text:
, B. and Senger, S. and Rossi, M. and Malorni, A. and Siciliano, R. A.},
   title = {Identification of transglutaminase-mediated deamidation sites in a recombinant alpha-gliadin by advanced mass-spectrometric methodologies},
   journal = {Protein Sci},
   volume = {12},
   number = {11},
   pages = {2434-42},
   note = {Mazzeo, Maria Fiorella
De Giulio, Beatrice
Senger, Stefania
Rossi, Mauro
Malorni, Antonio
Siciliano, Rosa Anna
Journal Article
Research Support, Non-U.S. Gov't
United States
Protein Sci. 2003 Nov;12(11):2434-42.},
   abstract = {Celiac disease is a permanent immune-mediated food intolerance triggered by ingestion of wheat gliadins in genetically susceptible individuals. It has been reported that tissue transglutaminase plays an important role in the onset of celiac disease by converting specific glutamine residues within gliadin fragments into glutamic acid residues. This process increases binding affinity of gliadin peptides to HLA-DQ2/DQ8 molecules, thus enhancing the immune response. The aim of the present study was to achieve a detailed structural characterization of modifications induced by transglutaminase on gliadin peptides. Therefore, structural analyses were carried out on a recombinant alpha-gliadin and on a panel of 26 synthetic peptides, overlapping the complete protein sequence. Modified glutamine residues were identified by means of advanced mass-spectrometric methodologies on the basis of MALDI-TOF-MS and tandem mass spectrometry. Results led to the identification of 19 of 94 glutamine residues present in the recombinant alpha-gliadin, which were converted into glutamic acid residues by a transglutaminase-mediated reaction. This allowed us to achieve a global view of the modifications induced by the enzyme on this protein. Furthermore, results gathered could likely be utilized as relevant information for a better understanding of processes leading to T-cell recognition of gliadin peptides involved in celiac disease.},
   keywords = {Amides/*chemistry/metabolism
Amino Acid Sequence
Animals
Gliadin/*chemistry/metabolism
Guinea Pigs
Mass Spectrometry/*methods
Molecular Sequence Data
Recombinant Proteins
Transglutaminases/*chemistry/metabolism},
   ISSN = {0961-8368 (Print)
0961-8368},
   Accession Number = {14573857},
   DOI = {10.1110/ps.03185903},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Meyer, K. G. and Fasshauer, M. and Nebel, I. T. and Paschke, R.},
   title = {Comparative analysis of conventional training and a computer-based interactive training program for celiac disease patients},
   journal = {Patient Educ Couns},
   volume = {54},
   number = {3},
   pages = {353-60},
   note = {Meyer, Kirsten G
Fasshauer, Mathias
Nebel, Istvan T
Paschke, Ralf
Clinical Trial
Comparative Study
Journal Article
Multicenter Study
Randomized Controlled Trial
Ireland
Patient Educ Couns. 2004 Sep;54(3):353-60.},
   abstract = {Gluten-free diet (GFD) protects against the complications of celiac disease (CD). However, training in the dietetic field is rare in Germany. Thus, CD patients are likely to benefit from a computer-based interactive training program (CBITP) combined with interactive exercises. We compared a CBITP and a conventional training for CD patients regarding increased knowledge, transferability and sustainability. In that context we analyzed whether CD patients are more able to judge the risk of a food or a situation after practicing with the interactive training software. Sixty-four CD patients were included and randomized in two groups. While the first group used the CBITP, the control group received written instructions. Before and after taking part in the training program and 3 weeks later, the participants filled in a questionnaire for celiac knowledge. The results show that both intervention and control groups increased knowledge about CD. However, the intervention group showed significantly better outcome. A CBITP significantly increases knowledge and sustainability as compared to a conventional training for CD patients. CBITPs can enhance patients' training and treatment.},
   keywords = {Adult
Analysis of Variance
Celiac Disease/*diet therapy
*Computer-Assisted Instruction
Educational Measurement
Germany
Humans
Multimedia
Patient Education as Topic/*methods
User-Computer Interface},
   ISSN = {0738-3991 (Print)
0738-3991},
   Accession Number = {15324987},
   DOI = {10.1016/j.pec.2003.12.006},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Molberg, O. and Solheim Flaete, N. and Jensen, T. and Lundin, K. E. and Arentz-Hansen, H. and Anderson, O. D. and Kjersti Uhlen, A. and Sollid, L. M.},
   title = {Intestinal T-cell responses to high-molecular-weight glutenins in celiac disease},
   journal = {Gastroenterology},
   volume = {125},
   number = {2},
   pages = {337-44},
   note = {Molberg, Oyvind
Solheim Flaete, Nina
Jensen, Tore
Lundin, Knut E A
Arentz-Hansen, Helene
Anderson, Olin D
