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PubMedDate not supplied

[The provocation test in children with cow-milk protein and gluten intolerance: evaluation of the clinical response and lesions in the mucous membrane of the small intestine].

Provocation test (re-introduction of the noxious protein) was carried out in two groups of patients: (a) with intolerance to the cow-milk proteins (41 children) treated with milk-free diet for 6-24 months, and (b) with gluten intolerance (26 children) treated with gluten-free diet for 6-36 months. The following parameters were compared: type and frequency of the clinical symptoms seen in these patients prior to the introduction of allergen-free diet. Moreover, the type of observed morphological changes in the small intestine mucosa following provocation test were analysed in the groups of 7 patients. A two-year elimination of milk from the diet produces milk tolerance in about 61% patients; clinical symptoms in the remaining children are diversified. Re-introduction of gluten with the diet (provocation test) produces recurrence of gluten intolerance in 96% of children treated with gluten-free diet for 2-3 years. Recurrence of the disease was accompanied by the atrophy of the intestinal villi.

Atrophy↗

PubMed1987

Experience with a gluten free diet in the treatment of linear IgA disease.

A study was undertaken to determine whether the skin eruption of linear IgA disease (LAD) was gluten dependent. Six patients with LAD were treated with a gluten free diet (GFD) for an average period of 33 months (range 19-48). Although one patient with LAD had an enteropathy which was clearly gluten sensitive, there was no convincing evidence that the rash of any of the patients responded to a GFD. Four of the six patients showed no significant alteration in their drug requirements. The remaining 2 patients showed a fall in minimum drug requirement but there was no increase after gluten challenge indicating that they were entering spontaneous remission. This contrasts to the situation in dermatitis herpetiformis, where both the rash and the enteropathy are gluten dependent. These data add further to the evidence that LAD and dermatitis herpetiformis are separate entities.

Adult↗

PubMed1987

Relationship of dietary gluten intake to dapsone dose in dermatitis herpetiformis.

The gluten intake was quantitated utilizing a dietary history method in 43 patients with dermatitis herpetiformis on non-restricted diet. The mean daily gluten intake was 15 g. The individual intake of gluten was related to the maintenance dose of dapsone. It was significantly higher in patients on 100-150 mg dapsone daily than in those taking 0-25 mg daily. There was a significant correlation between amount of gluten in the diet and the dapsone dose (p less than 0.01, rs = 0.43). Villous atrophy was not related to the dapsone dose. It is suggested that the gluten-sensitive enteropathy changes the intestinal permeability and thus contributes to the development of blisters.

Adolescent↗

PubMedDate not supplied

[Clinico-histological behavior of celiac patients after gluten load following the definitive diagnosis].

In the last 18 years we have followed 330 children with Coeliac Disease (CD), diagnosed according to the ESPGAN criteria (with 3 jejunal biopsies: during the acute phase, after a gluten-free diet and after a gluten challenge). One to fifteen years after the diagnosis, 61 of them asked to be exposed to a second gluten challenge to see if their intolerance was persistent. Ten percent of them had already started the challenge by themselves, the others were on Gluten Free Diet (GFD). To all 61 serial clinical controls, one-hour-blood-xylose absorption test every three months and a jejunal biopsy was suggested. The jejunal biopsy was performed when symptoms recurred, or when xylose-test showed an impaired absorption, or after 2 years. If the first jejunal biopsy showed a villous atrophy the GFD was restarted, while if a normal mucosa was found the gluten challenge was continued and the jejunal biopsy repeated every year. 52 children (85%) showed a villous atrophy after 1.5 to 72 months. 6 (10%) did not show a clinical or histological relapse, 2 refused the jejunal biopsy because symptomless, and 1 had to restart the GFD because she developed a dermatitis herpetiformis. One-hour-blood-xylose test was performed in 29 children and 20 (69%) showed a low absorbtion, the majority of them in the first year of challenge, and the remaining refused it. 36 of the relapsed children presented with mild clinical symptoms while 16 were symptomless.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1988

In mice, gluten in maternal diet primes systemic immune responses to gliadin in offspring.

