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PubMed1996

The coeliac disease task force " Free from Gluten," " Improved knowledge to cure coeliac disease".

Gluten has recently been introduced into the diet of the Mediterranean and European population, but a considerable proportion has not adapted to this change and has developed intolerance to gluten. At least one million EEC citizens are gluten intolerant. In Italy each year 12 million ECU is spent in the diagnosis of uncomplicated gluten intolerance, 10 million ECU for complex diagnosis and 32 million ECU for long-term complications and malignancies. The total financial load of gluten intolerance, in its present state, is about 150 million ECU/year in Italy. Four million ECU is actually needed to develop a genetic probe, which may make the population screening feasible. A National Task Force "Free from Gluten" has been set up by the Italian Coeliac Society to stimulate fund-raising activities supporting genetic and basic research on gluten intolerance.

Adult↗
PubMed1981

Some characteristics of immunofluorescence tests for antibodies against gluten, using wheat grain sections or gliadin coated sepharose beads.

Antibodies against gluten and gliadin were determined by the indirect immunofluorescence technique, using frozen wheat grain sections or gliadin-coated Sepharose beads. The methodological characteristics and diagnostic usefulness of the two techniques were evaluated. The reproducibility of both was improved by introducing a fluorometric reading-off procedure. Antibody quantitations were preferably performed as end-point titrations. The two techniques had different dose-response relationships. The grain section technique was more discriminative for small variations in antibody concentration than the bead technique. The latter was, however, more reproducible. Besides antibodies against gliadin, a number of patients with gluten enteropathy had antibodies against the main septa of wheat grains. Fluorescence intensity was preferably expressed in multiples of background intensity. A reaction was visually perceived when the fluorometrically-measured fluorescence intensity reached 2.5 times the background intensity. Using this value as the limit for positive reactions, antibodies were demonstrated in 81% of the cases with verified gluten intolerance, compared with 28% in cases with other intestinal allergies and 8% in normals. The diagnostic specificity of both the grain section and Sepharose bead technique for gluten enteropathy increased with increasing antibody concentration and was apparently 100% when the fluorescence intensity produced by a 1/10 serum dilution reached a value 7 to 8 times that of the background. Antibodies against reticulin were demonstrated in 1/4 of the cases having anti-gluten antibodies but in none of those with non-gluten-induced gastro-intestinal symptoms. Antibodies of the IgG class against cow's milk were demonstrated more often and in higher titre in cases with anti-gluten antibodies than in those without them.

Adolescent↗
PubMed1975

Confirming persistence of gluten intolerance in children diagnosed as having coeliac disease in infancy.

In young infants the clinical and investigative features of coeliac disease (CD) may be mimicked by other conditions such as cow's milk intolerance or secondary disaccharidase deficiency. It is therefore especially important to confirm a diagnosis of CD by later gluten challenge in such infants. Sixteen children in whom the diagnosis of CD had been made before the age of 12 months had an oral gluten challenge, after being treated with a gluten-free diet for periods of one month to 5 years. In 15 we showed intestinal xylose malabsorption by the one-hour blood xylose level within 1-28 days of starting ingestion of gluten. One child, with a persistently normal one-hour blood xylose test after gluten challenge for 3 months, had normal absorption and normal jejunal histology after 18 months on a gluten-containing diet; she is considered not to have CD. The one-hour blood xylose test before and after gluten challenge can help to confirm the diagnosis in coeliac patients diagnosed in infancy.

Biopsy↗
PubMed1976

Standardised approach to gluten challenge in diagnosing childhood coeliac disease.

