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At least 919 records · Page 51Linked to original sources
PubMed1992

Joint manifestations in gastrointestinal diseases. 2. Whipple's disease, enteric infections, intestinal bypass operations, gluten-sensitive enteropathy, pseudomembranous colitis and collagenous colitis.

This review addresses the clinical picture of rheumatic diseases seen in Whipple's disease, gluten-sensitive enteropathy, pseudomembranous colitis, collagenous colitis and that developing after enteric infections and intestinal bypass operations for morbid obesity. These disorders exemplify the interplay between antigen entrance through the gastrointestinal canal, specific bacterial properties and genetic host factors such as HLA B27. In most cases such as interplay results in formation of circulating immune complexes causing the development of peripheral joint disease.

Bacterial Infections↗
PubMed1995

Antibody response against wheat, rye, barley, oats and corn: comparison between gluten-sensitive patients and monoclonal antigliadin antibodies.

The antibody response of patients with gluten-sensitive enteropathy and dermatitis herpetiformis against alcohol-soluble prolamines of wheat, rye, barley, oats and corn assessed by immunoblotting was compared to the staining patterns produced by monoclonal antigliadin antibodies. Both monoclonal antibodies (MAbs) and patient serum reacted with wheat, rye, barley and oats, the patient serum showing individual variation both in IgA and IgG stainings. A broad reactivity with polypeptides from 30 to 68 kD was, however, typical for patient serum and comparable to the reactivity of two broadly reacting antigliadin MAbs. This kind of broad reactivity of the MAb may suggest that it binds to glutamine-repeating sequences of highly homologous gliadin polypeptides. Glutamine- and proline-containing motifs Pro-Ser-Gln-Gln and Gln-Gln-Gln-Pro are also included in the peptides toxic to the celiac small intestinal mucosa. Our study indicates that the humoral response of the patients may detect similar structures, in oat prolamines as well. Patient serum and one of the MAbs also reacted with a 22-kD polypeptide of corn extract. The meaning of this reactivity is not known, and further characterization of the antigenic epitopes of different cereals will be important.

Amino Acid Sequence↗
PubMed2001

Morphologic features suggestive of gluten sensitivity in architecturally normal duodenal biopsy specimens.

We studied small bowel biopsy specimens with architecturally normal villi from 78 adult patients with potential gluten sensitivity (GS) and correlated them with outcome to characterize morphologic features that would allow a pathologist to suggest GS. No patient had a previous GS diagnosis. Twelve study patients had GS. The mean number of intraepithelial lymphocytes (IELs) per 20 enterocytes from the tips of 5 random villi was significantly greater in GS than non-GS biopsy samples, but the groups overlapped significantly, making the number diagnostically useful only when markedly increased. Crypt mitoses counts had similar relationships. Twelve patients had an even distribution of IELs along villus sides and over tips (3/66 [5%] non-GS patients, 9/12 [75%] GS patients). Non-GS patients had a decrescendo pattern of IELs along the sides of villi. Architecturally normal small bowel biopsy specimens with an appreciable, continuous, even distribution of IELs along the sides and tips of villi and a mean of 12 or more IELs in the tips of several villi are suggestive of GS. Pathologists should be watchful for these morphologic features in small bowel biopsy specimens to suggest GS.

Adolescent↗
PubMed1986

Nitrogen balance and amino acid disappearance from the small intestine in calves fed soybean meal-, toasted soybean meal- or corn gluten meal-supplemented diets.