We have demonstrated recently immunological tolerance to gliadin in mice maintained on a diet that contains gluten. The aim of this study was to investigate whether oral tolerance is recreated in each generation by the ingestion of dietary gluten at weaning, or whether it is transferred from mother to young (as immune status or via passage of antigen) before birth or during lactation. Surprisingly, instead of transfer of tolerance we found priming of the immune response to gliadin in young mice. Mice born to mothers from normal, gluten-containing diet colonies had significantly greater systemic immune responses to gliadin after parenteral immunization than mice born to mothers from a gluten-free diet colony. Furthermore, feeding mothers gluten-containing diet for defined periods before and during pregnancy and during lactation also resulted in priming of the specific systemic immune responses of the offspring. These findings indicate that, in mice, sensitization to maternal dietary antigens readily occurs in utero or shortly after birth. This animal model should allow investigation of the immunological mechanisms concerned.

Animals↗

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↗

PubMed1980

Gluten-sensitive diarrhea without evidence of celiac disease.

Eight adult female patients suffering from abdominal pain and chronic diarrhea which was often incapacitating and frequently nocturnal, had dramatic relief on a gluten-free diet and return of symptoms after gluten challenge. Previous nonspecific measures and a milk-free diet were ineffective. Multiple jejunal biopsies showed minor, but significant changes in cellularity which returned to normal on the gluten-free diet. Apart from a slight increase in jejunal cellularity, no immunological abnormalities were found after gluten challenge. Steatorrhea or other biochemical defects, common in celiac disease, were not found. It was concluded that these patients had a gluten-sensitive diarrhea, but had no evidence of celiac disease.

Adult↗

PubMed1997

[Mineral content in bones of children with symptomless celiac disease and gluten-free diet].

Osteoporosis is a complication of adult celiac disease. The gluten-free diet improves but does not normalize bone mineral density. Only few and conflicting data are known about the influence of the disease and diet on bone mineralization in children. The aim of this study was to evaluate the radial bone mineral content (BMC) and density (BMD) in children and adolescents who are asymptomatic on gluten-free diet. The BMD and BMC values of non-dominant radius midshaft in ninety-one children (53 girls and 38 boys, mean age: 11.7 years, mean duration of disease: 8.7 years) were determined by single photon absorptiometry. At the diagnosis and at least three years after gluten-free diet, serum calcium, phosphorous and albumin concentrations and alkaline phosphatase activities were determined in all, and additionally intact parathormone concentrations in 16 patients. The mean BMC Z-score value in the entire study population did not differ from the value of normal age-matched population (mean Z-score: -0.27), but in female adolescent group was significantly lower than the normal value (mean Z-score: -1.04, p < 0.01). In contrast, the mean BMC Z-score value was significantly higher than in normal value in girls (mean Z-score: +1.36, p < 0.001), in boys (mean Z-score: +0.53, p < 0.02) as well as in the total patients group (mean Z-score: +1.01, p < 0.001). The diameter of radius midshaft was significantly smaller in all age group than the normal mean value. Serum laboratory parameters of asymptomatic patients were in the normal range. The serum parathormone value in treated patients was significantly lower than in untreated celiac children (mean +/- SD: 3.77 +/- 1.07 versus 7.89 +/- 2.54, p < 0.01), but significantly higher compared to controls (2.89 +/- 0.9, p < 0.05). The data indicate that the gluten-free diet alone is not able to normalize bone mineralization in children. The significant increase of serum parathormone level in treated asymptomatic patients may be explained by the lower calcium content of gluten-free diet. The authors suppose that low calcium supply in children similarly to adult patients can lead to increased parathormone secretion, which can cause the retardation of bone growth even in treated patients with celiac disease.

Adolescent↗

PubMed2004

Psychological support counselling improves gluten-free diet compliance in coeliac patients with affective disorders.

BACKGROUND: Anxiety and depression are common features of coeliac disease. Depression is cause of non-compliance to treatment in chronic illness. AIM: To evaluate the useful of psychological support counselling to improve affective disorders and gluten-free diet adherence in coeliac disease with anxiety and depression. METHODS: A total of 66 coeliac disease patients with state anxiety and current depression were enrolled. Patients were randomized in two groups: in group A psychological support was started at the beginning of gluten-free diet, while group B was free of psychological support. Both groups were followed every 2 weeks for 6 months. State and Trait Anxiety Inventory test Y-1 and the modified Zung self-rating depression scale were administered before (T0) and after 6 months of gluten-free diet (T1). RESULTS: At T1 no difference was found between groups in the percentage of state anxiety, while a significant lower percentage of depressed subjects was found in group A with respect to group B (15.1% vs. 78.8%; P=0.001). In the follow-up period, a significant lower compliance to gluten-free diet was found in group B with respect to group A (39.4% vs. 9.1%; P=0.02). CONCLUSIONS: In coeliac disease patients with affective disorders psychological support seems to be able to reduce depression and to increase gluten-free diet compliance.

