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PubMed1975

[Structural differences between various quality glutens and between their protein components].

The rheological differences between glutens of varying quality are determined by the non-uniform "packing density" of the protein components in the gluten complex which is due to the different amounts of the structure-stabilizing disulphide and hydrogen linkages. There is no direct relationship between the gluten quality and the protein composition of the gliadine fraction. On the contrary, it is apparent that structural differences between the gluteline fractions from glutens of varying quality are essential. Some recent knowledge concerning such differences is discussed.

Amino Acids↗
PubMed2004

[A great imitator for the allergologist: intolerance to gluten].

Intolerance of gluten, resposible for Coeliac disease, is essentially shown by an auto-immune enteropathy, even if the cutaneous manifestation (herpetiform dermatitis) and perhaps certain neurological signs (cerebral syndrome, peripheral neuropathy) may be independent as well as associated with the intestinal illness. This affection is of immunological nature, occuring in a genetic field that predisposes to the illness (familial form: concordance of 70% in homozygote twins; 90% of patients show an HLA molecule of type DQ2, DQ8 in almost all the other cases. The exogenous factor is the gluten content contained in wheat, rye and barley, more precisely by the intermediary "the prolamines" which are the "reactive" element that induces a the same time an inflammatory reaction of type TH11 locally (expressed by the histological aspect of a duodenal biopsy evolving as villous atrophy) and a humoral response with production of anti-gliadine and anti-transglutaminase antibodies (the role of the latter enzyme is intervention in the local transformation of antigens to make them antigenic). It is an illness of adults as well as children and this point must now be emphasized. Recent epidemiological studies insist on a high prevalence (1/300 in Europe). Clinical expression, at the start very polymorphic and so misleading, before the appearance of the more classical signs of malabsorption and development, always feared, towards a lymphoma. These signs are haematological (anemia of various types, hyper platelets by hyposplenism, haemorrhagic signs) cutaneous (herpetiform dermatitis, cutaneous vasculitis) mucosal (aphtose), hepatic (cytolysis), neurophysical (fatigue, troubles of behaviour, cerebral syndrome, neuropathy) and osteo-articulitis (osteopenia, arthralgias, diffuse pains). The association of certain auto-immune illnesses must be emphasized (diabetes, Hashimoto thyroiditis, Gougerot disease, primitive biliary cirrhosis). To think early of the possibility of intolerance to gluten, is to give the means of a very easy diagnosis (measurement of anti-gliadin, anti-endomysium and anti-transglutaminase, and secondarily duodenal biopsy if necessary), and it is early elimination of gluten food which will make the various clinical manifestations disappear and so prevent the risk of evolution to a tumoral pathology.

Adolescent↗
PubMed2005

Celiac disease and gluten-associated diseases.

Celiac disease develops from an autoimmune response to specific dietary grains that contain gluten. Diagnosis can be made based on the classical presentation of diarrhea, fatty stools, and abdominal bloating and cramping, as well as the presence of specific serum antibodies. In addition, gluten ingestion has increasingly been found to be associated with other conditions not usually correlated with gluten intolerance. The subsequent diversity of the clinical presentation in these cases can complicate decision-making and delay treatment initiation in conditions such as ataxia, headaches, arthritis, neuropathy, type 1 diabetes mellitus, and others. This review explores the etiology and pathology of celiac disease, presents support for the relationship between gluten and other diseases, and provides effective screening and treatment protocols.

Celiac Disease↗
PubMedDate not supplied

[Biochemical markers of bone turnover in children with celiac disease on gluten-free diet].