Nine crossbred (Hereford X Angus X Charolais) heifer calves (139 kg; 6 mo of age) with abomasal and ileal cannulas were used in a repeated design to evaluate N balance and amino acid disappearance in the small intestine. Calves were fed either soybean meal (SBM), toasted SBM (TSBM, 93 C for 90 min) or corn gluten meal (CGM) as supplemental protein sources. Each calf received approximately 83 g N/d from a cottonseed hull-corn based diet with 43% of the total dietary N supplied by the test proteins. Each experimental period consisted of a 10-d adaptation, 6-d digesta collection and 5-d excreta collection. Following the first 21-d period, calves were randomly re-allotted to treatment and the sampling process was repeated. Dry matter (64%) and N digestibilities (61%) and N retention (36.8 g/d) were similar (P greater than .10) among treatments. Nitrogen flow to the small intestine was similar for TSBM- and CGM-fed calves (119.1 g/d), but greater (P less than .01) than for those offered SBM (96.3 g/d). Offering TSBM and CGM resulted in greater quantities of essential, nonessential and total amino acids reaching the abomasum compared with SBM. Total amino acid flow to the small intestine was 100, 120 and 128% of intake for SBM, TSBM and CGM, respectively. Numerically, amino acid digestibility was lower in CGM-fed calves. Methionine digestibility was highest (64.6%), while histidine was lowest (43.7%). Feeding CGM may result in greater quantities of amino acids reaching the small intestine; however, several of these amino acids may be less digestible than for TSBM.

Amino Acids↗
PubMed2004

Response of lactating dairy cows to diets containing wet corn gluten feed or a raw soybean hull-corn steep liquor pellet.

We evaluated effects of wet corn gluten feed (WCGF) and a novel product (SHSL) containing raw soybean hulls and corn steep liquor on performance and digestion in lactating dairy cows. In Experiment 1, 46 multiparous Holstein cows were assigned to control (C), WCGF (20% of diet DM), or SHSL (20% of diet DM). Diets were fed as a total mixed ration beginning after calving. The C diet contained (dry matter [DM] basis) 30% alfalfa hay, 15% corn silage, 32% corn, 9.3% whole cottonseed, 4.4% solvent soybean meal (SBM), and 3.3% expeller SBM. The WCGF replaced 10% alfalfa hay, 5% corn silage, and 5% corn grain, while expeller SBM replaced solvent SBM to maintain diet rumen undegradable protein. The SHSL replaced 10% alfalfa hay, 5% corn silage, 3% solvent SBM, and 2% corn. Dietary crude protein averaged 18.4%. Milk, energy-corrected milk (ECM), DM intake (DMI), and ECM/DMI were similar among diets during the first 13 wk of lactation. During wk 14 through 30 postpartum, WCGF and SHSL improved milk, ECM, milk component yield, and ECM/DMI. In Experiment 2, 6 cows were used to evaluate digestibility and rumen traits. Dry matter intake and total tract digestibilities of DM, fiber, and crude protein were not different among diets. Diets did not affect ruminal liquid dilution rate, pH, or concentrations of total volatile fatty acids or ammonia, but acetate:propionate was higher for C (3.38) than for WCGF (2.79) or SHSL (2.89). The WCGF and SHSL products can serve as alternative feedstuffs in diets fed to lactating dairy cattle.

Animal Feed↗
PubMed1998

[The HLA-DR phenotype in Croatian children with gluten enteropathy].

Several studies of HLA and gluten enteropathy (GE) in European countries have found an association between this disease and certain DR phenotypes. However, no studies of DR phenotypes have been published in GE coming from Croatia. Therefore, we have studied HLA-A, B and DR specificities in 94 unrelated children with GE and in a group of healthy controls. In GE there was significant increase in the frequencies of A1 (61.70% v 24.50%; p < 0.0001) and B8 antigen (70.21% v 20.51%; p < 0.0001) compared with controls. The most frequent DR antigen was HLA-DR3 (87.23% v 18.82% in controls) with the relative risk of 29.65. The distribution of DR phenotypes in GE showed that the most frequent one was DR3/other DR (54.26%) and in decreasing order DR3/DR7 (17.02%), DR3/X (15.96%) and DR5/DR7 (8.51%). These phenotypes account for 95.75% of patients studied. A further 3.19% have DR4/DR5 phenotype. However, due to the frequency of certain antigen in controls, only phenotypes DR3/DR7 (relative risk: 28.92), DR3/X (relative risk: 13.29) and DR3/ other DR (relative risk: 10.04) were significantly associated with GE. The present study emphasizes the importance of studying the HLA-DR phenotypes in patients with GE.

