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PubMed1977

Wheat grains: a substrate for the determination of gluten antibodies in serum of gluten-sensitive patients.

A simple method of detecting gluten antibodies in serum is described. Cryostat sections of wheat grains proved to be an excellent substrate in the immunofluorescence technique. Rabbit antisera to gliadin and alpha-gliadin, and high percentage of sera from patients with gluten-induced enteropathy had antibodies that reacted with an internal structure of wheat grains. These antibodies could be absorbed with gliadin and with alpha-gliadin.

Adult↗

PubMed1977

The immunoglobulin-bearing cells in the lamina propria and the clinical response to a gluten-free diet in dermatitis herpetiformis.

In 17 patients with DH, multiple duodenal and jejunal biopsies were performed. In all patients the small-intestinal biopsy-specimens showed histopathological changes compatible with coeliac disease. Fourteen of the patients maintained a gluten-free diet (GFD) for more than 8 months. The small-intestinal lesions improved in all patients investigated during the GFD. The dosage of Dapsone needed to control the sin lesions could be reduced by more than 50% in 4 patients and the Dapsone could be stopped in 5 other patients on GFD. The immunoglobulin-bearing cells in the lamina propria were counted in 8 patients not on a gluten-free diet, in 6 patients on gluten-free diet, and in 8 healthy controls. The numbers of IgA-, IgM- and IgG-bearing cells were increased in most of the DH patients who were not on a gluten-free diet. The number of IgM-bearing cells in the DH patients who were on a gluten-free diet was the same as that in the control group. This may indicate a mainly IgM response in the lamina propria induced by gluten.

Adult↗

PubMed1977

Immunoglobulins in the jejunal mucosa in adult coeliac disease and dermatitis herpetiformis after the reintroduction of dietary gluten.

Cells containing immunoglobulin (IgA, IgG, IgM) have been measured and the distribution of extracellular and epithelial cell immunoglobulin assessed in treated patients with adult coeliac disease (ACD) and dermatitis herpetiformis (DH) before and after gluten was reintroduced to the diet. Patients with ACD and DH frequently had IgM and IgG cells above the normal range even before re-exposure to gluten, although the range of IgA cells was normal. In both diseases IgA and IgM cells increased after gluten with a proportionally greater rise in the latter, so that numbers of IgM cells, but not of IgA, exceeded the control range in all but one patient. There were increased quantities of IgA and IgM extracellularly in the lamina propria and in epithelial cells after challenge with gluten. Third component of complement was also found in some biopsies after re-exposure to gluten. These findings support the suggestion that gluten induces a humoral immunological response within the small intestinal mucosa and that both IgA and IgM systems are involved.

Adult↗

PubMed1976

Positive skin reactions to gluten in coeliac disease.

Following intradermal challenge with a peptic-tryptic digest of gluten, visible Arthus-type skin reactions were observed in 33 per cent of a group of 55 adults with coeliac disease. Of the 23 with untreated disease positive skin reactions occurred in 52 per cent. There was an invariable association between serum gluten antibodies and the presence of a skin reaction to gluten, indicating that gluten antibody combination with gluten in the skin provides the basis of the skin response. Since no false positive reactions were found in 52 normal controls, skin testing with gluten may provide a useful adjunct to the diagnosis and management of coeliac disease, especially in the outpatient department.

Adult↗

PubMed1979

Incidence of coeliac disease and transient gluten intolerance in children in a Swedish urban community.

The incidence of coeliac disease in children in the city of Malmö, South Sweden, was 1 : 982 during 1966 to 1975. The diagnostic criteria were: flat intestinal mucosa on gluten-containing diet, free of symptoms, and improvement in mucosal morphology on gluten-free diet, and morphological and/or evident clinical relapse (three times) on gluten challenge. 6 (12%) of 49 children with initially a flat mucosa still had a normal mucosa on a gluten-containing diet for two years or longer, having so-called transient gluten intolerance.

Celiac Disease↗

PubMed1979

Variability of gluten intolerance in treated childhood coeliac disease.

Fifty children consecutively attending a clinic for coeliac disease co-operated in a trial; 10 found to have flat mucosa were excluded. Forty children of mean age 9.8 years, whose duodenal or jejunal mucosa had returned to normal or near normal appearance after a mean of 5.8 years on gluten-free diets, were put back on normal diets. In 37, mucosal occurred in a mean of 16.9 months (four to 74 months). Four of the 37 had serial biopsies, in which mucosal enzymes (particularly lactase) fell and interepithelial lymphocyte counts rose before the mucosal morphology was regarded as definitely 'coeliac'. Three children had normal mucosal appearance after 58 to 73 months on normal diets, one of whom showed temporary mucosal abnormalities, another having occasionally low enzymes, in both suggesting underlying gluten sensitivity. Lactase suppression and raised IEL counts appear to be sensitive indicators of gluten intolerance. In our experience, a diagnosis of coeliac disease based on severe mucosal damage and a satisfactory response to a gluten-free but milk-containing diet implies a very strong likelihood of permanent or prolonged gluten intolerance, but with a striking variability in its expression.