Kjersti Uhlen, Anne
Sollid, Ludvig M
Journal Article
Research Support, Non-U.S. Gov't
United States
Gastroenterology. 2003 Aug;125(2):337-44.},
   abstract = {BACKGROUND & AIMS: The chronic, small intestinal inflammation that defines celiac disease is initiated by a HLA-DQ2 restricted T-cell response to ingested gluten peptides after their in vivo deamidation by tissue transglutaminase (TG2). To date, celiac disease can only be treated by a lifelong abstinence from foods that contain wheat, rye, or barley; better therapeutic options are hence needed. An attractive target would be to identify nontoxic wheat cultivars or components thereof with intact baking qualities. Because these qualities are mainly determined by the high molecular weight (HMW) glutenin proteins of gluten, it is critical to know if these proteins are toxic or, more specifically, if they will trigger the activation of T cells in the celiac lesion. METHODS: Different, highly purified HMW glutenins were isolated from wheat cultivars or expressed as recombinant proteins. The proteins were first tested for recognition by a large panel of gluten-specific T-cell lines established from celiac lesions and then applied during ex vivo challenges of celiac biopsies to allow for a direct identification of HMW specific T cells. RESULTS: Intestinal T-cell responses to TG2-deamidated HMW glutenins but not the corresponding native proteins were detectable in 9 of the 22 adult and childhood celiac disease patients tested. CONCLUSIONS: T cells within celiac lesions frequently recognize deamidated HMW glutenin proteins. This finding questions the possibility of implementing these proteins in novel food items destined to be nontoxic for celiac disease patients.},
   keywords = {Adult
Biopsy
Celiac Disease/*immunology
Child
Glutens/*analogs & derivatives/*immunology
Humans
Intestines/*immunology
Lymphocyte Activation
Molecular Weight
T-Lymphocytes/*immunology},
   ISSN = {0016-5085 (Print)
0016-5085},
   Accession Number = {12891534},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Mothes, T. and Stern, M.},
   title = {How gluten-free is gluten-free, and what does this mean to coeliac patients?},
   journal = {Eur J Gastroenterol Hepatol},
   volume = {15},
   number = {5},
   pages = {461-3},
   note = {Mothes, Thomas
Stern, Martin
Comment
Journal Article
England
Eur J Gastroenterol Hepatol. 2003 May;15(5):461-3.},
   abstract = {A gluten-free diet is the cornerstone treatment of coeliac disease. Until now, it is not known conclusively whether trace amounts of gluten might be allowed in the diet, as suggested by Codex Alimentarius. Gluten-free foods intended for dietary use can now be analysed reliably for residual gluten by the new R5 enzyme-linked immunosorbent assay (ELISA) system. Some major problems of gluten analysis (sensitivity, specificity, reproducibility) can be solved by the new method. Therefore, the information given by the new test system is relevant and superior to earlier methods. Further clinical studies using small dose challenges and dietary records including gluten analysis are necessary until a more meaningful discussion on standards for gluten-free foods can be started.},
   keywords = {Celiac Disease/*diet therapy
Enzyme-Linked Immunosorbent Assay/methods
Food Analysis/*methods
Glutens/administration & dosage/*analysis
Humans},
   ISSN = {0954-691X (Print)
0954-691x},
   Accession Number = {12702900},
   DOI = {10.1097/01.meg.0000059124.68845.8c},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Mowat, A. M. and Donachie, A. M. and Parker, L. A. and Robson, N. C. and Beacock-Sharp, H. and McIntyre, L. J. and Millington, O. and Chirdo, F.},
   title = {The role of dendritic cells in regulating mucosal immunity and tolerance},
   journal = {Novartis Found Symp},
   volume = {252},
   pages = {291-302; discussion 302-5},
   note = {Mowat, Allan McI
Donachie, Anne M
Parker, Lucy A
Robson, Neil C
Beacock-Sharp, Helen
McIntyre, Lindsay J
Millington, Owain
Chirdo, Fernando
Journal Article
Research Support, Non-U.S. Gov't
Review
England
Novartis Found Symp. 2003;252:291-302; discussion 302-5.},
   abstract = {The intestinal immune system discriminates between invasive pathogens and antigens that are harmless, such as food proteins and commensal bacteria. The latter groups of antigens normally induce tolerance and a breakdown in this homeostatic process can lead to diseases such as coeliac disease or Crohn's disease. The nature ofthe intestinal immune response depends on how antigen is presented to CD4+ T cells by dendritic cells (DCs). Both oral tolerance and priming are influenced by the numbers and activation status of DCs in the gut and its draining lymphoid tissues, and our current work indicates that dietary proteins are taken up preferentially by DCs in the lamina propria of the small intestine. These then migrate to interact with antigen-specific CD4+ T cells in the mesenteric lymph node. In vivo and in vitro studies using purified lamina propria DCs suggest these may play a unique role in the regulation of intestinal immune responses. We propose that local DCs are the gatekeepers of the mucosal immune system, inducing tolerance under physiological conditions, but being sufficiently responsive to inflammatory stimuli to allow T cell priming and protective immunity when necessary. In addition, we will discuss evidence that adjuvant vectors such as ISCOMS may be effective mucosal vaccines due to an ability to activate intestinal DCs.},
