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 937 records · Page 52Linked to original sources
PubMed1988

Gluten-sensitive enteropathy in a cynomolgus monkey.

A malabsorption syndrome was observed in a cynomolgus macaque. Clinical signs included weight loss despite increased appetite, and diarrhea, characterized by an increased volume of soft, tan, malodorous feces. Clinicopathologic findings included hypoalbuminemia, generalized dilation of bowel loops with a prolonged transit time, steatorrhea and markedly diminished absorption of D-xylose. Biopsies of the duodenum and jejunum had total villous atrophy, crypt hyperplasia and a plasmacytic-lymphocytic infiltrate of the lamina propria. The monkey's diet was changed to a semi-synthetic diet containing no grain products. Subsequently, stool characteristics, body weight and intestinal villous morphology returned to normal. This response to removal of grain products from the diet suggests a syndrome similar to gluten-sensitivity enteropathy in human beings.

Animals↗
PubMed1988

Preferential activation of CD4 T lymphocytes in the lamina propria of gluten-sensitive enteropathy.

The distribution and activation of T-lymphocyte subsets in the small intestinal mucosa of coeliac disease and dermatitis herpetiformis subjects on a normal diet has been studied and compared to normal controls. Double-labelling immunofluorescence techniques with monoclonal antibodies were used on cryostat tissue sections. Intestinal epithelial cells demonstrated staining for HLA-DR, the intensity being proportional to the degree of enteropathy. In both patients and controls nearly all (97%) intra-epithelial lymphocytes were of the CD8 subset and not activated as judged by HLA-DR expression. In the lamina propria there was an approximate 50-fold increase in T cells in the patients as compared with the controls. Whilst the ratio of total CD4 to total CD8 cells was unchanged, the CD4 subset was preferentially activated in the patients. Thus in the normal controls the median ratio of activated CD4 cells to activated CD8 cells was 1.67 whilst for dermatitis herpetiformis and coeliac disease it was 3.42 and 6.07 respectively. These findings suggest that the lamina propria is a site of vigorous T-cell activity in gluten-sensitive individuals and is consistent with the view that the enteropathy of dermatitis herpetiformis and coeliac disease is the result of a delayed-type hypersensitivity against gliadin.

Adolescent↗
PubMed1986

Gliadin antibody detection in gluten enteropathy.

Circulating antigliadin antibody has been described in patients with gluten enteropathy although the prevalence varies in different studies. It has been suggested that the investigation for antigliadin antibody might be useful as a screening test. The object of the present study was to evaluate two different techniques for assaying these antibodies - an indirect immunofluorescent method and an enzyme-linked immunosorbent assay (ELISA). Antibodies were assayed in the sera of 102 patients in whom jejunal biopsies were also obtained. The specificity of both tests was greater than 95%, and the correlation between the presence of antibody and histology was significant (p < 0.005), though the sensitivity of each test was less than 70%.

Adolescent↗
PubMed1983

Factor V deficiency and its reversal with gluten restriction. In a patient with celiac disease.

Hemorrhagic manifestations in patients with celiac disease are uncommon and, when present, are usually due to a deficiency of the vitamin K-dependent clotting factors. A patient with celiac disease was seen with a severe bleeding diathesis associated with deficiencies of factor V. The deficiencies of vitamin K-dependent clotting factors were rapidly reversed with parenteral administration of phytonadione. Factor V levels returned to normal levels only after gluten restriction.

Adult↗
PubMedDate not supplied

[Late treatment results with a gluten-free diet in celiac disease in adults].

The efficacy of the treatment with an agluten diet of celiac disease of the adults was studied in 45 patients over time, the observation periods ranging from 6 months to 6 years. The results were assessed from the patients' clinical examination that included study of absorption function of the small intestine (daily mass and fat loss with feces, absorption of D-xylose), determination of hemoglobin, total protein in blood serum, and morphological study of the jejunum mucosa obtained on aspiration enterobiopsy. Analysis of the data has shown that the patients who strictly observed the agluten diet noted a clinical remission with a tendency towards morphological improvement of the structure of small intestinal mucosa. No such an improvement was recorded in patients given gluten on a periodic basis.