Adolescent↗

PubMed1979

[Chronic inflammatory neuromyopathies in adults treated for gluten-sensitive enteropathy. A report on three cases with microvascular nerve and muscle lesions (author's transl)].

Neuromyopathies developed in three patients with gluten-sensitive enteropathy, a long time after they had been cured of their digestive disease by following a gluten-free diet. These cases differed radically from typical deficiency neuropathies by the presence of microvascular inflammatory lesions in nerves and muscles. The semiological findings were similar in all 3 cases, and were distinguished by the association of signs eveking lesions of the largest myelinated nerves fibers to the posterior rami with lesions in the muscles. Corticotherapy improved the condition but did not affect its chronic course. Nerve and muscle biopsies revealed the presence of segmentary microrascularitis, mainly lymphohistiocytic. The probable mechanism of these histological changes is alterations in the circulating immune-complexes, usually found in gluten-sensitive enteropathy, producing various types of associated disorders. Some of these immune-complexes would not be related straight to digestive intolerance to gluten, but would persist during the gluten-free diet period, and could be responsible for the micro-angiitis.

Adult↗

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↗

PubMed2016

Identification of food-grade subtilisins as gluten-degrading enzymes to treat celiac disease.

Gluten are proline- and glutamine-rich proteins present in wheat, barley, and rye and contain the immunogenic sequences that drive celiac disease (CD). Rothia mucilaginosa, an oral microbial colonizer, can cleave these gluten epitopes. The aim was to isolate and identify the enzymes and evaluate their potential as novel enzyme therapeutics for CD. The membrane-associated R. mucilaginosa proteins were extracted and separated by DEAE chromatography. Enzyme activities were monitored with paranitroanilide-derivatized and fluorescence resonance energy transfer (FRET) peptide substrates, and by gliadin zymography. Epitope elimination was determined in R5 and G12 ELISAs. The gliadin-degrading Rothia enzymes were identified by LC-ESI-MS/MS as hypothetical proteins ROTMU0001_0241 (C6R5V9_9MICC), ROTMU0001_0243 (C6R5W1_9MICC), and ROTMU0001_240 (C6R5V8_9MICC). A search with the Basic Local Alignment Search Tool revealed that these are subtilisin-like serine proteases belonging to the peptidase S8 family. Alignment of the major Rothia subtilisins indicated that all contain the catalytic triad with Asp (D), His (H), and Ser (S) in the D-H-S order. They cleaved succinyl-Ala-Ala-Pro-Phe-paranitroanilide, a substrate for subtilisin with Pro in the P2 position, as in Tyr-Pro-Gln and Leu-Pro-Tyr in gluten, which are also cleaved. Consistently, FRET substrates of gliadin immunogenic epitopes comprising Xaa-Pro-Xaa motives were rapidly hydrolyzed. The Rothia subtilisins and two subtilisins from Bacillus licheniformis, subtilisin A and the food-grade Nattokinase, efficiently degraded the immunogenic gliadin-derived 33-mer peptide and the immunodominant epitopes recognized by the R5 and G12 antibodies. This study identified Rothia and food-grade Bacillus subtilisins as promising new candidates for enzyme therapeutics in CD.

Bacteria↗

PubMed1979

Response of intestinal mucosa to gluten challenge in autistic subjects.

Eight autistic patients with steatorrhoea, hypocalciuria, and alleged behavioural improvements on gluten restriction, were fed ordinary diets plus 20 g gluten/day for 4 weeks. None of the patients had any significant change in body-weight or bowel habit as a result of gluten challenge, nor were any histological abnormalities detected on jejunal biopsy. The data suggest that the steatorrhoea and hypocalciuria seen in some autistic subjects cannot be accounted for by the presence of coeliac disease. Furthermore, these patients should not be confined to gluten-free diets, unless rigorous behavioural studies demonstrate a statistically significant improvement in behaviour as a result of the diet, or deterioration during challenge.

Autistic Disorder↗

PubMed1978

Gluten-sensitive enteropathy: genetic analysis and organ culture study in 35 families.

The genetic marker histocompatibility antigen HLA-B8 is present in 80% of patients with gluten-sensitive enteropathy (GSE). We studied 35 families with at least one affected member to determine whether an HLA-region gene alone could determine susceptibility to GSE. The incidence of HLA-B8 in the patients was 69% vs 22% for normals (P less than 0.001). The incidence of GSE in HLA-genotype-identical siblings of patients was only 8%, and in HLA-B8-haplotype-identical siblings and parents of patients was only 14% and 5%, respectively. In addition, intestinal biopsies of HLA-identical or partially identical relatives of patients were studied in an in vitro organ culture system capable of detecting gluten sensitivity in subjects ingesting a normal diet. The results confirmed the low incidence of gluten sensitivity in these individuals. The organ culture system could not differentiate mucosa obtained from unaffected parents or siblings of patients with GSE (who presumably carry the HLA-associated genetic information) from mucosa obtained from normals. We conclude that the genetic material inherited with HLA-B8 alone is not sufficient to produce clinical or subclinical disease. Other genetic and environmental factors appear to be important for disease pathogenesis.

