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PubMed1996

Evidence that intestinal intraepithelial lymphocytes are activated cytotoxic T cells in celiac disease but not in giardiasis.

To further define intraepithelial lymphocytes (IELs) in celiac disease (CD) and giardiasis, IELs were probed for the presence of cytolytic granules containing granzyme B (GrB) and T-cell-restricted intracellular antigen (TIA)-1. The expression of TIA-1, GrB, CD3 (T-cell-receptor-associated complex), and Leu-7 (subset of natural killer cells) was studied by a sensitive three-step immunoperoxidase technique. Stained IELs were determined quantitatively, and results were expressed as number of stained IELs per 100 epithelial cells (ECs). The relative content in labeled lamina propria lymphocytes was determined and expressed as the percentage of all lamina propria cells counted. When compared with controls, CD3+ and GrB+ IELs were significantly increased (P < 0.0004) in CD paralleled by an increase in TIA-1+ IELs (P < 0.0004). In CD, the highest numbers of IELs containing GrB were found in subjects with a flat mucosa (median, 38 IELs/100 ECs, P < 0.0004), followed by cases with shortened and blunted villi (median, 8 IELs/100 ECs, P < 0.0004) and, finally, CD patients with an intact villous architecture (median, 0.5 IELs/100 ECs, P < 0.02). Except for cases with giardiasis, Leu-7+ IELs were virtually absent in all groups as were GrB+ IELs in the controls and in subjects with giardiasis. In the lamina propria of CD subjects, GrB+ lymphocytes were also significantly increased (P < 0.001), whereas controls and cases with giardiasis were essentially free of GrB+ cytotoxic T lymphocytes. The percentage of CD3+ lamina propria lymphocytes was nearly equal in all groups. In humans and mice, extensive studies revealed a GrB expression to be absolutely restricted to activated cytotoxic T lymphocytes and natural killer cells. TIA-1, on the other hand, is considered a marker of resting T lymphocytes possessing cytolytic potential. We therefore conclude that IELs are cytotoxic T cells that are in a resting state in the normal small bowel and in giardiasis. In CD, they become activated as suggested by the GrB positivity of their granules.

Adolescent↗
PubMed1991

IgA antiendomysial antibody test. A step forward in celiac disease screening.

Serum IgA antiendomysial antibodies (EmA) were found in 61 (87%) of 70 adults and children with untreated celiac disease, whereas IgA antigliadin antibodies (AGA) and IgA R1-antireticulin antibodies (R1-ARA) were positive in 71% and 47%, respectively, of the same patients. Two of the nine untreated celiacs negative for IgA EmA showed positivity for IgA AGA. While IgA AGA and R1-ARA disappeared in all the celiacs tested one year after gluten-free diet, IgA EmA persisted at low titer in seven (18%) of these 38 subjects, although the jejunal biopsy showed a complete regrowth of jejunal villi. All the disease control patients as well as the blood donors tested were always negative for the three IgA antibodies. Our results state that the search for both IgA EmA and AGA gives the best results in the screening of celiac disease, since the positivity for at least one of these two antibodies allows identification with a 100% specificity of the 90% of untreated celiac patients.

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↗
PubMed1996

In vitro toxicity testing of alcohol-soluble proteins from diploid wheat Triticum monococcum in celiac disease.

Peptic-tryptic digests of alcohol-soluble proteins from flours of 10 accessions of Trificum monococcum with contrasting storage protein compositions and bread-making characteristics were found unable to agglutinate K562(S) cells even at a peptide concentration as high as 14 g/L, agglutination being strongly correlated with toxicity in celiac disease. When fractionated by affinity chromatography on Sepharose-6B coupled with mannan, peptic-tryptic digests separated into three fractions. Fraction C peptides were shown to agglutinate K562(S) cells, whereas peptides in fractions A and B and in the mixed fraction B + C were inactive, suggesting that fraction B contains "protective" peptides that interfere with toxic peptides in fraction C in their agglutinating activity. These results offer an opportunity to study the biochemical and genetic bases of wheat toxicity at the diploid level. Moreover, the reduced toxicity, if any, of Triticum monococcum in the celiac disease, along with the good grain characteristics of some "monococcum" accessions, greatly increases the economical prospects of this wheat species.

