10/39 (25.6%, 95% CI 13-42.1%) coeliacs with oesophagitis and in 23/32 (71.8%, 95% CI 53.2-86.2%) non-coeliac subjects with oesophagitis. CONCLUSION: Coeliac patients have a high prevalence of reflux oesophagitis. That a gluten free diet significantly decreased the relapse rate of GORD symptoms suggests that coeliac disease may represent a risk factor for development of reflux oesophagitis.

Adolescent↗

Neuropathy associated with gluten sensitivity.

OBJECTIVES: To prospectively study the clinical, neurophysiological and neuropathological characteristics of axonal neuropathies associated with positive antigliadin antibodies and the prevalence of such neuropathies in a cohort of patients with sporadic axonal neuropathy. METHODS: Prospective screening (using antigliadin, antiendomysium and tissue transglutaminase antibodies) of patients with peripheral neuropathy attending a neurology clinic. RESULTS: 215 patients with axonal neuropathy were screened. 141 patients had symmetrical sensorimotor neuropathy, 47 had mononeuropathy multiplex, 17 had motor neuropathy and 10 had small-fibre neuropathy. Despite extensive investigations of the 215 patients, 140 had idiopathic neuropathy. Positive immunoglobulin (Ig)G with or without IgA antigliadin antibodies was found in 34% (47/140) of the patients with idiopathic neuropathy. This compares with 12% prevalence of these antibodies in the healthy controls. The prevalence of coeliac disease as shown by biopsy in the idiopathic group was at least 9% as compared with 1% in the controls. The clinical features of 100 patients (47 from the prevalence study and 53 referred from elsewhere) with gluten neuropathy included a mean age at onset of 55 (range 24-77) years and a mean duration of neuropathy of 9 (range 1-33) years. Gluten-sensitive enteropathy was present in 29% of patients. The human leucocyte antigen types associated with coeliac disease were found in 80% of patients. CONCLUSIONS: Gluten sensitivity may be aetiologically linked to a substantial number of idiopathic axonal neuropathies.

Adolescent↗

Antibodies in relation to gluten intake.

Serum reticulin, endomysial and gliadin antibody tests are used in serological screening and case finding of coeliac disease, as well as the novel tissue transglutaminase antibody test. None of these tests are 100% predictive, however. Reticulin/endomysial antibodies predict forthcoming coeliac disease in individuals with normal small-bowel mucosal morphology. The effect of a gluten-free diet can be monitored with serological tests. A positive test result often indicates an inadequate gluten-free diet. However, slight dietary transgressions and minor mucosal damages cannot always be revealed with the serological tests. Therefore, small-bowel mucosal biopsy remains the most sensitive method to monitor the effect of a gluten-free diet.

Autoantibodies↗

Genetics of the immune response to gluten in coeliac disease.

Accumulating evidence indicates that coeliac disease (CD) is a multifactorial disorder where several heritable factors in conjunction with environmental factors are involved in the disease development. Gluten proteins are a critical environmental factor as the presence of disease in affected individuals is strictly dependent on dietary gluten exposure. Most likely coeliac patients have genetically shaped immune responses to gluten proteins that cause intestinal pathology. Many of the CD genes thus supposedly encode variants of proteins with immune functions. HLA has been identified as a major genetic factor, but yet no further genes have been identified. There probably exist several predisposing non-HLA genes, but available data indicate that the heritable contribution by each of them can be small. Combined genetic and functional studies will hopefully identify additional predisposing genes in the future.

Celiac Disease↗

Effects of adding dietary lysine to a low gluten diet on the brain protein synthesis rate in aged rats.

The purpose of this study was to find whether the addition of dietary lysine affected the rate of brain protein synthesis in aged rats fed on a gluten diet. Experiments were done on two groups of aged rats (30 wk) given the diets containing 5% gluten or 5% gluten + 0.3% lysine for 10 d. The fractional rates of protein synthesis in brain, liver, and kidney increased with an addition of dietary lysine. In brain, liver, and kidney, the RNA activity [g protein synthesized/(g RNA x d)] was significantly correlated with the fractional rate of protein synthesis. The RNA concentration (mg RNA/g protein) was not related to the fractional rate of protein synthesis in any organ. The results suggest that the addition of the limiting amino acid for the low quality protein elevates the rate of protein synthesis in the brain of aged rats, and that RNA activity is at least partly related to the fractional rate of brain protein synthesis.