UNLABELLED: Celiac disease is known to predispose patients to disturbances in bone metabolism. However, little information is available on the biochemical bone turnover markers in celiac children treated with gluten-free diet. AIM: The aim of presented study was to assess bone resorption and formation processes by biochemical bone turnover markers in children with celiac disease on gluten-free diet. SUBJECTS AND METHODS: We studied 20 children with celiac disease (age range 1.5 - 16 yr; 11 girls, 9 boys). The mean age of diagnosis was 2.6 +/- 1.9 yr and the mean duration of gluten-free diet was 7.8 +/-5.1 yr. Results were compared with those obtained in 130 healthy children. Serum levels of bone-specific alkaline phosphatase and osteocalcin as bone formation indices and serum level of C-telopeptide of type I collagen as bone resorption index were measured by immunoenzymatic methods. Additionally, serum vitamin D, calcium and phosphorus were also estimated. RESULTS: Lower median values of C-telopeptide of type I collagen were observed in about 50% tested celiac patients. Some of them also had lower osteocalcin level. However, in most patients ranges of values of bone turnover markers were similar to those in the controls. During our observation, all tested children had normal serum concentration of vitamin D as well as of calcium and phosphorus. CONCLUSIONS: Our data show normal bone resorption and formation processes in most patients with celiac disease on gluten-free diet. However, some cases had changes in the pattern of bone turnover markers. Further studies of these patients are needed to assess their predisposition to osteopenia and osteoporosis.

Adolescent↗
PubMedDate not supplied

Effects of small amounts of gluten in the diet of coeliac patients.

A diet excluding wheat, oats, rye and barley is the cornerstone of the treatment of coeliac patients. Such a gluten-free diet (GFD) is recommended irrespective of the presence of symptoms. Maintenance of a strict GFD is not a simple matter, as small amounts of gluten capable of causing relapse have been identified in several previously unsuspected sources, thanks to the recent availability of sensitive detection assays. To date there is no definition as to what amount of gluten in the diet might be tolerable. Compliance to the GFD is a problem, particularly in certain groups of patients (e.g. adolescents). Small amounts of gluten in the diet often do not cause clinical symptoms, nor increased serum levels of antigliadin antibody, nor gross changes of the jejunal histology; nevertheless, they seem to be able to activate mucosal cell-mediated immunity. This finding represents a warning in view of the recently reported protective effect of GFD against malignancies. In conclusion, all present evidences give strong support for advising all patients to adhere to a strict GFD for life.

Adolescent↗
PubMed1990

[Physiologic requirements for casein protein and wheat gluten in 4-month-old rats].

Sources of casein protein and wheat gluten were analysed for the content of proteins, fats, saccharides, water and amino acids. The chemical score of the amino acids and the ratio of essential and non-essential amino acids (E/N) were determined. In rats (males) at the age of 120 days, given the diets for 14 days, the optimal and maintenance physiological daily rations were determined from the changes of body nitrogen, body water and weight dependent on the protein intake, using the method of increasing casein protein and wheat gluten content from 0 to 40 per cent in the diet. In 120-134-day-old rats, the optimal daily dose was 1.75 g of casein protein (7.5 per cent of all proteins in the diet) and 2.46 g of wheat gluten protein (10 per cent of all proteins in the diet). As to the maintenance rations determined from the weight changes, body nitrogen and body water in dependence on the protein intake, in these rats the successive daily rations were 1216 mg, 1214 mg and 1302 mg for the casein protein, and 1731 mg, 1760 mg and 1861 mg for the wheal gluten protein.

Age Factors↗
PubMedDate not supplied

[Class IgA antigliadin antibodies and monitoring of compliance to gluten-free diet in celiac disease].

Antibodies to gliadin (AGA), detected by ELISA, were found in the sera of 37 (88%) of 42 patients with untreated adult celiac disease. IgG class AGA showed a higher sensitivity for the diagnosis of celiac disease than IgA AGA, but, while IgA AGA had a specificity of 100% for celiac disease, false positives of IgG class were present in 19% of 37 patients with ulcerative colitis and in 27% of 26 patients with Crohn's disease. Twenty-eight out of our 42 adult celiac patients were tested after 6-12 months of gluten free diet: IgG AGA persisted in 43% of them showing antibody titres lower than those observed in untreated celiac disease. IgA AGA became negative after gluten withdrawal and there was regrowth of jejunal villi in all but 2 adult celiac patients (7%), who continued to present IgA AGA positivity and subtotal villous atrophy. These 2 patients did not comply to the gluten free diet. Our study confirms the specificity of IgA AGA for untreated celiac disease and emphasizes their usefulness in monitoring the compliance with gluten free diet in adult celiac disease.