Agglutination↗
PubMed2004

Regional cerebral hypoperfusion in patients with celiac disease.

BACKGROUND: Neurological and psychiatric disorders occur in approximately 10% of patients with celiac disease. Although some of these alterations respond to a gluten-free diet, the etiology of these abnormalities is uncertain. Because of a case report that cerebral hypoperfusion in a celiac patient resolved after a gluten-free diet, we studied brain perfusion changes in untreated celiac patients, treated celiac patients, and healthy controls. METHODS: A total of 15 untreated celiac patients without conditions affecting brain perfusion were enrolled; none had neurological or psychiatric disorders other than anxiety or depression. We also studied 15 celiac patients who were on a gluten-free diet for almost 1 year, and 24 healthy volunteers of similar sex and age. All subjects underwent cerebral single photon emission computed tomography examination. RESULTS: Of the 15 untreated celiac patients, 11 (73%) had at least one hypoperfused brain region, compared with only 1 (7%) of the 15 celiac patients on a gluten-free diet and none of the controls (P = 0.01). Cerebral perfusion was significantly lower (P <0.05) in untreated celiac patients, compared with healthy controls, in 7 of 26 brain regions. No significant differences in cerebral perfusion were found between celiac patients on a gluten-free diet and healthy controls. CONCLUSION: There is evidence of regional cerebral blood flow alteration in untreated celiac patients.

Adult↗
PubMedDate not supplied

Anti-alpha-gliadin antibodies are not predictive of celiac disease in juvenile chronic arthritis.

Some authors have recently reported an increased level of antigluten antibodies in rheumatoid arthritis, both in the adult and juvenile form. The real meaning of these antibodies is still unclear. We ascertained the levels of antigluten antibodies in a group of children with juvenile chronic arthritis to determine if these antibodies were linked with celiac disease and/or to increased intestinal permeability. In 18 of 53 patients (33.9%), the levels of antigluten antibodies (IgA or IgG) were higher than normal. No correlation was found between the increase in antigluten antibodies and the positive lactulose/mannitol test, used for determining increased intestinal permeability. In all eight patients undergoing intestinal biopsy due to abnormal levels of antigluten antibodies (IgA class), intestinal mucosa was normal. In conclusion, our study shows that in patients with juvenile chronic arthritis, immunological response to gluten is neither related to celiac disease nor to increased intestinal permeability.

Adolescent↗
PubMed1996

Measurements of the jejunal unstirred layer in normal subjects and patients with celiac disease.

Normal intestinal absorption of nutrients requires efficient luminal mixing to deliver solute to the brush border. Lacking such mixing, the buildup of thick unstirred layers over the mucosa markedly retards absorption of rapidly transported compounds. Using a technique based on the kinetics of maltose hydrolysis, we measured the unstirred layer thickness of the jejunum of normal subjects and patients with celiac disease, as well as that of the normal rat. The jejunum of humans and rats was perfused with varying maltose concentrations, and the apparent Michaelis constant (Km) and maximal velocity (Vmax) of maltose hydrolysis were determined from double-reciprocal plots. The true Km of intestinal maltase was determined on mucosal biopsies. Unstirred layer thickness was calculated from the in vivo Vmax and apparent Km and the in vitro Km of maltase. The average unstirred layer thickness of 11 celiac patients (170 micron) was seven times greater than that of 3 controls (25 micron). The unstirred layer of each celiac exceeded that of the controls. A variety of factors could account for the less efficient luminal stirring observed in celiacs. Although speculative, villous contractility could be an important stirring mechanism that would be absent in celiacs with villous atrophy. This speculation was supported by the finding of a relatively thick unstirred layer (mean: 106 micron) in rats, an animal that lacks villous contractility. Because any increase in unstirred layer slows transport of rapidly absorbed compounds, poor stirring appears to represent a previously unrecognized defect that could contribute to malabsorption in celiac disease and, perhaps, in other intestinal disorders.

