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PubMedDate not supplied

Dermatitis herpetiformis: problems, progress and prospects.

Dermatitis herpetiformis (DH) is an IgA mediated blistering skin disease characterized by the presence of granular deposits of IgA in papillary dermis. The major significant advances in our understanding of DH have been the demonstration that DH patients also have coeliac diseases (CD) and that the rash is also gluten dependent. As a result, it is now possible to cure patients by gluten withdrawal from the diet. The other major significant finding has been the presence of IgA in the uninvolved, now used as the diagnostic criterion for the disease. Despite the fact that it has been known for over fifty years that gluten causes the enteropathy of CD, and for over thirty years the rash of DH, it is still not known how gluten produces these effects. Future immunological studies may look at ways of inducing tolerance to gluten peptides once the toxic ones have been identified. Vaccination against gluten peptides may also be possible in those affected with gluten sensitive disorders.

Adolescent↗
PubMed1990

Effect of dietary proteins on the plasma immunoreactive insulin-like growth factor-1/somatomedin C concentration in the rat.

Plasma immunoreactive insulin-like growth factor-1/somatomedin C (IR-IGF-1) was determined in rats fed for 1 week on a protein-free diet, or diets containing gluten, gluten supplemented with lysine and threonine, maize-gluten meal (with arginine), maize-gluten meal (with arginine) supplemented with tryptophan and lysine, or casein. IR-IGF-1 concentration was higher in the arterial plasma of rats fed on a diet containing casein at 120 g/kg diet (4-8 U/ml) than in rats fed on a protein-free or a low-casein (50 g/kg diet) diet (1.5-2 U/ml). The plasma of rats fed on gluten or maize-gluten meal as the protein source showed intermediate values. However, giving a diet containing an amino acid mixture as recommended by the National Research Council (1978) but deprived of lysine or tryptophan did not affect significantly the plasma IR-IGF-1 concentration. Total IGF-1 concentration (which was measured immunologically after extraction of the plasma with acid-ethanol) was also lower in the rats fed on the protein-free diet than in those fed on the casein (120 g/kg diet) diet. The ratio IR-IGF-1:total IGF-1 was higher in the rats fed on the casein diet (120 g casein/kg diet) than in those fed on the protein-free diet. The results suggest an important influence of IR-IGF-1 or IR-IGF-1:total IGF-1 ratio on protein anabolism and nutrition. IR-IGF-1 and total IGF-1 were found in the fractions of molecular weights 40 kDa and 150 kDa after gel filtration of rat plasma. A larger amount of IGF-1 was recovered in the fraction of 150 kDa in the rats fed on the casein diet. 125I-IGF-1 added to the plasma of rats fed on the protein-free diet was found mainly in the fraction of 40 kDa after gel-filtration. On the other hand, 125I-IGF-1 added to the plasma of rats fed on the gluten or casein diets was mainly recovered in the free IGF-1 fraction. The results suggest that IGF-binding protein(s) of molecular weight about 40 kDa was not saturated with IGF-1 in the rats fed on the protein-free diet. The results indicate the important role of IGF-1 and its binding proteins in the regulation of protein metabolism in rats.

Animals↗
PubMed1990

Serum antibodies to dietary antigens: a prospective study of the diagnostic usefulness in celiac disease of children.

We examined 1,541 consecutive serum samples from 707 children with suspected food intolerance and 32 with treated celiac disease (CD) for IgG and IgA antibody reactivities to antigens from gluten, egg, and cow's milk by an enzyme-linked immunosorbent assay (ELISA). Samples from 72 patients showed increased IgA and/or IgG reactivity to gluten antigens; four were known CD patients not complying with a gluten-free diet, 13 were suspected CD patients challenged with gluten, and 30 most likely had CD as suggested by small intestinal villous atrophy and histological and/or clinical improvement on a gluten-free diet. The remainder with increased antigluten activity had other disorders that might have affected mucosal permeability. Nevertheless, the median IgA reactivity to gluten was significantly higher in the CD group, and the probability for CD increased from 25 to 100% when this reactivity was above 2.4 optical density (OD) units in our ELISA. Sixteen CD patients (but none of those without CD) had IgA reactivity to gluten higher than 2.4 OD units. We conclude that ELISA determinations of levels of serum antibodies reacting to dietary antigens is a valuable adjunct in the diagnosis of CD in children.

Adolescent↗
PubMed1986

Intestinal and serum antibody in coeliac disease: a comparison using ELISA.