Adolescent↗
PubMed1999

Recombinant human tissue transglutaminase ELISA for the diagnosis of gluten-sensitive enteropathy.

BACKGROUND: Tissue transglutaminase (TGc) has recently been identified as the major, if not the sole, autoantigen of gluten-sensitive enteropathy (GSE). We developed and validated an ELISA based on the human recombinant antigen and compared it to existing serological tests for GSE [guinea pig TGc ELISA and endomysium antibody (EMA) test]. METHODS: Human TGc was expressed in the human embryonic kidney cell line 293-EBNA as a C-terminal fusion protein with the eight-amino acid Strep-tag II allowing one-step purification via streptavidin affinity chromatography. We carried out ELISA assays for IgA antibodies against TGc using calcium-activated human and guinea pig TGc. The sera were also tested on monkey esophagus sections by indirect immunofluorescence for IgA EMA. We examined 71 serum samples from patients with GSE (38 with celiac disease, 33 with dermatitis herpetiformis), including 16 on therapy, and 53 controls. RESULTS: The human TGc could be expressed and purified as an active enzyme giving a single band on a Coomassie-stained gel. The mean intra- and interassay CVs for the human TGc ELISA were 3.2% and 9.2%, respectively. The area under the ROC curve was 0.999. The specificity and sensitivity were 98.1% (95% confidence interval, 95.7-100%) and 98.2% (95.9-100%), respectively. CONCLUSIONS: The human TGc ELISA was somewhat superior to the guinea pig TGc ELISA, and was as specific and sensitive as the EMA test. The human TGc-based ELISA is the method of choice for easy and noninvasive screening and diagnosis of GSE.

Adolescent↗
PubMed2000

Is villous atrophy always and only the result of gluten sensitive disease of the intestine?

'Flat and flexible truths are beat out by every hammer' (Sir Thomas Browne, writer and physician) The prevalence of gluten-sensitive enteropathy (GSE) or coeliac disease is likely to be as high as 1:200 to 1:400 in the developed world. Current medical practice leaves a significant proportion of these cases undiagnosed. An association between untreated coeliac disease and intestinal malignancy is well described so it is possible that patients with undiagnosed coeliac disease constitute a significant reservoir of preventable gastrointestinal malignancy. However, it is not clear whether all patients with coeliac disease are equally at risk of malignancy nor are all cases of intestinal malignancy necessarily associated with wheat protein sensitivity. Thus the precise links between GSE, villous atrophy and malignancy have not yet been established. However, there is evidence that products of activated T-cell clones, be they antigen specific or malignant, influence epithelial cell proliferation, differentiation and function thus contributing to the histological lesion characteristic of GSE or small bowel lymphoma.

Animals↗
PubMed2000

Humoral and cellular immune responses in gluten-treated suckling or hand-fed rats.

We analyzed the immune response to gliadin in suckling rats and rats hand-fed with an artificial milk formula, an animal model of gluten enteropathy. Animals of both groups were intragastrically given either gliadin or albumin (control animals) or gliadin from birth till day 55. When compared to the controls, spleen lymphocytes from both groups of gliadin-treated rats cultivated in vitro exhibited a significant increase of spontaneous 3H-thymidine incorporation. Moreover, the proliferation of spleen and mesenteric lymph node (MLN) lymhocytes from both groups of gliadin-treated suckling and hand-fed rats was specifically increased by the in vitro gliadin challenge. Spleen B cells from gliadin-treated rats spontaneously produced higher amounts of gliadin-specific antibodies than those from the controls, however, in vitro stimulation by gliadin caused no further increase in antibody production. Apoptotic DNA fragmentation in MLN cells was higher in gliadin-treated rats than in albumin-treated ones, independently of the milk diet during the suckling period.