Animals↗
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↗
PubMed2002

Human genome search in celiac disease: mutated gliadin T-cell-like epitope in two human proteins promotes T-cell activation.

Discovery of a number of novel and known human genes whose protein products bear striking similarity to two or more wheat gliadin domains raised the possibility that human intestinal non-HLA peptides homologous to celiac T-cell epitopes could play a role in non-HLA gene specification in celiac disease. Database searching of the entire human genome identified only 11 gut-expressed proteins with high T-cell epitope homology, particularly to the DQ2-gamma-I-gliadin epitope (i.e. TFIIA, FOXJ2 and IgD; mean BestFit quality score=40 versus random value of 24). Others were similar to DQ2-alpha-I-gliadin (i.e. PAX9; BestFit quality 46 versus 20 for random), or DQ2-alpha-II-gliadin (PHLDA1, known in mice as the T-cell death-associated gene; BestFit quality 43 versus 30 for random) epitopes. Among proteins previously screened for gliadin homology, noteworthy was achaete scute homologous protein (DQ2-alpha-I-gliadin; BestFit quality 41 versus 22 for random). With the exception of IgD, all are nuclear factors. Paying particular attention to the position of potential major histocompatibility complex (MHC) anchor residues, several were selected for testing in a DQ2-gamma-I-gliadin-restricted T-cell system. All native 10-mer peptides were inactive, even when deamidated, but V96F substitution of deamidated TFIIA amino acid residues 91-100 stimulated IL-2 release at levels exceeding the wheat gliadin positive control. Also active, but only slightly, was L1009F substitution of AIB3 amino acid residues 1004-1013. PlotSimilarity alignment of TFIIAs from eight species revealed subthreshold similarity score in the peptide region, in contrast to the highly conserved amino and carboxy termini. Molecular modeling of TFIIA[V96F] peptide points to an important juxtaposition of an upwardly projecting phenylalanine residue at peptide position 6 that likely contacts a receptor complementarity-determining region, and a downwardly projecting glutamic acid residue that fits into the shallow MHC P7 pocket. These observations tentatively point to a new multi-gene hypothesis for the initiation of celiac disease in which deamidated free human peptides with T-cell epitope homology (particularly those made more homologous by mutation) escape negative selection, as per deamidation of the HEL(48-62) peptide in the hen egg lysozyme model of autoimmunity. Deamidation following peptide release due to injury triggers inflammation, thereafter repeatedly provoked by dietary gliadin immunodominant peptides concentrated in the proximal small intestine.

Amino Acid Sequence↗
PubMed2002

Gut mucosal immunity to tissue transglutaminase in untreated celiac disease and other gastrointestinal disorders.

Tissue transglutaminase antibodies have not previously been measured in gut secretions. IgA anti-tissue transglutaminase and anti-endomysium antibodies were measured in paired serum and whole gut lavage fluid samples from patients with untreated celiac disease (N = 36), other gastrointestinal diseases (N = 235), and healthy volunteers (N = 13). HLA DQ2 typing was performed in the celiac patients. Whole gut lavage IgA anti-tissue transglutaminase antibody concentrations were raised in 83% of celiac patients, 4% of disease controls, and 8% of volunteers, and the antibody concentrations were significantly higher in celiac patients than in controls (P < 0.0001). Whole gut lavage IgA anti-endomysium antibodies were positive in 67% of celiac patients, but in none of the controls. Whole gut lavage, but not serum, IgA anti-tissue transglutaminase antibody concentrations were significantly higher in DQ2 positive than negative celiac patients. In conclusion, whole gut lavage IgA anti-tissue transglutaminase antibody concentrations are higher in untreated celiac disease than in other gastrointestinal diseases.

Adolescent↗
PubMed2005

Nutritional status in adolescents and young adults with screen-detected celiac disease.