Thirty-five children, in whom coeliac disease had been diagnosed on inadequate grounds and who had been on a gluten-free diet for one to 10 years, were challenged with gluten in accordance with a standardised procedure. All children were admitted to hospital for 48 hours for general assessment, two one-hour blood xylose tests, and the introduction of gluten. Thirty children underwent a pre-challenge peroral jejunal mucosal biopsy; the specimens were either normal or showed slight non-specific abnormalities. Gluten powder 20 g/day was given in addition to an otherwise gluten-free diet. The children were reassessed as outpatients every two weeks, when a one-hour blood xylose test was performed. Repeat biopsy was performed when xylose absorption fell or after three months. Seventeen children had abnormal post-challenge biopsy appearances compatible with coeliac disease in relapse; 14 of these children completed their challenge within eight weeks. Seventeen children had completely normal biopsy appearances at the end of three months and were returned to a normal diet. One to two years later eight underwent repeat biopsies, which showed nothing abnormal. In only one child, the oldest in the series, were the histological findings equivocal. In the 17 children in whom coeliac disease was confirmed the duration of gluten challenge was not related to age, duration of gluten-free diet, histological findings on the pre-challenge biopsy, or HLA status.

Adolescent↗
PubMed1970

The effect on jejunal mucosa of withdrawing and adding dietary gluten in cases of idiopathic steatorrhoea.

Biopsy studies of the jejunal mucosa in patients with idiopathic steatorrhoea after periods on a gluten-free diet showed that the epithelium improved quickly in respect of surface cell height, mucosal thickness, and mitosis count, and more slowly in respect of villous height and width. In no case was recovery complete in every particular. Appearances seen through the dissecting microscope improved slowly and incompletely. Gluten loading after a period on a gluten-free diet partially reversed some of these mucosal changes in as short a time as five to seven days. Measuring such changes may help to hasten the diagnosis in some patients with suspected gluten-sensitive enteropathy in whom there is otherwise difficulty in assessing the clinical response to a gluten-free diet. The histological response of the jejunum to a gluten-free diet and to subsequent gluten loading may help to clarify the aetiological relationship between carcinoma and jejunal mucosal atrophy.

Adult↗
PubMed1978

Cell-mediated immunity to gluten fraction III in adult coeliac disease.

A migration inhibition test was used to assess sensitisation of blood leucocytes, and thus cell-mediated immunity, to gluten fraction III in controls and patients with coeliac disease. Migration indices were significantly less (indicating sensitisation) in untreated and in treated patients than in controls, and significantly less in treated patients than in untreated patients. At a concentration of 1 mg/ml gluten fraction III, 13% of untreated patients and 54% of treated patients had migration indices in the sensitised range. At 2 mg/ml gluten fraction III, sensitisation was demonstrated in 8% of untreated patients and 48% of treated patients. After starting a gluten free diet, migration indices fell into the sensitised range in all patients followed. After at least nine months on a gluten free diet, migration indices were significantly higher in those patients with a normal interepithelial lymphocyte count than in those patients with a raised interepithelial lymphocyte count. Cell-mediated immunity to gluten fraction III can be detected in the peripheral blood of certain patients with coeliac disease. Detectable sensitivity is related to the time on a gluten free diet, and the interepithelial lymphocyte count.

Adult↗
PubMed1992

Dietary modulation of gluten sensitivity in a naturally occurring enteropathy of Irish setter dogs.

Gluten sensitivity in a naturally occurring enteropathy of Irish setter dogs, and the effects of excluding dietary cereal from birth on the subsequent response to gluten challenge were investigated. Peroral jejunal biopsy specimens were obtained at 1 year of age for morphometric and biochemical examinations, and intestinal permeability was assessed using 51Cr-ethylenediaminetetraacetic acid. Affected setters, reared on a normal wheat containing diet, exhibited partial villus atrophy, intraepithelial lymphocyte infiltration, reduced brush border alkaline phosphatase activity, and increased intestinal permeability. Gluten sensitivity was shown by introduction of a gluten free diet, which resulted in resolution of morphological and biochemical abnormalities and decreased intestinal permeability, and subsequent gluten challenge, which resulted in relapse. In contrast, littermates reared exclusively on a cereal free diet showed minimal changes when challenged with gluten, apart from intraepithelial lymphocyte infiltration. These findings document a gluten sensitive enteropathy in Irish setters and indicate that exclusion of dietary cereal from birth may modify subsequent expression of the disease.