Adult↗
PubMed1989

[The effect of 6-month provocation with gluten on the height and weight of children with celiac disease].

Gluten challenge was performed in 22 coeliac children in the period of histological remission. Gluten in dose 0.5 g/kg was administered for 6 months. Before the Provocation Test over 60% of children have had body weight over 50 c for normal children in Warsaw. Standardized mean body weight (+ 0.13 +/- 1.1) and height (+ 0.04 +/- 1.05) of the investigated coeliac children did not differ significantly from the values of normal Warsaw population (p greater than 0.005). A 6 month provocation with gluten leading to the histological relapse did not affect body weight and height of tested children; over 50% have had body weight and height over 50 c. Mean standardized body weight (- 0.002 +/- 1.0) and height height (-0.07 +/- 0.91) did not differ significantly from the normal values (p greater than 0.05) and corresponding values before the provocation (p greater than 0.05). It seems that Provocation Test with gluten carried out in the above way does not inhibit physical development of children with coeliac disease.

Body Height↗
PubMed1989

[Diet among patients with celiac disease. Do patients comply with a gluten-free diet?].

We studied dietary compliance retrospectively among 28 coeliac patients, 18 adults (15-68 years) and 10 children (1-14 years) by means of a self-administered frequency questionnaire. 50% of the participants ate foods that were not guaranteed to be gluten-free. Four adult patients (22%) with certainty did not keep to a strictly gluten-free diet. Lack of dietary compliance was not detected among children. The patients had received information on diet shortly after the disease had been diagnosed during the period 1964-81. The most frequent source of information about gluten-free diet was the physician, but information from the Norwegian Coeliac Association and from clinical nutritionists was rated as more useful. 24 patients reported experiencing social and practical problems related to the gluten-free diet.

Adolescent↗
PubMed1989

Serum interleukin-2-receptor in coeliac disease: response to treatment and gluten challenge.

Concentrations of the soluble interleukin-2 receptor (sIL-2R) in the serum of 33 patients with coeliac disease were measured by ELISA. The levels of sIL-2R were significantly raised in 15 patients with untreated coeliac disease compared with treated patients and age- and sex-matched symptomatic and non-symptomatic control groups. Longitudinal studies in individual coeliac patients showed that serum sIL-2R fell following commencement of a gluten-free diet. Gluten challenge of 16 treated coeliac patients for 1 week resulted in a significant increase in serum sIL-2R, which returned to prechallenge levels within 4 weeks of recommencement of a gluten-free diet. We suggest that serum sIL-2R levels in patients with coeliac disease reflect specific immunological activation in response to gluten ingestion. Measurement of serum sIL-2R may therefore be useful in the assessment of response to treatment in patients with coeliac disease.

Adolescent↗
PubMedDate not supplied

The contribution of some constitutional factors to the development of cow's milk and gluten intolerance in children.

The role of some constitutional factors in the development of cow's milk and gluten intolerance among hospitalized children was the subject of analysis made by the authors. The patients were hospitalized at the Clinic of Infectious Diseases of Children during 1973-1982. The age of 45 children varied from 5 months to 5 years (gluten intolerance group) and of 50 children it amounted to from 2 months to 5 years (cow's milk intolerance group). In 34% of the family members of the children with milk intolerance and in 4.4% of the family members of the children with gluten intolerance the symptoms of this trait were found. Coeliac disease was observed in 13.3% of the family members of the gluten intolerance group of children and 10.8% psychic and/or diabetes disease among the members. It has been suggested that above illnesses of the family members occur more frequently compared to control group and this finding can speak for the participation of s constitutional (genetic?) factor in the development of this type of intolerance among the members of the family of affected children.