Intestinal and serum antibody to antigens derived from gluten and other food proteins in 16 children with coeliac disease and 15 control subjects was measured using an enzyme-linked immunosorbent assay (ELISA). High concentrations of antibody to gluten antigens were found in children with coeliac disease who were on a diet which contained gluten. This antibody was predominantly in the IgA and IgM classes in intestinal fluid, and in the IgG and IgA classes in serum. When coeliac children transferred to a gluten-free diet for 6 months or more, anti-gluten antibody fell much more rapidly in serum than in intestinal fluid. Although no single measure of antibody, in any immunoglobulin class, to a gluten-derived antigen proved sufficiently discriminating to be suggested as a diagnostic test for coeliac disease, serum antibody, particularly in the IgA class, may be of value in following the progress of patients and in assessing their adherence to a gluten-free diet.

Adolescent↗
PubMed2003

Self-rated quality of life in celiac disease.

As much as 1% of the gluten-consuming world is gluten-intolerant. New screening methods are increasingly identifying gluten intolerance in individuals previously free from health problems. The often-abrupt major change in diet may adversely affect the patient's quality of life. Our aim was to evaluate self-perceived quality of life in a large cohort of adult celiac patients after at least one year of a gluten-free diet. In all 581 members (410 females) of five regional celiac societies were on a gluten-free regimen for at least one year. In this cross-sectional study, a modified version of the Zung Self-Rating Depression Scale was administered to the 581 patients from five Italian regions. Most patients correctly defined celiac disease, and compliance with the gluten-free diet was high, although reporting bias cannot be excluded. Most felt well (83.6% "very well" and "well"); consequently, anxiety and depression scores were low. Happiness also scored low. Most participants did not feel that a gluten-free life differentiated them from the general population. Women and patients diagnosed after 20 years of age had better dietary compliance, but more problems in their social life. Happiness scores were higher in patients diagnosed before 20 years of age. Anxiety and depression were infrequent in this group; however, anxiety was frequently related to feeling different from the general population, and depression to an unsatisfactory sexual life. In conclusion, celiac disease does not appear to be associated to a low level of self-perceived quality of life in members of the Italian Celiac Society.

Adult↗
PubMed2000

Concordance of dermatitis herpetiformis and celiac disease in monozygous twins.

Celiac disease can be defined as the classical manifestation of gluten sensitivity, which primarily affects the small intestine. Gluten sensitivity has also a skin manifestation, i.e., dermatitis herpetiformis. Both diseases have a strong genetic association with HLA DQ on chromosome 6. In this study we tried to estimate how much different clinical expressions of gluten sensitivity are determined by genetic factors, and hence how feasible they are for genetic mapping; therefore, we studied all six monozygous twin pairs found among 1292 prospectively collected patients of dermatitis herpetiformis in Finland. Three of the six twin pairs were concordant for dermatitis herpetiformis and for simultaneous enteropathy, celiac disease. Two other twin pairs were partially discordant, one of each pair had dermatitis herpetiformis and celiac disease, whereas the other had solely the gut manifestation of gluten sensitivity, i.e., celiac disease. Only one pair was found to be discordant for gluten sensitivity. All the pairs had typical risk alleles for gluten sensitivity, i.e., either HLA DQ2 or DQ8. These results demonstrate that the genetic component in gluten sensitivity as broadly defined is very strong (5/6 concordant). Genetically identical individuals can have clearly distinguished phenotypes, either dermatitis herpetiformis or celiac disease, suggesting that environmental factors determine the exact phenotype of this multifactorial disease. These findings are of importance in genetic linkage analyses, which focus to only certain phenotypic properties of a complex trait.

Adult↗
PubMedDate not supplied

Sites of digestion in beef steers fed bermudagrass hay and supplemented with high-nitrogen feeds alone or mixed with tallow.