Alkaline Phosphatase↗
PubMed2002

Long-term follow-up of celiac adults on gluten-free diet: prevalence and correlates of intestinal damage.

BACKGROUND AND AIMS: Celiac disease is the most common severe food intolerance in the Western world and is due to gluten ingestion in genetically susceptible children and adults. Intestinal biopsy is the golden standard for evaluation of mucosal damage associated with celiac disease. Gluten-free diet is the key treatment for celiac disease. Data on the long-term control of celiac disease are few and limited to small series of patients. The study reports data on the control of celiac disease and on its correlates in a large cohort of celiac adults during long-term treatment with gluten-free diet. METHODS: The study cohort comprises 91 men and 299 women having undergone treatment with a gluten-free diet for at least 2 years and with complete records for visits at the time of diagnosis of celiac disease (baseline). Data collection included gender, age, education, weight, bowel habit, blood hemoglobin, plasma albumin and cholesterol, serum antiendomysium antibodies (EMA), dietary compliance to gluten-free diet (coded as good, low, or very low), and intestinal damage at biopsy (coded as absent, mild, or severe). RESULTS: The duration of follow-up was 6.9 +/- 7.5 years (mean +/- SD, range 2-22 years). At follow-up visit, intestinal damage was absent in 170 patients (43.6%), mild in 127 (32.6%), and severe in 93 (23.8%). At follow-up, intestinal damage was significantly associated with dietary compliance, EMA, and plasma albumin (follow-up value and change value from baseline to follow-up). Baseline education significantly predicted dietary compliance and intestinal damage at follow-up. CONCLUSIONS: Celiac disease is often poorly controlled in the majority of patients on long-term treatment with a gluten-free diet as demonstrated by intestinal biopsy. Lack of adherence to strict gluten-free diet is the main reason of poorly controlled disease in adults. Laboratory and clinical information have a high positive predictive value and low negative predictive value for intestinal damage on long-term treatment. Dietary compliance as assessed by interview is the best marker of celiac disease control due to low cost, noninvasivity, and strong correlation with intestinal damage.

Adult↗
PubMed1978

Effect of dietary wheat gluten in lipid metabolism in growing rats.

The effect of dietary wheat gluten on liver and spleen lipogenesis in rats was studied in vitro and in vivo. Weanling rats were fed for 2 or 3 weeks an experimental diet containing wheat gluten as the only protein source and compared to other rats fed a casein control diet. Rats fed gluten showed enhanced in vitro lipogenesis as measured by conversion of (1(-14) C)-acetate into liver and spleen lipids. These results indicated that the gluten-fed rats had a significantly higher hepatic capacity than the control rats to synthesize all lipid classes. On the other hand, the in vivo study of hepatic lipogenesis showed smaller differences between the group fed gluten and that fed casein. This suggests that the accumulation of lipids in fatty livers of gluten-fed rats is mostly due to increased rate of biosynthesis and not a result of impairment in the lipids' transport system. In the spleens of the gluten-fed groups, the enhanced in vitro lipogenesis was also found in vivo, indicating that accumulation of lipids in fatty spleens may be a result of biosynthesis only, with no other effects that can take place in vivo.

Animals↗
PubMed2001

Macroamylasemia attributable to gluten-related amylase autoantibodies: a case report.