Adult↗

PubMed1981

New immunofluorescent blood test for gluten sensitivity.

A new test for the detection of antibodies to gliadin in the sera of children who are gluten sensitive is described. This test is based on the observation that wheat protein binds selectively to connective tissue fibres in cryostat sections of mammalian tissues. Sera containing antibodies to gliadin give a reticulin pattern of staining on section pretreated with wheat gliadin if tested by indirect immunofluorescence. Antibodies to gliadin were detected in this manner in sera fom all of 32 children with coeliac disease, in 16 of whom a provisional diagnosis had been given and in 16 an established diagnosis confirmed by gluten challenge. The incidence of reticulin antibodies detected on untreated sections (in the absence of gliadin) was only 28%. Gliadin antibodies were also present in sera from 15% of 152 children with gastroenterological disorders other than coeliac disease, but most of these non-positive results for coeliac disease were in patients with transient gluten in tolerance, cows' milk-sensitive enteropathy, or Crohn's disease. This new test, although not specific for coeliac disease, promises to be of value as an indicator of gluten sensitivity, and when negative excludes a diagnosis of coeliac disease. It may also be useful in monitoring diet, and in determining when rebiopsy after gluten challenge in appropriate.

Adolescent↗

PubMed1981

Morphological and morphometric assessment of human duodenal biopsies maintained in organ culture. In vitro influences of gluten in coeliac disease.

Duodenal biopsy specimens from 51 coeliac patients (children and young adults) and 13 non-coeliac controls were maintained in organ culture for 24 h. Morphometric determinants were compared after culture in the presence of different gluten fractions, after culture on gluten-free medium, and in non-cultured specimens. Biopsies from patients with untreated coeliac disease were susceptible to gluten fractions, which provoked disorganization of crypt architecture, reduced height and irregularities of enterocytes and crypt cells, together with detrition of surface epithelial cells and even tissue necrosis. In latent coeliac disease (silent relapse) biopsies were more resistant to gluten, and higher concentrations were required to induce signs of morphological deterioration. Remission mucosa and biopsies from non-coeliac controls showed no signs of impairment after gluten exposure in vitro.

Adolescent↗

PubMed2002

Gluten-sensitive enteropathy (celiac disease): more common than you think.

Gluten-sensitive enteropathy or, as it is more commonly called, celiac disease, is an autoimmune inflammatory disease of the small intestine that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons. Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease. Recent studies in the United States suggest that the prevalence of celiac disease is approximately one case per 250 persons. Gluten-sensitive enteropathy commonly manifests as "silent" celiac disease (i.e., minimal or no symptoms). Serologic tests for antibodies against endomysium, transglutaminase, and gliadin identify most patients with the disease. Serologic testing should be considered in patients who are at increased genetic risk for gluten-sensitive enteropathy (i.e., family history of celiac disease or personal history of type I diabetes) and in patients who have chronic diarrhea, unexplained anemia, chronic fatigue, or unexplained weight loss. Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anemia.

Celiac Disease↗

PubMed2005

[Gluten enteropathy--occurrence, diagnosis, therapy].

Gluten enteropathy is a chronic all-life disease, characterized by typical inflammatory changes of the small bowel mucosa. It is the genetically determined autoimmune disease with permanent intolerance to gluten. Its clinical signs are very heterogeneous and also the severity of intestinal changes varies considerably. It frequently presents with atypical symptoms, as many as 80% of adult patients have no gastrointestinal troubles at all. The present estimated prevalence is 1:200 - 1:250. The diagnosis is based on criteria of the European Society of Paediatric Gastroenterology, Hepatology and Nutrition revised in 1990, above all on the detection of serum antibodies to endomysium and tissue transglutaminase. The five forms are distinguished: classic, subclinical, latent, potential and silent. Coeliac disease and dermatitis herpetiformis are considered to be two identical forms of the gluten enteropathy manifestations. Coeliac disease is frequently associated with other autoimmune diseases--diabetes mellitus, autoimmune thyreoiditis, hepatitis, IgA deficiency. Permanent gluten free diet is the cornerstone of the therapy; untreated gluten enteropathy is a serious illness, considered to be a significant precancerosis.