Five crossbred beef steers (329 kg) were used in a 5 x 5 Latin square experiment with 14-d periods to determine the effects of supplementation with high-nitrogen (N) feeds alone or mixed with tallow on sites of digestion with a basal diet of bermudagrass hay. Hay was 1.93% nitrogen, 75% neutral detergent fibre and fed at 1.83% of body weight (dry matter; DM). Supplements were basal (B; 105 g DM): 81.8% dried molasses product (DMP) and 18.2% calcium carbonate (CC); soybean meal (S; 942 g DM): 88.0% soybean meal, 9.8% DMP and 2.2% CC; S mixed with 9.8% tallow (SF; 1041 g DM); corn gluten and blood meals (CB; 662 g DM): 62.5% corn gluten meal, 20.8% blood meal, 13.6% DMP and 3.0% CC; CB mixed with 13.2% tallow (CBF; 757 g DM). Total N intake was 117, 185, 187, 174 and 172 g/d, and duodenal N flow was 121, 148, 143, 162 and 169 g/d for B, S, SF, CB and CBF, respectively, being lower for B than for other treatments and higher for supplements with the corn gluten and blood meal mix than for soybean meal (P less than 0.05). Duodenal microbial N flow was 39, 51, 49, 38 and 45 g/d for B, S, SF, CB and CBF, respectively, being greater (P less than 0.05) for supplements with soybean meal than with corn gluten and blood meals. Duodenal flow of feed N was greater (P less than 0.05) with than without high-N feeds and for supplemental corn gluten and blood meals than for soybean meal (78, 90, 86, 117 and 116 g/d for B, S, SF, CB and CBF, respectively). In conclusion, mixing of tallow and high-N feeds did not affect the extent of ruminal N disappearance, and soybean meal supplementation increased duodenal N flow less than did supplementation with corn gluten and blood meals. Increased duodenal N flow with soybean meal was associated with about equal elevations of ruminal outflow of microbial and feed N, whereas the corn gluten-blood meal mix affected the intestinal protein supply by increasing ruminal escape of feed protein.

Animal Feed↗
PubMed1986

Malt sprouts as a source of supplemental protein for ruminants.

Nitrogen solubility, ruminal degradation, and amino acid composition of pelleted malt sprouts, pelleted corn gluten feed, and soybean meal were studied. Four rumen-cannulated steers were fed diets containing 45% pelleted malt sprouts or 45% pelleted corn gluten feed in a 2 X 2 crossover design with 15-d periods. Ruminal degradation of dry matter and nitrogen from malt sprouts or corn gluten feed was estimated by disappearance of these components from polyester bags after 1, 2, 3, 4, 6, 8, 10, 12, 16, or 24 h of in situ fermentation. For comparison, degradation of soybean meal after 2, 4, 8, or 24 h was measured. Malt sprouts had less soluble nitrogen than corn gluten feed, but available crude protein contents were similar. Malt sprouts dry matter was degraded more slowly than was corn gluten feed dry matter. Nitrogen degradation rates of the two feeds, after correction for unavailable nitrogen, did not differ. Malt sprouts had higher concentrations of arginine, lysine, and aspartate than corn gluten feed; however, corn gluten feed had higher concentrations of the other amino acids measured. Malt sprouts would be expected to provide more amino acids of feed origin to the lower gut of ruminants, provided passage rates of the supplements are similar.

Animal Feed↗
PubMed1992

[Living with celiac disease].

Celiac disease (CD) is caused by ingestion of gluten-containing foods by gluten-sensitive individuals. The gluten causes malabsorption by damaging their intestinal mucosa. Adherence to a gluten-free diet is not simple, because the composition of foods stocked on store shelves is often not known, Patients with CD, particularly when adolescent, often refuse to comply with the diet; and parents are occasionally unable, or unwilling, to prepare gluten-free food. Furthermore, school teachers are usually ignorant of the specific dietary requirements of these patients. We examined physical, scholastic, and social aspects of CD patients in comparison with their siblings in the same age groups (10-18 years) to determine whether CD and the need to keep a diet influence these parameters. 25 CD patients and 14 of their siblings were interviewed at home where they filled a questionnaire. The mean adherence to a gluten-free diet was 96.6%; the heights of the patients were comparable to those of their siblings. We did not find significant differences in scholastic achievement and social adjustment between patients and siblings. It appears that children and adolescents with CD can live with their disease and keep a gluten-free diet while performing satisfactorily in school. However, some complained of difficulties, such as feeling uneasy at social gatherings, wanting to discuss their disability with friends, and feeling unhappy. Some were angry at society for pitying them and considering them as having a disease, while the patients considered themselves as having a food sensitivity.

Achievement↗
PubMed2003

Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies.