BACKGROUND: Macroamylasemia (MA) is a benign condition caused by circulating macroamylase complexes of pancreatic or salivary amylase bound to plasma proteins, which cannot be cleared by the renal glomeruli. In most cases, the macromolecular amylase represents a complex of normal amylase and either immunoglobulin A or G and may be a specific antigen-antibody complex. Celiac disease (CD) is a permanent intolerance to ingested gluten that results in immunologically mediated inflammatory damage of the small intestinal mucosa. Several recent population-based serologic surveys have shown CD to be a common disorder, possibly affecting 1 in 200 to 250 individuals in most countries studied, including the United States, where overt CD is rare, indicating a high proportion of subclinical disease. The diagnosis of CD currently rests on the histological demonstration of the characteristic lesion in the small intestine and the subsequent clinical response to the introduction of a gluten-free diet. MA associated with CD has been described in adult patients, and in a few cases, MA decreased or resolved after a strict gluten-free diet. A few single cases of MA have been described in childhood, but no association with CD has been reported so far. We report a girl with CD, autoimmune thyroiditis, and MA, in whom CD-related antibodies to amylase and to exocrine pancreas tissue resolved with a gluten-free diet. CASE REPORT: An 11-year-old girl was referred for chronic abdominal pain and growth retardation associated with persistent hyperamylasemia and suspected chronic pancreatitis. We confirmed elevated serum amylase, normal serum lipase, and very low 24-hour urine amylase and amylase clearance/creatinine clearance ratio, consistent with MA. Serologic tests for CD were positive, and the diagnosis was confirmed by small bowel biopsy showing subtotal villous atrophy. Thyroid function tests showed a pronounced hypothyroidism, associated with high titers of thyroid microsomal and thyroglobulin antibodies. Screening for other autoantibodies-including antinuclear, islet cell, glutamic acid decarboxylase, protein tyrosine phosphatase islet antigen 512, adrenal gland, and cytoplasmic neutrophil granulocyte antibodies-was negative. A diagnosis of CD, MA, and hypothyroidism attributable to autoimmune thyroiditis was made. A gluten-free diet and oral replacement with L-thyroxine was started with clinical improvement. Serum amylase and amylase clearance/creatinine clearance ratio normalized, consistent with resolution of MA. STUDY DESIGN AND METHODS: The patient's serum samples were obtained at the time of CD diagnosis and at 3 and 12 months after instituting a gluten-free diet. Serum samples from 10 consecutive untreated celiac children were disease controls, and 39 participants with no gastrointestinal symptoms and no family history of CD served as healthy controls. The origin of MA as determined by complexes of amylase with circulating immunoglobulins was tested by the measurement of amylase on supernatants after precipitation of immune complexes with either protein A Sepharose or polyethylene glycol. The precipitation of >60% of amylase activity was consistent with the presence of MA. Immunoglobulin G (IgG) and immunoglobulin A (IgA) circulating autoantibodies to amylase were measured using recently developed enzyme-linked immunosorbent assay (ELISA), using porcine amylase as antigen. Results were expressed as arbitrary units (AUs). Statistical analysis was performed by Student's t test for unpaired data. IgA and IgG antibodies to exocrine pancreas tissue were detected by indirect immunofluorescence on human pancreas cryosections. RESULTS: Serum immunoprecipitation with either protein A Sepharose or polyethylene glycol reduced amylase activity from 1698 to 89 U/L (94.8%) and to 75 U/L (95.6%), with only marginal reduction in control serum samples. The ELISA for autoantibodies to amylase detected high values, both IgA (3531 AU) and IgG (1855 AU), in the serum sample from the patient at CD diagnosis. IgA autoantibodies (mean +/- standard deviation) were 3.4 +/- 2.5 AU in healthy controls, and 2.1 +/- 1.2 AU in celiac controls; IgG autoantibodies were 10 +/- 4.8 AU in healthy controls and 8.5 +/- 3.2 AU, respectively. Autoantibodies to exocrine pancreas tissue were documented in patient sera at the time of CD diagnosis, both IgA and IgG, but not in control groups. Preincubation of patient's serum with excess of alpha-amylase specifically inhibited antibody binding to coated amylase in the ELISA, and partially inhibited immunoreactivity to exocrine pancreas. Autoantibodies to alpha-amylase and to exocrine pancreas declined in CD patients after institution of a gluten-free diet. CONCLUSIONS: Few cases of MA have been described in children, and in all amylase determination was part of the clinical investigation for abdominal pain or trauma. (ABSTRACT TRUNCATED)

Amylases↗
PubMed1988

Wet corn gluten feed as a supplement for lactating dairy cattle and growing heifers.