Adult↗
PubMed1980

[Effect of a protein-deficient diet (5 p. 100 gluten) and of balanced refeeding (15 p. 100 casein) on potential lipase, colipase-dependent lipase and phospholipase A2 activities. I. In the growing rat pancreas].

The intake of a 5 p. 100 gluten diet as the only protein source caused an overall protein synthesis deficiency that immediately stopped the rat growth. At first, the pancreas was less affected than the rest of the organism, but after 29 days of malnutrition, there was a 40 p. 100 decrease in body and pancreatic weight. The protein level of the deficient pancreas remained at that of the controls. Refeeding caused a considerable but temporary increase in that level after 24 h. The specific enzyme activities (AS) showed high variations from one day to the other, but only phospholipase A2 AS was significantly affected by the deficiency (--50 p. 100). Total lipase activities of the pancreas were reduced by 50 p. 100 and those of phospholipase A2 by 70 p. 100. Refeeding caused a considerable increase in lipase activities in 12 h and in phospholipase A2 activity in 48 h, but this process was brief and did not indicate complete recovery of those activities. After 27 days of refeeding, only phospholipase A2 showed good levels. Adding methionine to the deficient diet only changed the colipase level; this constitutes one more argument in favor of a distinct synthesis for this factor and for lipase.

Animals↗
PubMed1995

Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet.

The prevalence of hypertransaminasemia and the effect of gluten-free diet (GFD) were evaluated in 158 consecutive adult celiac patients, 127 women and 31 men, aged 18 to 68 years (mean, 32). At diagnosis, 67 patients (42%) had raised aspartate and/or alanine transaminase levels (AST and ALT; mean, 47 IU/L, range, 30 to 190; and 61 IU/L, range, 25 to 470, respectively), whereas 91 patients had normal liver function tests (LFT). Patients with and without hypertransaminasemia were comparable for epidemiological data, body mass index (18.5 vs. 19.6), and severity of intestinal histological involvement. All patients were given a strict GFD and were followed for 1 to 10 years (median, 4). At 1 year, a highly significant improvement in intestinal histology was observed in both groups (P < .0001). In the 67 patients with raised transaminase levels body mass index (BMI) also increased significantly (from 18.5 to 21.0, P < .001), and transaminase levels normalized in 60 (95%). In the other seven cases liver biopsy showed fatty infiltration in two and chronic active hepatitis (CAH) in the other five, related to chronic infection with hepatitis B virus in three and hepatitis C virus in one, and to autoimmune type in the fifth. We conclude that in adult celiac patients elevated serum transaminases are a frequent finding and normalize in most cases after GFD. When they persist, liver biopsy is mandatory to further investigate hepatic involvement, which is our series was mainly attributable to CAH.

Adolescent↗
PubMed1995

Epstein-Barr virus in primary gastrointestinal T cell lymphomas. Association with gluten-sensitive enteropathy, pathological features, and immunophenotype.

Forty-three primary gastrointestinal T cell lymphomas were investigated for the presence of Epstein-Barr virus (EBV) by polymerase chain reaction, RNA in situ hybridization, and immunohistochemistry. In addition, the association between EBV and clinicopathological characteristics of these lymphomas was investigated. Five of the thirty-eight cases that could be evaluated expressed EBV-encoded nonpolyadenylated RNA-1 in most tumor cells. Two of these five cases were EBV latent membrane protein-1 positive. All five cases were CD30 positive. In three of these five EBV-associated T cell lymphomas, the tumor cells were considered to be the neoplastic counterparts of activated cytotoxic T cells as shown by the expression of granzyme B. There was no association with histological characteristics of gluten-sensitive enteropathy, angioinvasion, necrosis, eosinophilia, or epitheliotropism of the tumor cells. The substantial percentage (58%) of EBV DNA polymerase chain reaction-positive cases was largely the result of the presence of EBV-encoded RNA-1-positive reactive cells. In conclusion, EBV might have an important etiological role in only 13% of the primary gastrointestinal T cell lymphomas. This percentage is similar to the findings in primary lymph node and lung T cell lymphomas.