Animals↗
PubMed2002

[Diagnosis of gluten enteropathy and efficiency of its treatment].

AIM: To develop screening diagnosis of gluten enteropathy (GEP), indications to administration of glucocorticoid hormones and objective criteria of effective treatment. MATERIAL AND METHODS: Clinical, immunological (antibodies-Abs to alpha-gliadin, reticulin and endomisium) examinations, enterobiopsy with morpho- and stereometry of small intestinal mucosa were made in 200 GEP patients. The examination was repeated 6 months to 5 years and later after the discharge from the hospital. RESULTS: Mean values of Abs to alpha-gliadin was 6 times higher than normal values. Positive titers of Abs to endomisium and reticulin were in 100 and 87.5% patients, respectively. Formed stool was registered 1.5 times more frequently, polyfecalia occurred 2.5 times less frequently, hypovitaminosis and trophic disorders were relieved 3 times more frequently, malabsorption syndrome reduced in patients given prednisolone vs those untreated with it. CONCLUSION: Screening diagnosis of GEP may be based on Abs tests to alpha-gliadin, reticulin and endomisium. Improvement of clinical condition of GEP patients can be stated by decreased diarrhea, polyfecalia and malabsorption symptoms. The treatment efficacy may be judged by clinical improvement, recovery of morphological structure of small intestinal mucosa, normalization of concentration of Abs to alpha-gliadin, reticulin, endomisium. Administration of prednisolone provides more complete and rapid rehabilitation of the patients.

Adult↗
PubMed2002

Antiendomysial and antitissue transglutaminase antibodies in gluten-induced enteropathy.

Although the gold standard for diagnosis of coeliac disease remains the small bowel biopsy, the broad spectrum and the non-specific nature of many of the clinical manifestations makes biopsy as the initial investigation impossible. So, much effort has been put into the identification of serological screening tests with adequate sensitivity and specificity. The aim of this study was to identify antiendomysial and antitissue-transglutaminase antibodies as serum markers of coeliac disease in a group of patients admitted in the 3rd Medical Clinic, 4th Medical Clinic and 1st Pediatric Clinic as well as in the general population. The study was made on serum samples collected from 64 persons, adults and children with or without documented coeliac disease. Antitissue transglutaminase (anti-tTG) antibodies were determined by the sandwich ELISA technique, using a commercial kit. Antiendomysium (EMA) antibodies were dosed by indirect immunofluorescence. Twenty-four subjects were positive for IgA anti-tTG and 23 for EMA. We found that IgA anti-tTG were 100% positive in patients with clinical suspicion of coeliac disease, the diagnosis being confirmed by biopsy. All, but two patients on a gluten-free diet had small or zero EMA levels. We also found that serum EMA levels correlated perfectly with the degree of histological alterations. A very good correlation was found between the serum concentrations of the two antibodies studied

Adolescent↗
PubMed2002

[Diagnostic value of determination of autoantibodies in gluten-sensitive enteropathy].

The study is focused on the immunopathological mechanisms of development of gluten-sensitive enteropathy (coeliac disease). It describes environmental factors and the role of autoantibodies and autoaggressive cells in the bowel inflammation. Attention is paid to the autoantibodies used in routine laboratory diagnosis of coeliac disease. The objective is a summary of rational diagnostic algorithms used in screening, diagnostics, treatment and dispensary care of patients with coeliac disease, especially with latent forms associated with other organ-specific immunopathological diseases. Exploration of anti-gliadin and anti-endomysial antibodies in diabetes mellitus type I were submitted. Furthermore, indications of these tests in the routine laboratory practice was analyzed.

Adult↗
PubMedDate not supplied

[Adult celiac disease(gluten enteropathy].

Celiac sprue is a disease in which there is malabsorption of nutrients by that portion of the small intestine which is damaged, a characteristic though not specific lesion of the small intestinal mucosa and prompt clinical improvement following withdrawal of certain cereal grains from the diet. We present a 41 years old patient with a history of diarrhea, treated as enterocolitis for several years, in which the gluten-free diet brought a clinical improvement.