A lactation trial and a heifer growth trial were conducted to evaluate use of wet corn gluten feed by dairy herds. Twelve multiparous and 4 primiparous Holsteins were assigned to 4 x 4 Latin squares blocked according to previous production or parity. Animals received increasing amounts of wet corn gluten feed, up to 36% of ration DM, in place of a dry corn and soybean meal concentrate mixture. Each kilogram of wet corn gluten feed DM replaced .9 kg concentrate DM. Diets were based on ensiled forage with 33% of forage DM from wilted alfalfa silage and the remainder from corn silage. Forage and supplement were fed separately. Milk production, composition, and DM intake were not affected by increased feeding of wet corn gluten feed. Higher producing cows performed well on this feed. Wet corn gluten feed was generally acceptable when fed separately, but two animals refused sizable portions when fed the highest amount. Wet corn gluten feed can be utilized in traditional stall feeding of dairy cattle, and individual feeding should allow better management of this feed resource by limiting the amount offered to cattle that find it unpalatable. Wet corn gluten feed is also an adequate supplement for raising dairy replacements, allowing more rapid utilization of this perishable feed resource by the dairy herd.

Animal Feed↗
PubMed1975

The pathogenesis of gluten-sensitive enteropathy.

Gluten-sensitive enteropathy is characterized by flattening of intestinal villi and malabsorption caused by the toxic effect of gluten, a wheat protein. Gluten activates an endogenous mechanism of toxicity that may be the local mucosal immune system: local mucosal immunoglobulin and antigluten antibody production occur soon after gluten ingestion. Approximately 80% of patients with this disease possess HL-A8, a second segregant series antigen. This association also occurs in dermatitis herpetiformis, a disease with vesicular skin lesions and gluten-sensitive flattening of intestinal villi. The association suggests that the fundamental abnormality in enteropathy is a binding reaction involving gluten protein and a binding site on a cell surface, determined in part by the histocompatibility gene; this reaction then results in a local mucosal immune response to gluten. Alternatively, the fundamental abnormality may be the presence of an abnormal immune-response gene linked to the HL-A8 gene or acting in concert with it; this immune-response gene results in local mucosal production of antigluten antibody.

Adult↗
PubMed2003

[Compliance with gluten free diet, physical development and bone mineral status in patients with celiac disease].

OBJECTIVES: The aim of the study was the assessment of the influence of a gluten free diet on physical development and bone mineral density (BMD) in patients with celiac disease. MATERIALS & METHODS: 59 patients (40 girls, 19 boys) aged 10-20 years with celiac disease, diagnosed according to ESPGAN criteria were included in the study. Patients were divided in 3 groups: 1--strict gluten free diet, II--not entirely compliant i.e. faults in gluten free diet 1-2 times per week, III--gluten free diet not followed or frequent faults. Daily calcium (Ca) intake and physical activity was assessed. BMD of the lumbar spine L2-L4 was measured by dual-energy-X-ray absorptiometry with LUNAR DPX-IQ. Physical development was assessed by anthropometric measurements: growth and weight. RESULTS: Gluten free diet was strictly followed by 16 (27%) patients (group I), group II consisted of 23 (39%) patients. Diet was not followed by 20 (34%) patients. Thirty five (59%) patients had low Ca intake and they made up the majority of the patients in every group. High physical activity declared 35 (59%) patients. No statistically significant differences in BMD were found between group I and II. BMD was lower in group III in comparison to group I (p = 0.01) and group II (p = 0.003). BMD was higher in patients with high Ca intake (p = 0.002). Physical activity had no significant influence on BMD. There was no statistically significant difference in physical development between groups. CONCLUSIONS: Majority of the patients with celiac disease did not strictly follow gluten free diet. Poor compliance to the diet had no significant influence on physical development. BMD was lower in patients who were not compliant to the gluten free diet, occasional faults in the diet had no influence on the BMD.

Absorptiometry, Photon↗
PubMed1991

Gluten challenge in patients with celiac disease: evaluation of alpha 1-antitrypsin clearance.