Celiac Disease↗
PubMed1995

Gluten-sensitive enteropathy.

Peptides originating from wheat gluten during digestion in the alimentary tract are known to cause primary intolerances in genetically-predisposed individuals. Other cereals such as rye, barley and probably oats are also toxic for coeliac patients, whereas rice and maize are considered to be non-toxic. The mechanism by which prolamine-derived peptides produce jejunal lesions is not fully understood. Most investigators favour a dysregulated immune response to gliadins as the underlying abnormality in coeliac disease, but according to other authors a non-immuno-mediated cytotoxic activity of gliadin peptides on the small intestine seems to be the primary cause of intestinal mucosal damage in coeliac patients. This paper is a critical appraisal of current theories on the pathogenic mechanism underlying this disease. Moreover, many in vitro systems needed to investigate the cereal toxicity are described.

Celiac Disease↗
PubMed1998

Families with multiple cases of gluten-sensitive enteropathy.

UNLABELLED: Early detection of oligosymptomatic gluten-sensitive enteropathy (GSE) may contribute to the prevention of late complications, such as malignancy. Family members of known GSE patients are at higher risk of being affected. To evaluate the frequency and clinical significance of multiple occurrence, we routinely offered an antiendomysium antibody (EmA)-based non-invasive screening to affected families. Among 997 family members of 396 GSE patients, we identified 89 subjects with EmA positivity and/or severe jejunal villous atrophy. In 83 cases GSE has been verified, four patients refused the biopsy and two subjects are under further observation for latent celiac disease. Prevalence of GSE was 8.5% (80/943) among the first-degree relatives, with significantly higher values in the siblings (13.8%) and offsprings (12.0%) than in the parents (4.2%) of the probands (p < 0.001). In 55 families (13.9% of the families studied) two, in ten families (2.5%) three, in one family four and in one other family six members were affected. Combinations of the clinical presentations of index and screening-detected cases were highly variable, with a high percentage of silent and atypical forms in the relatives. GSE cases presenting both with and without dermatitis herpetiformis occurred in 15 families. Six GSE cases with atypical or mild dermatitis herpetiformis were detected in consequence of the screening. CONCLUSIONS: EmA-assisted family screening resulted in the detection of a clinically significant number of additional GSE patients.

Adolescent↗
PubMed1998

Evidence for a compensatory increase in synthesis of brush border enzymes in the jejunum of Irish Setters with gluten-sensitive enteropathy.

OBJECTIVE: To determine whether biosynthesis of aminopeptidase N (ApN), alkaline phosphatase (AP), and total microvillus membrane protein is altered in Irish Setters with gluten-sensitive enteropathy (GSE). ANIMALS: A litter of 6 Irish Setters with GSE and 3 healthy Greyhounds. PROCEDURES: Explants obtained from affected dogs at 4 and 12 months were maintained in vitro and were compared with material from healthy control dogs. Biosynthesis of ApN and AP was monitored by incorporation of [35S]methionine and immunoprecipitation of these enzymes. RESULTS: Jejunal explants from affected Irish Setters had significantly higher rates of biosynthesis of total protein, microvillus membrane protein, AP, and ApN, compared with control tissue. Two forms of ApN with apparent molecular mass of 155 and 135 kd and 4 forms of AP with apparent molecular mass of 210 to 260, 150, 130, and 105 kd were identified in total membrane fractions from control and affected dogs. CONCLUSIONS: Reduced activities of ApN and AP in dogs with GSE are not attributable to decreased synthesis of these proteins and document enhanced synthesis of microvillar membrane proteins, which may be a compensatory response to enterocyte damage. The 150-kd form of AP was most prominent in tissue from the most affected dogs, probably representing an early form of this enzyme. In contrast, the 105-kd form was most intense in tissue from controls and less intense in tissue of affected dogs.

Alkaline Phosphatase↗