CONTEXT: Dietary factors modifying type 1 diabetes mellitus (DM) risk have been proposed, but little is known if they trigger the islet autoimmunity that precedes clinical disease. OBJECTIVE: To determine whether breastfeeding duration, food supplementation, or age at introduction of gluten-containing foods influences the risk of developing islet autoantibodies. DESIGN AND SETTING: Prospective natural history cohort study conducted from 1989 to 2003 in inpatient/outpatient clinics in Germany. PARTICIPANTS: The BABYDIAB study follows newborn children of parents with type 1 DM. Eligibility requirements were met in 1610 children. Blood samples were obtained at birth, age 9 months, 2, 5, and 8 years. Dropout rate was 14.4% by age 5 years. Breastfeeding data were obtained by prospective questionnaires (91% complete), and food supplementation data were obtained by family interview (72% for food supplementation and 80% for age of gluten introduction). MAIN OUTCOME MEASURE: Development of islet autoantibodies (insulin, glutamic acid decarboxylase, or IA-2 antibodies) in 2 consecutive blood samples. RESULTS: Life-table islet autoantibody frequency was 5.8% (SE, 0.6%) by age 5 years. Reduced total or exclusive breastfeeding duration did not significantly increase the risk of developing islet autoantibodies. Food supplementation with gluten-containing foods before age 3 months, however, was associated with significantly increased islet autoantibody risk (adjusted hazard ratio, 4.0; 95% confidence interval, 1.4-11.5; P =.01 vs children who received only breast milk until age 3 months). Four of 17 children who received gluten foods before age 3 months developed islet autoantibodies (life-table 5-year risk, 24%; SE, 10%). All 4 children had the high-risk DRB1*03/04,DQB1*0302 genotype. Early exposure to gluten did not significantly increase the risk of developing celiac disease-associated autoantibodies. Children who first received gluten foods after age 6 months did not have increased risks for islet or celiac disease autoantibodies. CONCLUSION: Ensuring compliance to infant feeding guidelines is a possible way to reduce the risk of development of type 1 DM autoantibodies.

Autoantibodies↗
PubMed2000

Faecal occult blood in children with coeliac disease.

UNLABELLED: It has recently been suggested that in adults with coeliac disease, faecal blood loss may play a role in the development of iron deficiency. A group of 45 children diagnosed with coeliac disease during 1996 and 1997 were therefore prospectively evaluated for the presence of gluten in their diet, iron deficiency anaemia, and faecal occult blood. Sixty children admitted for elective surgery or asthma served as controls. Faecal occult blood was found in four iron deficient children on normal diet, of whom three were newly diagnosed. Occult blood loss disappeared in three of the four children when gluten was removed from their diet. Faecal occult blood was found in 26.7% of children on gluten-containing diet, but not in children on gluten-free diet (P = 0.01), or in control children (P = 0.001). CONCLUSION: Our data suggest that the incidence of occult blood loss in coeliac disease occurs mainly in newly diagnosed cases and responds to a gluten-free diet. Occult blood testing may not be warranted in the absence of iron deficiency anaemia nor in children with iron deficiency anaemia who are on a gluten-free diet.

Adolescent↗
PubMed1995

Dermatitis herpetiformis.

Dermatitis herpetiformis (DH) is a relatively rare skin disorder with an estimated incidence of 1:10,000 in the UK. It is characterized by urticarial plaques and blisters on the elbows, buttocks, and knees, although other sites may also be involved. The eruption tends to be persistent: only 10-15% of patients have spontaneous remission over a 25-year study period. The disease is characterized by the presence of IgA deposits in the upper dermis of uninvolved skin and the diagnosis should not be made in the absence of these deposits. Two-thirds of patients have a small intestinal enteropathy with villous atrophy as seen in coeliac disease (CD). However, the remaining third also show evidence of a gluten sensitivity in the intestine, as judged by increased lymphocytic infiltration of the epithelium. Villous atrophy also ensues after gluten challenge in those patients with previous normal villous architecture. The initial treatment of the rash is with one of the following three drugs, dapsone, sulphapyridine or sulphamethoxypyridazine. However, the rash also clears with gluten withdrawal. It must be stressed, however, that the average time to achieve significant reduction in drug requirements is 6 months and it can be over 2 years before drugs are no longer required. On re-introduction of gluten the eruption recurs. Patients with DH have a high incidence of auto-immune disorders, thyroid disease, pernicious anaemia, and insulin-dependent diabetes, and should be screened for those diseases on a yearly basis. As with coeliac disease there is also an increased incidence of lymphoma and a gluten-free diet appears to protect patients from this complication. The mechanism by which gluten causes the skin lesions has still to be elucidated, but current investigations implicate lymphocytes and cytokines in the pathogenesis. The original hypothesis of an antigen-antibody reaction in the skin with complement activation causing the skin lesions, may not be correct.