Our aim in this study was to monitor changes of the intestinal structure by alpha 1-antitrypsin clearance (alpha 1-ATCL) in order to offer an alternative to the gluten challenge biopsy. In addition, we evaluated the possibility of reducing the time of gluten challenge. Twelve patients had a presumptive diagnosis of celiac disease based on clinical and histological grounds. They were studied when the jejunal histology was normal after gluten-free diet and an alpha 1-ATCL was normal. The gluten was introduced by returning to a normal diet. The challenge lasted 4 wk. We measured alpha 1-ATCL at the end of the 1st and 4th wk, and a new jejunal biopsy was obtained at the end of the 4th wk. By wk 1, alpha 1-ATCL was abnormal in 11 patients but normal in one. By wk 4, alpha 1-ATCL was abnormal in 10 patients and still normal in one. The post-challenge biopsies showed atrophy in 11 and was normal only in the patient with normal alpha 1-ATCL at wk 1 and 4. One patient with abnormal alpha 1-ATCL had to stop the challenge at the first week. The patient with normal clearance at wk 1 and 4 and normal biopsy at wk 4 had abnormal results at 6 months. These data support our hypothesis that alpha 1-ATCL can be used as evidence of gluten toxicity after gluten challenge, and that this test can be abnormal as early as 1 wk after gluten is reintroduced.

Adolescent↗
PubMed1990

Effects of a gluten-free diet in primary IgA nephropathy.

In an uncontrolled study a gluten-free diet was given to 29 patients affected by primary IgA nephropathy (IgAGN). All of them followed the diet for 6 months, 23 patients for 1 year and 9 for 2 to 4 years. Mean levels of IgA containing circulating immune complexes (IgAIC), detected by a specific conglutinin assay and by measuring IgA content in 2.5% polyethylene glycol precipitates, on an unrestricted diet, significantly decreased after 6 months of gluten-free diet (p less than 0.01) and remained reduced during the follow-up. A decrease in IgAIC levels was evident in 85.7% of the cases with basal positive data, with complete normalization in 64.3% of them. IgA to gluten antigens (ethanol- or saline-soluble gliadin, glutenin and the lectin fraction termed glyc-gli) as well as to heterologous bovine and egg albumins were found to be significantly increased on an unrestricted diet in the group of 14 IgAGN patients with basal positive IgAIC. The mean levels of IgA to most dietary antigens significantly decreased after 6 months to 1 year of a gluten-free diet. A decrease in IgA to ethanol-soluble gliadin was evident in 81.8% of the cases with basal positive data, with complete normalization in 63.6%. A subgroup of 27.5% of IgAGN patients showed positive IgAIC values associated with increased IgA values to a variety of dietary antigens. A gluten-free diet induced in 75% of the cases a parallel improvement in these abnormal immunological data. Mean proteinuria values were found to be significantly decreased after 6 months of the diet and a reduction was also observed in microscopic hematuria. However, mean blood creatinine levels showed a significant increase after the gluten-free diet. The data of this study indicate that a gluten-free diet can modify some immunological abnormalities in a group of IgAGN patients, reducing levels of IgAIC and IgA to dietary antigens. The clinical course does not seem to be favorably influenced, since a relentless progression towards renal failure was observed.

Adult↗
PubMed1989

Gluten-induced experimental IgA glomerulopathy.