Adolescent↗

PubMed1977

Failure to detect specific gluten antigens associated with the immune aggregates in the skin in dermatitis herpetiformis.

The univolved skin of 10 patients with dermatitis herpetiformis (DH) was examined for the presence of gluten antigens with the immunofluorescence technique using a rabbit anti-gliadin antiserum, human antibodies to wheat and to reticulin conjugated to fluorescein-isothiocyanate (FITC) and class-specific anti-human IgA immunoglobulin. In all patients, IgA deposits were found in the tips of the dermal papillae of the uninvolved skin. With the anti-wheat and anti-reticulin conjugates, as well as with the rabbit anti-gliadin antiserum, no specific immunofluorescence was observed in any of the skin specimens. Skin biopsy sections of three DH patients were treated with an acid solution (pH 3.2) in an effort to dissociate antigen-antibody complexes that might be present. After the elution procedure the sections showed undiminished IgA fluorescence, and retesting with the anti-wheat- and anti-reticulin antisera again gave negative results. The skin eluates, two of which contained IgA, had no antibodies to wheat or reticulin. These findings do not give support to the hypothesis that the antigens in the suspected immune complexes in the DH skin consist of gluten.

Animals↗

PubMed1976

An alternative mechanism for gluten toxicity in coeliac disease.

The pathogenesis of gluten-sensitive enteropathies is unknown, although a peptidase deficiency and an immune defect have been postulated. The effect of plant-derived lectins on cells has led to an alternative concept in which a defect of the cell surface membrane allows gluten to act as a lectin and this reaction initiates cell toxicity. The proposed abnormality is viewed as a structural change produced by incomplete oligosaccharide chains in surface-membrane glycoproteins.

Animals↗

PubMed1976

Role of gluten, prednisone, and azathioprine in non-responsive coeliac disease.

A case of severe "non-responsive" coeliac disease has been shown to be sensitive to gluten whilst under prednisone therapy, but not without prednisone. This adds an additional dimension to the criteria for diagnosis of coeliac disease. Cases of non-responsive coeliac disease may require both prednisone and gluten exclusion to induce a remission. In this patient, azathioprine induced and sustained a remission when unacceptably high doses of prednisone had failed, and may prove to be a valuable immunosuppressive in non-responsive coeliac disease.

Administration, Oral↗

PubMed1977

Skin test for coeliac disease using a subfraction of gluten.

Gluten and various of its fractions and subfractions have been used for intradermal testing in 10 patients with coeliac disease and in 20 healthy control subjects. All the coeliac patients gave positive Arthus-type reactions (type III) to the subfractions of gluten, whereas all the control subjects were negative. The subfraction B2 evoked strong reactions in almost all the coeliac subjects. If tests with larger series confirm the present results, skin testing with B2 may prove to be a useful screening test for coeliac disease. As B2 has already been found to stimulate the lymphocytes of coeliac patients, the present findings are also of interest in relation to the pathogenesis of coeliac disease.

Adolescent↗

PubMed1977

Reversible insensitivity to androgens in men with untreated gluten enteropathy.

Plasma androgen and gonadotrophin concentrations have been measured before and during treatment of 23 men with gluten enteropathy. Before treatment, there was marked rise in total plasma-testosterone, free testosterone concentration (as assessed by the free testosterone index), and plasma-luteinising-hormone concentration. In contrast, 5 alpha-dihydrotestosterone concentrations were lower than normal. All these abnormalities reverted towards normal with successful treatment of the jejunal mucosal lesion. These data are consistent with a reversible tissue resistance to circulating plasma-testosterone in men with gluten enteropathy and subtotal villous atrophy.

Adult↗

PubMed1979

Immunologic reaction of psychotic patients to fractions of gluten.

Production of a leukocyte migration inhibition factor by peripheral blood lymphocytes in response to challenge with gluten fractions was studied in hospitalized patients with schizophrenia and other psychoses compared with normal individuals and with children and adolescents with celiac disease. The schizophrenic and other psychotic patients could be subdivided into two groups, one that responded in the leukocyte migration inhibition factor test as the celiac patients did and one that responded as the normal control subjects did. The psychotic and schizophrenic patients did not show any evidence of malabsorption. The authors speculate that gluten may be involved in biological processes in the brain in certain psychotic individuals.

Adolescent↗

PubMedDate not supplied

[Two cases of gluten intolerance presenting as dwarfism (author's transl)].

Two patients with dwarfism were found to have intolerance to gluten. The authors describe the clinical, biological and radiological signs which enable the growth disorder to be related to its true cause, when obvious signs of a celiac syndrome are lacking. In fact, a small intestine biopsy is the essential diagnostic procedure. The hormonal changes found in such patients are discussed, and include normal HGH levels, reduced somatomedin activity which becomes normal after a gluten-free diet, and low blood insulin levels in the basal state as in insulin tolerance tests.

Adolescent↗