OBJECTIVE: To describe the nutritional status in patients with screen-detected celiac disease (CD). METHODS: Nutritional status was assessed by serum tests and anthropometric measures in 26 subjects (16 to 25 years of age) with biopsy-proven CD and 29 healthy control subjects (16 to 21 years of age) with negative tissue transglutaminase antibodies (16 to 22 years of age); all the subjects were selected from the cohort of 3654 schoolchildren. RESULTS: Compared with control subjects, CD patients had lower median values of whole blood folic acid (91 versus 109 nmol/L; P = 0.01), serum ferritin (14 versus 27 microg/L; P = 0.028) and pre-albumin (0.21 versus 0.28 g/L; P </= 0.001) and higher transferrin receptor (1.3 versus 1.1; P = 0.008) and serum transferrin receptor-ferritin index (1.2 versus 0.7; P = 0.006). Folic acid concentration was subnormal in 31% of the CD subjects (versus 14% of the controls) and iron status (transferrin receptor-ferritin index) was subnormal in 30% (versus 14%). Body mass index was not different in females of the CD and control groups (22 versus 22 kg/m2) or in the males of the respective groups (25 versus 24 kg/m2). Females with CD were shorter than the controls (mean 162 versus 167 cm; P = 0.018), but no difference was found in males. No association was found between the nutritional status and the markers of mucosal injury (villous-crypt measures), but titer of transglutaminase was associated with whole blood folic acid (r = -0.5; P = 0.016) and with transferrin receptor-ferritin index (r = 0.4, P = 0.05). CONCLUSIONS: One third of screen-detected adolescent CD subjects have abnormalities in folate or iron status that call for early diagnosis and dietary treatment of the disease to prevent nutritional deficiencies.

Adolescent↗
PubMed1996

MALTectomy (appendectomy/tonsillectomy) does not influence the occurrence or mode of presentation of adult celiac disease.

OBJECTIVE: Recent reports suggest that appendectomy may protect against the development of ulcerative colitis. Depletion of mucosal helper T-cells is the suggested mechanism. Because mucosal T-cell activity has an even more critical role in the pathogenesis of celiac disease, our objective was to determine whether the development or mode of presentation of this disorder is influenced by appendectomy and/or tonsillectomy. METHODS: One hundred fifty consecutive adult celiac patients were compared with 138 consecutive patients examined at orthopedic clinics. One hundred twenty consecutive patients with ulcerative colitis from the same ethnogeographic population were included as positive disease control. RESULTS: Contrary to the previous findings in ulcerative colitis, which were again confirmed in this study, appendectomy and/or tonsillectomy did not influence the occurrence of celiac disease. In addition, presenting features, predefined in the study protocol, did not differ significantly in the appendectomy and nonappendectomy celiac patients. CONCLUSION: Resection of mucosa-associated lymphoid tissue (MALT) does not influence the occurrence or the mode of presentation of adult celiac disease. Therefore, in this classical example of a T-cell-mediated disorder, the hypothesis that surgical depletion of mucosal T-cells has a protective effect or influences the clinical manifestations cannot be supported.

Adult↗
PubMed2006

Splenic hypofunction and the spectrum of autoimmune and malignant complications in celiac disease.

BACKGROUND & AIMS: We investigated the prevalence of functional hyposplenism in autoimmune disorder (AID)-associated and complicated celiac disease (CD). In addition, because the association between hyposplenism and overwhelming infections caused by Streptococcus pneumoniae in patients with CD is well known, we investigated whether immunoglobulin (Ig)M memory B cells, which are responsible for protection against infections by encapsulated bacteria and require the spleen for their generation and/or survival, mirror the reduced splenic function in CD. METHODS: Peripheral blood samples were collected from 73 adult CD patients (27 with AID, 36 without AID, and 10 with CD-related complications including enteropathy-associated T-cell lymphoma, refractory sprue, and ulcerative jejunoileitis). Thirty-four non-CD patients with AID, 35 healthy volunteers, and 29 splenectomized patients also were studied. Counting of erythrocytes with membrane abnormalities (pitted red cells) was used as an indicator of splenic function, and flow cytometry was performed to analyze peripheral blood B cells. RESULTS: A significantly higher risk for hyposplenism was found in AID-associated CD (59%) and complicated CD (80%) than in uncomplicated CD without AID (19%). In AID-associated CD, the degree of splenic function did not correlate to the duration of gluten-free diet. In AID-associated and complicated CD, the frequency of circulating IgM memory B cells was significantly lower than in CD patients without AID or healthy subjects. A significant inverse correlation between IgM memory B cells and pitted red cells was found in all 73 CD patients. CONCLUSIONS: The prevalence of splenic hypofunction is increased in CD with AID and in complicated CD, and is not related to the duration of gluten-free diet. IgM memory B cells are reduced in AID-associated and complicated CD. This defect, which is related to the impairment of splenic function, might predispose hyposplenic CD patients to infections by encapsulated bacteria.