Adult↗
PubMed1992

[Gluten enteropathy].

The authors relate the results of 10 years of observations of 113 patients suffering from gluten enteropathy (GE) of the adults. In all the patients, the diagnosis was supported by the presence of hyper-regenerative atrophy of the small intestinal mucosa (total in 70% and subtotal in 30%). Metabolic disorders and cellular immunity were investigated. At the onset of the observations 70.7% of the patients demonstrated malabsorption, stage III gravity, and 29.3% stage II. It has been proved that permanent and strict adherence to the agluten diet and administration of corticosteroids in the most severe cases in combination with pathogenetic therapy of diarrhea and metabolic disorders permit attaining a steady clinical remission, improvement of normalization of the biochemical and immunological characteristics, a tendency toward normalization of the small intestinal mucosa, and even the recovery of its normal structure in part of the cases.

Adolescent↗
PubMedDate not supplied

Cobalamine deficiency associated with neuropathy and oral mucosal melanosis in untreated gluten-sensitive enteropathy.

A 32-year-old woman was admitted with complaints of difficulty in walking and hypoaesthesia and tingling in her legs. She had short stature and brown-black hyperpigmentation, cheliosis, dental irregularities and scars in the axillary regions. Neurological examination revealed mild, symmetric, predominantly distal weakness of the legs; deep tendon reflexes were depressed. There was glove-and-stocking decrease in pinprick and temperature perception but proprioception and light touch were normal. Investigations established a diagnosis of celiac disease; her neurological features improved on gluten-free diet, but oral pigmentation persisted.

Adult↗
PubMed2006

[Effects of nitrogen, phosphorus and potassium fertilization on sucrose accumulation in flag leaf and starch accumulation in kernel of weak gluten wheat].

With weak gluten wheat Yumai 50 as test material, this paper studied the sucrose accumulation in flag leaf and starch accumulation in kernel under effects of nitrogen, phosphorus and potassium fertilization. The results showed that nitrogen and potassium fertilization increased the sugar content in flag leaf at early and late filling stage, respectively, while phosphorous fertilization had little effect. Nitrogen, phosphorous, and potassium fertilization increased the sucrose-synthase activity in flag leaf, but the effect differed with time, i. e., at mid filling stage for nitrogen fertilization, early filling stage for phosphorous fertilization, and early and mid stage for potassium fertilization. As for the sucrose phosphate-synthase activity in flag leaf, it was increased by nitrogen fertilization in 24 days after anthesis, by potassium fertilization at early and mid filling stage, and by phosphorus fertilization at late filling stage. Nitrogen, phosphorus and potassium fertilization increased the sugar and starch contents in kernel, and the effect of potassium fertilization was most significant. Phosphorus fertilization increased the accumulation of amylose, while potassium fertilization improved that of amylopectin in kernel.

Edible Grain↗
PubMed1978

Genetic basis of gluten-sentitive enteropathy.

Families of patients with gluten-sensitive enteropathy (GSE) were typed for HLA-A and -B antigens as well as for HLA-DW3 antigen(s) using appropriate typing alloantisera. In addition, patients and families were typed for GSE-associated B cell antigens using alloantisera obtained from mothers and wives of patients. The data obtained suggest that disease occurs within families when two conditions were fulfilled: (1) the family member is homozygous for the GSE-associated B cell antigens and (2) the family member also bears the HLA-DW3 antigen(s) or an antigen usually associated with DW3. In addition, with the family studies it was possible to show that the gene(s) controlling the DW3 antigen(s) and those controlling the GSE-associated B cell antigens are separate nonlinked genetic loci, a fact which leads to the conclusion that GSE has a genetic basis in at least two genes. It is speculated that the genes responsible for GSE code for surface proteins which are physically associated on lymphoid cell membranes and which form receptors important to the initiation of disease.

B-Lymphocytes↗