Adult↗
PubMed1985

Determination of physiological casein and wheat gluten protein requirements of adult rats aged 75-89 days.

Mounting doses of casein and wheat gluten protein (from 0% to 40% in the diet) were given to adult male rats aged 75-89 days for 14 days. The optimum physiological daily dose, determined from changes in body nitrogen, body water and body weight, was 2.76 g/d for casein protein (corresponding to a 10% casein protein diet) and 3.67 g/d for wheat gluten protein (corresponding to a 15% gluten protein diet). Determined from body weight changes, the daily maintaining dose of casein or wheat gluten protein was 1.054 and 1.511 mg/d respectively, from body nitrogen changes 970 and 1.514 mg/d and from body water changes 1.124 and 1.637 mg/d. Compared with newly weaned animals aged 35-49 days, the optimum physiological daily dietary protein doses for adult animals fall, while the maintaining doses rise.

Animals↗
PubMed1985

Specificity of leucocyte migration inhibition test in coeliac disease. A reassessment using different gluten subfractions.

Production of leucocyte migration inhibition factor by peripheral blood leucocytes in response to challenge with gluten fractions has been proposed as a reliable in vitro test for the diagnosis of coeliac disease. We have performed the leucocyte migration inhibition test with two different gluten fractions, GFIII and B2, in untreated and treated coeliac patients, patients with other intestinal diseases (abnormal controls) and healthy controls, and evaluated the sensitivity, specificity and positive and negative predictability of the test for the diagnosis of coeliac disease. Using GFIII as antigen leucocyte migration was significantly inhibited, compared to healthy controls, not only in treated and untreated coeliacs but also in abnormal controls. Using B2 gluten subfraction as antigen only treated coeliacs and abnormal controls differed significantly from healthy controls. The elevated number of abnormal controls showing migration inhibition consistently affected the diagnostic value of the test, which did not vary using B2 subfraction instead of GFIII as antigen. Our study confirms previous observations of gluten sensitization, as detected by leucocyte migration inhibition, in coeliac patients but strongly questions the claim that coeliac disease can be diagnosed on the basis of a positive leucocyte migration inhibition test without the need for intestinal biopsy.

Adolescent↗
PubMed1984

Antibodies to gliadin, gluten and reticulin glycoprotein in rheumatic diseases: elevated levels in Sjögren's syndrome.

An enzyme immunoassay was used to measure circulating antibodies to gluten, gliadin and to 'reticulin glycoprotein' in 25 patients with Sjögren's syndrome (SS), in 20 patients with rheumatoid arthritis without SS and in 19 patients with systemic lupus erythematosus without SS. Antibody levels to these three antigens were significantly higher in SS than in the other groups. In SS the level of antibodies to 'reticulin glycoprotein' correlated positively with the levels of antibodies to both gliadin and to gluten but not with the level of antibodies to SS-B antigen. Patients with primary SS had higher antibody levels to 'reticulin glycoprotein' than had patients with secondary SS, whereas no significant difference between primary and secondary SS was found in the levels of the antibodies to gliadin or to gluten. Circulating antibodies to gliadin, gluten and 'reticulin glycoprotein' have not been previously recognized in SS. Their occurrence suggests that small bowel injury may be a common finding in SS.

Adult↗
PubMed1984

Hyposplenism and gluten-sensitive enteropathy. Natural history, incidence, and relationship to diet and small bowel morphology.