Aging↗

Consumption of hypoallergenic flour prevents gluten-induced airway inflammation in Brown Norway rats.

Brown Norway rats were immunized with gluten, and then fed a diet containing hypoallergenic flour or an amino acid mixture. The rats were then made to inhale a solubilized gluten to induce gluten-specific bronchial asthma. The antibody levels in the serum of rats were measured by ELISA, and cell counts were done on cytospin preparations of bronchoalveolar lavage fluid. Body weight was decreased after allergen challenge in rats fed the amino acid mixture but not in rats fed the hypoallergenic flour. Antibody levels in the serum were significantly lower in rats fed hypoallergenic flour than in those fed the amino acid mixture. Differential cell counts in the bronchoalveolar lavage fluid showed that the numbers of eosinophils, lymphocytes, and neutrophils were significantly lower in rats fed the hypoallergenic flour than in those fed the amino acid mixture. These results suggest that hypoallergenic flour actively suppresses the allergic reactions, probably by inducing oral tolerance.

Animals↗

Effect of wheat gluten hydrolysate on the immune system in healthy human subjects.

Nine healthy volunteers were divided into a test group (n = 5) and a control group (n = 4). The test group consumed 3 grams per d of wheat gluten hydrolysate for 6 d, and their NK cell activity and hematological parameters were measured: The same assessments were performed in the control group, which did not receive wheat gluten hydrolysate. In the test group, NK cell activity increased significantly (P = 0.018) after wheat gluten hydrolysate intake. No adverse effects were observed in either group.

Adjuvants, Immunologic↗

Histologic follow-up of people with celiac disease on a gluten-free diet: slow and incomplete recovery.

To assess histologic recovery in response to gluten withdrawal in celiac disease, 158 patients seen in our hospital during a 15-year period underwent follow-up small intestine biopsies (SIBs) within 2 years after starting a gluten-free diet; further SIBs were done if villous atrophy was present. A modified Marsh classification was used (IIIA, partial villous atrophy; IIIB, subtotal villous atrophy; IIIC, total villous atrophy). Of patients with Marsh IIIA, IIIB, or IIIC lesions, histologic remission was seen in 65.0% within 2 years, 85.3% within 5 years, and 89.9% in long-term follow-up. Eleven patients (7.0%) with persisting (partial) villous atrophy had symptoms and signs of malabsorption and were considered to have refractory celiac disease; 5 of them developed an enteropathy-associated T-cell lymphoma. Children recovered up to 95% within 2 years and 100% in the long-term. Histologic recovery in celiac disease after starting a gluten-free diet takes time and is incomplete or absent in a substantial subgroup of patients (10.1% villous atrophy after 5 years). Systematic follow-up of patients with celiac disease and the malabsorption syndrome and secondary complications is needed.

Adolescent↗

Short-term gluten challenge in children with coeliac disease does not impair spontaneous growth hormone secretion.

BACKGROUND: Growth retardation in children with coeliac disease has been attributed to impaired growth hormone (GH) secretion observed in stimulation tests. OBJECTIVE: This study aimed at investigating the possible change in spontaneous GH secretion during a standardised gluten challenge. PATIENTS: Twelve children with previous enteropathy suggesting coeliac disease and a normal pre-challenge biopsy on a gluten-free diet were included; eight of them completed all parts of the study, including repeated 24-h GH sampling. METHODS: At the start and the end of a 5-6 weeks standardised gluten challenge, blood was drawn at a constant rate for 24 h and collected for GH analysis at 20-min intervals. The graph of plotted GH values was analysed by means of a computer program (PULSAR). RESULTS: No significant changes were seen in the measures of maximum GH peak, baseline GH values, area under the curve over the baseline (AUCb), the number of GH peaks or mean GH concentration. GH secretion rate (GHt) increased slightly. None of the characteristics of the 24-h profile was significantly correlated to the change of IGF-I. CONCLUSION: No impaired GH secretion was found. Thus, we speculate that decreased growth rate in celiac disease may not be primarily caused by changes in GH secretion. Instead it may be caused by changed peripheral sensitivity to GH.

Celiac Disease↗