   keywords = {Animals
CD4-Positive T-Lymphocytes/*immunology
Dendritic Cells/*immunology
Homeostasis
Humans
*Immune Tolerance
Immunity, Mucosal/*immunology
Immunophenotyping
Mice},
   ISSN = {1528-2511 (Print)
1528-2511},
   Accession Number = {14609226},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Mowat, A. M. and Parker, L. A. and Beacock-Sharp, H. and Millington, O. R. and Chirdo, F.},
   title = {Oral tolerance: overview and historical perspectives},
   journal = {Ann N Y Acad Sci},
   volume = {1029},
   pages = {1-8},
   note = {Mowat, Allan McI
Parker, Lucy A
Beacock-Sharp, Helen
Millington, Owain R
Chirdo, Fernando
Journal Article
Review
United States
Ann N Y Acad Sci. 2004 Dec;1029:1-8.},
   abstract = {Oral tolerance was first detailed almost 100 years ago, and since then, it has been shown repeatedly that feeding a wide variety of nonpathogenic antigens can inhibit subsequent systemic immune responses. All systemic immune responses are susceptible, but the degree and scope of the suppression depends on the nature and dose of the fed antigen. Oral tolerance has been described in most mammals, including humans, and it may be the homeostatic mechanism that prevents hypersensitivity to food antigens, as is found in celiac disease. A similar process may prevent the aberrant immune responses to commensal bacteria that occur in inflammatory bowel disease. The ability of oral tolerance to modulate experimental models of autoimmune and inflammatory disease has led to clinical trials in such diseases as rheumatoid arthritis, multiple sclerosis, and type I diabetes, with only variable success. Despite intense research, the exact mechanisms responsible for the systemic tolerance and the reasons why tolerance is the default response to many fed antigens remain controversial. Early studies suggested that CD8(+) "suppressor" T cells were important, but it is now accepted that it may involve either anergy/deletion of CD4(+) T cells, or the induction of regulatory CD4(+) T cells that produce IL-10 and/or TGFbeta. There may also be a role for CD4(+) CD25(+) T(reg), but how and when all these different mechanisms operate is still unclear. The ability of fed antigens to induce tolerance probably reflects their uptake by "quiescent" antigen-presenting cells in the intestine, with presentation to specific CD4(+) T cells in the absence of costimulation, or with the involvement of inhibitory costimulatory molecules. Dendritic cells in the Peyer's patches or mucosal lamina propria are the most likely APCs involved, but it remains to be determined exactly where these interactions occur and what the precise nature of the relevant dendritic cells is.},
   keywords = {Animals
Antigen-Presenting Cells/immunology
Dendritic Cells/immunology
Food Hypersensitivity/prevention & control
Humans
*Immunity, Mucosal
Mammals
Mouth/immunology
Peyer's Patches/immunology},
   ISSN = {0077-8923 (Print)
0077-8923},
   Accession Number = {15806729},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Natah, S. S. and Konttinen, Y. T. and Enattah, N. S. and Ashammakhi, N. and Sharkey, K. A. and Hayrinen-Immonen, R.},
   title = {Recurrent aphthous ulcers today: a review of the growing knowledge},
   journal = {Int J Oral Maxillofac Surg},
   volume = {33},
   number = {3},
   pages = {221-34},
   note = {Natah, S S
Konttinen, Y T
Enattah, N S
Ashammakhi, N
Sharkey, K A
Hayrinen-Immonen, R
Journal Article
Research Support, Non-U.S. Gov't
Review
Denmark
Int J Oral Maxillofac Surg. 2004 Apr;33(3):221-34.},
   abstract = {Recurrent aphthous ulcers represent a very common but poorly understood mucosal disorder. They occur in men and women of all ages, races and geographic regions. It is estimated that at least 1 in 5 individuals has at least once been afflicted with aphthous ulcers. The condition is classified as minor, major, and herpetiform on the basis of ulcer size and number. Attacks may be precipitated by local trauma, stress, food intake, drugs, hormonal changes and vitamin and trace element deficiencies. Local and systemic conditions, and genetic, immunological and microbial factors all may play a role in the pathogenesis of recurrent aphthous ulceration (RAU). However, to date, no principal cause has been discovered. Since the aetiology is unknown, diagnosis is entirely based on history and clinical criteria and no laboratory procedures exist to confirm the diagnosis. Although RAU may be a marker of an underlying systemic illness such as coeliac disease, or may present as one of the features of Behcet's disease, in most cases no additional body systems are affected, and patients remain otherwise fit and well. Different aetiologies and mechanisms might be operative in the aetiopathogenesis of aphthous ulceration, but pain, recurrence, self-limitation of the condition, and destruction of the epithelium seem to be the ultimate outcomes. There is no curative therapy to prevent the recurrence of ulcers, and all available treatment modalities can only reduce the frequency or severity of the lesions.},