Celiac Disease↗

PubMed1989

[Anti-endomysium antibodies: new serological markers for the diagnosis and follow-up of patients with gluten-sensitive enteropathy. Preliminary study].

The authors value the parameters of diagnostic efficacy in a preliminary study of anti-endomysium antibodies (EmA), in the diagnostic and follow-up of patients with gluten sensitive enteropathy. The study was made with 84 subjects distributed into four groups. Group I consisted of 21 patients with gluten sensitive enteropathy (GSE) who were eating gluten at the time of diagnosis. Group II consisted of 20 patients with gluten sensitive enteropathy with different periods of time of gluten free diet. Group III consisted of 16 subjects with non-evolutive neuropathies and without intestinal disease. This group was considered as controls. Group IV consisted of 27 patients with toddler diarrhoea. The sensitivity, specificity, positive predictive value, negative predictive value and efficiency were 100%.

Autoantibodies↗

PubMedDate not supplied

Severe osteomalacia due to gluten-sensitive enteropathy.

This report discusses a severe case of osteomalacia due to gluten-sensitive enteropathy: it stresses the clinical features and describes an atypical form of gluten-sensitive enteropathy, in which gastroenterological symptoms were absent. Wasting and osteomalacia causing skeletal deformation with spontaneous fractures were observed in a 31-year-old woman who had marked hypophosphoremia, a tendency to low serum calcium levels and slight multi-deficiency anaemia. The patient was in a state of depression. The causes of osteomalacia and then a general malabsorption syndrome were investigated. Anti-gliadin antibodies were positive. Histological tests on duodenal mucous revealed a pattern indicative of gluten-sensitive enteropathy. A gluten-free diet was prescribed and at a check-up one month later the patient had improved markedly. Skeletal symptoms are predominant in 30% of atypical forms of gluten-sensitive enteropathy. The severity of this case was due to a late diagnosis.

Acute Disease↗

PubMed1999

Glutenin is involved in the gluten-driven mucosal T cell response.

Gluten ingestion causes coeliac disease in susceptible individuals. Gluten is a heterogeneous mixture of glutenin and gliadin, the latter of which is considered responsible for disease induction. By combining high-performance liquid chromatography purification steps of gluten with a T cell bioassay and mass spectral analyses, we have identified a glutenin peptide (glt04 707-742) that activates T cells from the small intestine of a coeliac disease patient and results in the secretion of large amounts of IFN-gamma. The minimal T cell stimulatory core of the peptide (residues 724-734) is repetitively present in glutenin molecules. Moreover, it was observed that a large number of naturally occurring variants of this peptide are recognized by the T cells. These data suggest that the large heterogeneity of glutenin proteins dramatically increases the number of available T cell epitopes. Together, the results provide new insight into the nature of the gluten antigens that lead to coeliac disease and suggest that glutenin, next to gliadin-derived antigens, may be involved in the disease process.

Amino Acid Sequence↗

PubMed1981

[Changes in the biological protein value of wheat grain caused by manufacture into flour and gluten].

The authors determined the amino-acid composition of the proteins of whole wheat grain, flour and gluten, and calculated the biological protein values of these products from the data obtained. The decrease in the contents of the single amino acids was as follows: flour, 8--13% (as compared to whole grain); and gluten, 2--5% (as compared to flour). The decrease in the biological protein value according to Mitchell was: wheat flour, 5% (as compared to whole grain); and gluten, 8% (as compared to flour). The decrease in the biological protein value according to Oser was: flour, 9% (as compared to whole grain); and gluten, 26% (as compared to flour).

Amino Acids↗

PubMed2006

Dietary treatment of gluten neuropathy.

We studied the effect of a gluten-free diet in patients with idiopathic sensorimotor axonal neuropathy and circulating antigliadin antibodies. Consecutive patients underwent baseline neurophysiological assessment and were offered a gluten-free diet. Those who went on the diet formed the intention-to-treat group and those who did not were the control group. Repeat neurophysiological assessment and subjective evaluation of neuropathy symptoms were performed at 1 year. A total of 35 patients participated in the study, with 25 patients going on the diet and 10 not doing so. There was a significant difference in the change of sural sensory action potentials (pre-defined primary endpoint), with evidence of improvement in the intention-to-treat group and deterioration in the control group. Subjective change in neuropathy symptoms also showed significant differences, with patients in the intention-to-treat group reporting improvement and those in the control group reporting deterioration. Gluten-free diet may thus be a useful therapeutic intervention for patients with gluten neuropathy.

Aged↗