Splenic function was quantitatively assessed using "pitted" erythrocyte counts in 177 patients with gluten-sensitive enteropathy. Hyposplenism was found to be a common, but not inevitable, complication of gluten-sensitive enteropathy that fluctuated with disease activity. Splenic function improved after withdrawal of gluten from the diet and a close relationship was demonstrated between hyposplenism and the morphology of the small intestine. The severity of the hyposplenism increased with advancing age and prolongation of exposure to dietary gluten. Splenic function did not vary with the HLA-A, -B, and -DR antigens, but, due to the presence of HLA-B8 and -DR3 in the vast majority of patients, a role for this haplotype in the causation of the hyposplenism cannot be excluded.

Adolescent↗
PubMed1984

Gluten antibodies in patients with multiple sclerosis.

The level of gluten antibodies has been determined in plasma samples from 36 patients with MS using a haemagglutination technique. Only one of the 36 patients studied showed any evidence of gluten antibodies and the level of antibodies in this patient did not justify putting the patient on a gluten-free diet. This study has provided no evidence to support the use of a gluten-free diet as part of the management of MS.

Adult↗
PubMed1995

Intestinal calcium absorption as shown by stable strontium test in celiac disease before and after gluten-free diet.

OBJECTIVES: To investigate the effect of gluten-free diet on mineral and bone metabolism in women with celiac disease and, using the strontium test, to assess intestinal calcium absorption. METHODS: We studied body mass index, biochemical and bone mineral indices, strontium absorption test, and bone mineral density in 18 women (mean age 36.8 yr, range 18-68 yr) with celiac disease at diagnosis and after 12 months of gluten-free diet. RESULTS: Mean strontium absorption at diagnosis was markedly decreased with respect to control values (13.84 +/- 9.03% vs 22.47 +/- 4.21%, p < 0.0001), and 11 of the 18 patients (61%, subgroup A) had low values. In all patients, mean hemoglobin, serum potassium, magnesium, plasma calcium, urinary calcium, and phosphorus were significantly abnormal at diagnosis, whereas only the subgroup A had significantly reduced body mass index, 25 OH vitamin D, and elevated alkaline phosphatase. This subgroup differed in body mass index (p < 0.003) and calciuria (p < 0.035) with respect to the other patients. Strontium absorption correlated with body mass index, calcemia, and 25 OH vitamin D. After the gluten-free diet, all biochemical variables and strontium absorption normalized (23.23 +/- 5.54%), whereas bone mineral density did not change. CONCLUSIONS: At diagnosis, the patients frequently had intestinal calcium malabsorption, as demonstrated by strontium test, with an early renal compensatory mechanism. After the gluten-free diet, the normalization of calcium absorption and the decrease of mid-molecule parathyroid hormone suggested a normalization of mineral metabolism, although a positive effect on bone mineral density was not evident at that time.

Adult↗
PubMed1993

Extracts of wheat gluten activate complement via the alternative pathway.

We studied the ability of wheat gluten and its subfractions to activate complement directly. A sensitive sandwich ELISA employing a monoclonal antibody (MoAb) to a C9 neoepitope exposed in the terminal complement complex (TCC), a functional haemolytic assay for C5b6 generation, and Laurell's electrophoretic method of estimating C3 conversion to C3bi were used. On a weight-for-weight basis, enzyme solubilized Frazer's fraction three of gluten (FIII) produced approximately 75% of the complement activation seen with the potent activator zymosan. By contrast, activation with whole insoluble undigested gluten was very weak and similar to that seen with ovalbumin or beta-lactoglobulin. The results were the same using normal human serum or sera from patients with coeliac disease, dermatitis herpetiformis, or hypogammaglobulinaemia as the complement source. Activation by both zymosan and FIII was blocked in 0.01 M EDTA, but not in 0.01 M EGTA with 0.0025 M magnesium chloride. Zymosan and FIII activated complement in a serum from a patient with an intact alternative pathway but classical pathway haemolytic activity (CH50) of zero. Preferential heat inactivation of the alternative pathway inhibited both zymosan- and FIII-induced activation. Our results confirm that FIII is a strong activator of the alternative pathway. We discuss how gluten enteropathy might be initiated by complement.

Adult↗