The effect of alimentary gluten and of its lectin-like fraction gliadin in inducing IgA mesangial deposits in BALB/c mice was investigated. In the pilot study G1 (4 mice), G2 (4 mice) and G3 (6 mice) received ovalbumin, human gamma-globulins, and crude gluten, respectively. The antigens, 1 mg/ml, were given in drinking water for 14 weeks. G4 (20 mice) were fed with standard mouse fodder. Gluten, as well as other alimentary antigens, induced IgA mesangial deposits with intense IgA staining in each animal, however a positive IgA staining was also observed in 10 of 20 adult controls. Antigliadin IgA antibodies were detected in renal tissue eluates from gluten-immunized mice but were found in eluates from control animals too. IgA deposits and antigliadin IgA in renal tissue were also observed in 3 of 7 adult mice (G7) fed for 30 weeks with standard fodder, then for 1 month with a protein-free diet supplemented with 20% amino acids. Conversely, there were no IgA mesangial deposits or IgA anti-gliadin antibodies in renal eluates of 1- or 2-week-old mice (G5 and G6). For the definitive protocol, 4-week-old BALB/c mice were selected and fed with basal glutenfree diet. G8 (14 mice) did not receive any alimentary immunogen in the drinking water, whereas G9 (15 mice) and G10 (15 mice) received ovalbumin and gliadin, respectively. G11 (15 mice) had standard gluten-containing diet. IgA deposits semiquantified by immunofluorescence scores were found to be significantly greater in G9 and G10 than in G8 (Student' t-test p1 less than 0.003, Mann-Whitney test p2 less than 0.001 and p1 less than 0.01, p2 less than 0.007, respectively), and in G11 than in G8 (p1 and p2 less than 0.05). The presence of positive IgA staining (greater than or equal to 2/6 scores) was significantly less frequent in G8 in comparison to G9 (chi-square test p3 less than 0.002), G10 (p3 less than 0.02) and G11 (p3 less than 0.04). Total serum IgA were significantly higher in orally immunized G9 and G10 than in G8 control mice (p1 less than 0.005, p2 less than 0.002). Anti-gliadin IgA in circulation as well as in renal deposit eluates were significantly increased in gluten-eating mice (G10 and G11) as compared with the gluten-free control group G8. These observations indicate that gliadin does induce IgA immune deposits in BALB/c mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Dermatitis herpetiformis: relation between circulating antibodies against reticulin and gluten, small-intestinal mucosal status and absorptive capacity.

The status of the jejunal mucosa and of the intestinal absorptive capacity were investigated and related to the occurrence of antibodies against reticulin and gluten in 55 patients with dermatitis herpetiformis (DH), 28 on a normal, 11 on a gluten-reduced and 16 on a gluten-free diet. The mucosal status was characterized on the basis of histopathological findings and the numbers of intra-epithelial lymphocytes. Absorption was evaluated by 5-h urine and 1-h serum D-xylose tests. There was a positive correlation between the degree of pathological mucosal changes, malabsorption and the occurrence of circulating antibodies against reticulin and gluten. The serum xylose test was more sensitive than the urine xylose test for screening of the relatively mild enteropathy of DH and identified 88% of the patients with an abnormal mucosal status. The serological test (antibodies to reticulin and gluten) identified 80% of such patients. Among patients on a gluten-free diet there was some discrepancy between the serum xylose and the serological test, in that 5 of the 16 patients on this diet had an abnormal serum xylose test result, but no antibodies. In DH patients on a normal diet, the presence of antibodies to reticulin and gluten provided the same information about the presence of mucosal lesions as the serum xylose test. In the whole material a combination of the serum xylose test and the serological test identified 24 of 25 patients with an abnormal mucosal status.

Adult↗
PubMed1981

[Diagnostic value of the histological examination in gluten-sensitive enteropathy].

At 42 children with malabsorption syndrome 65 peroral intestinal biopsies have been taken. In 7 cases three consecutive biopsies - at the onset of symptoms (1.), after gluten withdrawal (2.) and after reintroduction of gluten (3.) - were obtained. In 3 cases two biopsies, the (2.) and the (3.) were examined. On the basis of the clinico-morphological analysis of 27 biopsies gluten sensitive enteropathy was diagnosed in 6 cases. In 4 cases the reaction of the intestinal mucosa on withdrawal and reintroduction of gluten indicated transient gluten intolerance. As an effect of the dietary treatment introduced according to the morphological alterations of intestinal mucosa normal development of children started. Authors believe that the diagnosis of the gluten sensitive enteropathy and it's differentiation from the transient gluten intolerance should be based on the morphological examination of the intestinal mucosa.

Biopsy↗