Acquired Immunodeficiency Syndrome↗
PubMed1963

CELIAC DISEASE.

Explore the source record for details and available documents.

Celiac Disease↗
PubMed1979

Celiac disease associated with immune complex glomerulonephritis.

A patient with immune complex glomerulonephritis and celiac disease without dermatitis herpetiformis or other underlying disease associated with glomerulonephritis is presented. Antibodies to wheat proteins were found in serum and withdrawal of gluten from the diet resulted in disappearance of immune complexes from serum and resolution of both renal and intestinal disease, suggesting a dietary source of antigen. Despite extensive immunopathologic studies of the renal biopsy, neither dietary nor endogenous brush border antigens were demonstrated in glomeruli.

Adult↗
PubMed2005

Cytokine production by intestinal intraepithelial lymphocyte subsets in celiac disease.

One of the earliest signs of mucosal immune activation in celiac disease (CD) is an increase in the intraepithelial lymphocyte (IEL) count in the small intestinal epithelium. Though most of those IELs express T cell receptor (TcR)-alphabeta chains, CD is characterized by an increase in TcR-gammadelta+ IELs and by the loss of CD3- IELs. There is currently little evidence that these changes in IEL subset distribution are of relevance in the pathogenesis of CD. We aimed to determine the pattern of cytokine production by IEL subsets isolated from duodenal biopsy specimens from control subjects and CD patients at different stages of the disease. We quantified the capacity of IEL subsets to produce IFN-gamma, TNF-alpha, IL-2, IL-4, and IL-10 by intracellular staining by flow cytometry. All IEL subsets studied displayed a type I cytokine profile in both CD and control subjects, with TcR-alphabeta+ IELs being the main IFN-y producers. Untreated CD exhibited a trend toward a superior accumulation of IFN-gamma per cell but a reduced proportion of INF-gamma+ cells in vitro in association with a significantly increased apoptotic rate of IELs. IL-4 was almost undetectable in all cases and IL-10 showed a tendency to increase in treated and "silent" celiac patients. IEL subsets have a similar Th1 profile in controls and CD patients, and the superior in vitro apoptosis of IELs from CD patients may reflect their superior in vivo activation. The induction of IL-10-dependent regulatory Tr1 responses may be of potential clinical significance in this disease and merits further investigation.

Biopsy, Needle↗
PubMed1995

Partial seizures, cerebral calcifications and celiac disease.

We describe the case of a 25 year old woman who has been clinically and instrumentally examined over a period of about 20 years. A diagnosis of celiac disease was made when she was four years old and, ten years later, CAT revealed the presence of bilateral cerebral calcifications. The partial occipital seizures were controlled by adopting a gluten-free diet, which is still being followed four years after the discontinuation of anti-epileptic treatment.

Adult↗
PubMedDate not supplied

Progressive cerebral calcifications, epilepsy, and celiac disease.

A case with progressive cerebral calcifications, white matter involvement, and drug-resistant epilepsy in a 9-year-old boy is described. The final diagnosis was celiac disease (CD). The relationship of CD with epileptogenic lesions is considered, and the possible significance of this association is discussed.

Brain Diseases↗