Adolescent↗
PubMed2005

Pathomechanisms in celiac disease.

Celiac disease is an inflammatory disorder of the small intestine caused by an immune response to ingested wheat gluten and similar proteins of rye and barley. It affects at least 1 in 200 individuals, corresponding to roughly three million patients in Western Europe and Northern America alone. Data accumulated since the discovery of gluten specific T cells in the intestine of celiac disease patients the early 1990s have allowed the deciphering of the interplay between the triggering environmental factor, gluten, the main genetic risk factor, the HLA-DQ2/8 haplotypes and the autoantigen; the enzyme tissue transglutaminase (tTG). This established a key role of adaptive immunity orchestrated by lamina propria T cells responding to a set of gluten derived peptides. More recent work points to an important contribution of innate immunity triggered by a distinct gluten peptide and driven by the proinflammatory cytokine Interleukine-5 (IL-15). Together, these observations provide a unique explanation for the disease inducing capacity of gluten.

Celiac Disease↗
PubMed1983

IgA antigliadin antibodies: a marker of mucosal damage in childhood coeliac disease.

Antigliadin antibodies in serum samples of 31 children with coeliac disease were measured by an enzyme-linked immunosorbent technique. In young patients (less than 2 years) tested before gluten withdrawal IgA antigliadin antibody levels were invariably above the levels of 36 controls. The titres fell rapidly when gluten was eliminated from the diet and rose on its reintroduction. The titres were not always greater than the control level in older untreated patients. IgA antigliadin antibodies seem to be a good marker of the immune reaction in the jejunum triggered by gluten. In 2 IgA-deficient patients gluten challenge caused an increase in IgM antigliadin antibodies, and at the same time the number of IgM-containing cells increased in the jejunal mucosa. Rising IgG antigliadin antibody levels after gluten elimination were seen in 6 patients, 5 of whom had very low complement C3 levels before gluten elimination.

Age Factors↗
PubMed2005

Future therapeutic options for celiac disease.

Celiac disease is a disorder of the small intestine caused by an inappropriate immune response to wheat gluten and similar proteins of barley and rye. At present, the only available treatment is a strict gluten-exclusion diet; hence the need for alternative treatments. Recent advances have improved our understanding of the molecular basis for this disorder and there are several attractive targets for new treatments. Oral enzyme supplementation is designed to accelerate gastrointestinal degradation of proline-rich gluten, especially its proteolytically stable antigenic peptides. Complementary strategies aiming to interfere with activation of gluten-reactive T cells include the inhibition of intestinal tissue transglutaminase activity to prevent selective deamidation of gluten peptides, and blocking the binding of gluten peptides to the HLA-DQ2 or HLA-DQ8 molecules. Other possible treatments include cytokine therapy, and selective adhesion molecule inhibitors that interfere with inflammatory reactions, some of which are already showing promise in the clinic for other gastrointestinal diseases.

Celiac Disease↗
PubMed1999

Changing jejunal gamma delta T cell receptor (TCR)-bearing intraepithelial lymphocyte density in coeliac disease.

The function of jejunal intraepithelial gamma delta+ T cells is obscure, but they are commonly implicated as playing a role in inflammatory and autoimmune conditions. In coeliac disease (CoD), there are controversial reports as to gluten dependency of these cells. We have now studied the small bowel mucosal intraepithelial T cell densities, and the ratios of gamma delta+ to CD3+ T cells and gamma delta+ to alpha beta+ T cells during early disease development and on a gluten-free diet. Nine children initially excluded for CoD were followed up and rebiopsy after 0.8-4.5 years showed mucosal deterioration. Further, 21 biopsy specimens from newly diagnosed CoD patients were studied, together with 20 specimens taken from children on a gluten-free diet. During CoD development the density of gamma delta+ and alpha beta+ T cells as well as the ratios of gamma delta+ to CD3+ T cells and gamma delta+ to alpha beta+ T cells increased. In the latent stage of CoD when the small bowel mucosal architecture was still normal, two children had clearly normal densities of gamma delta+ (< 2.5 cells/100 epithelial cells) and alpha beta+ (< 25.0 cells/100 epithelial cells) T cells, and low ratios as well. In patients with newly diagnosed CoD the densities decreased significantly on a long-term gluten-free diet. We conclude that the density of intraepithelial gamma delta+ T cells as well as alphabeta+ T cells in CoD is gluten-dependent. CoD can develop in a child ingesting normal amounts of gluten and having normal jejunal mucosal morphology on biopsy and a normal density of gamma delta+ T cells.

Adolescent↗
PubMed2000

Increase in T-cell subsets of oral mucosa: a late immune response in patients with treated coeliac disease?

BACKGROUND AND AIMS: In coeliac disease, the gut involvement is gluten-dependent. Following the introduction of a gluten-free diet, inflammatory cell infiltration decreases in the small intestinal mucosa. Our hypothesis was that the oral mucosa might mirror the changes found in coeliac disease similarly to the mucosa of the small intestine. Thus, the number of inflammatory cells in the oral mucosa would decrease in patients with coeliac disease on a gluten-free diet. METHODS: The distribution CD45RO+ and CD3(+) T cells, T-cell subpopulations (CD4(+), CD8(+), T-cell receptor (TCR)alpha beta+ and TCR gamma delta+ cells) and HLA DR expression were studied in the buccal mucosa of 15 untreated and 44 gluten-free diet treated coeliac disease patients, and of 19 controls. All 15 patients with untreated coeliac disease were immunglobulin (Ig)A endomysial antibody positive and all 44 patients on gluten-free diet except one were endomysial antibody negative, as were all control subjects. RESULTS: Untreated coeliac disease patients did not differ from controls in the densities of CD45RO+ cells, CD3(+) cells or of T-cell subsets. In contrast, in treated coeliac disease patients, a significant increase in the numbers of mast cells, CD3(+) and CD4(+) lymphocytes was found in the lamina propria of oral mucosa as compared with patients with untreated coeliac disease and controls. The increase in CD3(+) T cells was in part owing to an increase in lymphocytes expressing no TCR. No differences were found in the expression of human leucocyte antigen (HLA) DR in the epithelium or in the lamina propria in the patient groups studied or in the controls. In treated coeliac disease patients only a few TCR gamma delta+ T cells were found intraepithelially and in the lamina propria, but these cells were not detected in the lamina propria of oral mucosa of patients with untreated coeliac disease or in the controls. CONCLUSIONS: The infiltration of T cells into oral mucosa was increased in treated coeliac disease patients in spite of adherence to a gluten-free diet. Because the CD3(+) T cell count was higher than those of the TCR alpha beta+ and TCR gamma delta+ T cells, there must be other cells involved, probably natural killer (NK) cells. The increase in T-cell subsets in the treated coeliac disease patients seems not to result from poor dietary compliance, but might occur as a late immune response in coeliac disease and reflect chronic immunologic stimulation followed by regeneration of memory T cells.

Adult↗
PubMed1998

Mycotoxins in ingredients of animal feeding stuffs: II. Determination of mycotoxins in maize and maize products.

Analytical methods have been developed for the reliable detection and estimation of 22 mycotoxins in maize gluten and other maize products used in the animal feed industry. The mycotoxins are aflatoxins B1, B2, G1 and G2, ochratoxins A and B, citrinin, cyclopiazonic acid, zearalenone, sterigmatocystin, deoxynivalenol, nivalenol together with seven related trichothecene mycotoxins, fumonisins B1 and B2 and moniliformin. For most of the mycotoxins, recoveries obtained were 60% or greater and reproducibility data were better than +/- 40%. In general, the analysis of maize gluten proved more difficult than for other maize products. In total 40 samples of maize gluten, and 27 samples of other maize products were examined. Aflatoxins were not found above the reporting limit (1-5 micrograms/kg) in any sample while ochratoxin A was detected in only two samples of maize gluten at 2 micrograms/kg. No sterigmatocystin or cyclopiazonic acid were detected although the limits of detection for these toxins were poor. Twenty percent of maize gluten samples contained zearalenone at up to 500 micrograms/kg while all other maize products also contained this mycotoxin. Highest levels occurred in screenings and meal while the lowest amounts were in flaked maize and germ. Many samples contained a multi-toxin mixture of trichothecenes, fumonisins and moniliformin. The most highly contaminated samples of maize screenings and maize meal contained a mixture of zearalenone, deoxynivalenol, nivalenol, fumonisin B1 and B2, moniliformin, each in mg/kg amounts and lower amounts of other trichothecenes such as 15-acetoxy deoxynivalenol, HT-2 toxin and T-2 toxin. Fumonisins occurred in all except two gluten samples and occurred up to a level of 32 mg/kg in maize screenings, 13 mg/kg in maize meal and 8 mg/kg in maize germ.

Animals↗