   keywords = {Adolescent
Adult
Female
Humans
Male
Middle Aged
Recurrence
Stomatitis, Aphthous/etiology/*physiopathology/prevention & control},
   ISSN = {0901-5027 (Print)
0901-5027},
   Accession Number = {15287304},
   DOI = {10.1006/ijom.2002.0446},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Nieuwenhuizen, W. F. and Pieters, R. H. and Knippels, L. M. and Jansen, M. C. and Koppelman, S. J.},
   title = {Is Candida albicans a trigger in the onset of coeliac disease?},
   journal = {Lancet},
   volume = {361},
   number = {9375},
   pages = {2152-4},
   note = {1474-547x
Nieuwenhuizen, W F
Pieters, R H H
Knippels, L M J
Jansen, M C J F
Koppelman, S J
Journal Article
Research Support, Non-U.S. Gov't
England
Lancet. 2003 Jun 21;361(9375):2152-4.},
   abstract = {Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans-hyphal wall protein 1 (HWP1)-contains aminoacid sequences that are identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium.},
   keywords = {Antibody Formation
Candida albicans/*pathogenicity
Celiac Disease/*immunology/*microbiology
Fungal Proteins/immunology/metabolism
Genetic Predisposition to Disease
Gliadin/immunology
Humans
Intestinal Mucosa/immunology/metabolism
Membrane Glycoproteins/immunology/metabolism
Transglutaminases/metabolism
Virulence},
   ISSN = {0140-6736},
   Accession Number = {12826451},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Nowson, C. A. and Diamond, T. H. and Pasco, J. A. and Mason, R. S. and Sambrook, P. N. and Eisman, J. A.},
   title = {Vitamin D in Australia. Issues and recommendations},
   journal = {Aust Fam Physician},
   volume = {33},
   number = {3},
   pages = {133-8},
   note = {Nowson, Caryl A
Diamond, Terrence H
Pasco, Julie A
Mason, Rebecca S
Sambrook, Philip N
Eisman, John A
Journal Article
Research Support, Non-U.S. Gov't
Australia
Aust Fam Physician. 2004 Mar;33(3):133-8.},
   abstract = {BACKGROUND: A significant number of Australians and people from specific groups within the community are suffering from vitamin D deficiency. It is no longer acceptable to assume that all people in Australia receive adequate vitamin D from casual exposure to sunlight. OBJECTIVE: This article provides information on causes, consequences, treatment and prevention of vitamin D deficiency in Australia. DISCUSSION: People at high risk of vitamin D deficiency include the elderly, those with skin conditions where avoidance of sunlight is required, dark skinned people (particularly women during pregnancy or if veiled) and patients with malabsorption, e.g. coeliac disease. For most people, deficiency can be prevented by 5-15 minutes exposure of face and upper limbs to sunlight 4-6 times per week. If this is not possible then a vitamin D supplement of at least 400 IU per day is recommended. In cases of established vitamin D deficiency, supplementation with 3000-5000 IU per day for at least 1 month is required to replete body stores. Increased availability of larger dose preparations of cholecalciferol would be a useful therapy in the case of severe deficiencies.},
   keywords = {Accidental Falls
Australia
Dietary Supplements
Humans
Vitamin D/*therapeutic use
Vitamin D Deficiency/etiology/physiopathology/*therapy},
   ISSN = {0300-8495 (Print)
0300-8495},
   Accession Number = {15054977},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Peraaho, M. and Collin, P. and Kaukinen, K. and Kekkonen, L. and Miettinen, S. and Maki, M.},
   title = {Oats can diversify a gluten-free diet in celiac disease and dermatitis herpetiformis},
   journal = {J Am Diet Assoc},
   volume = {104},
   number = {7},
   pages = {1148-50},
   note = {Peraaho, Markku
Collin, Pekka
Kaukinen, Katri
Kekkonen, Leila
Miettinen, Sanna
Maki, Markku
Journal Article
Research Support, Non-U.S. Gov't
United States
J Am Diet Assoc. 2004 Jul;104(7):1148-50.},
   abstract = {Finnish celiac disease and dermatitis herpetiformis patients have used oat-containing gluten-free diets since 1997. The aim of this study was to evaluate how the use of oats has been adopted. The use of oats and the effect of oats on symptoms and quality of life were investigated in 1,000 randomly selected members of the Celiac Society. Altogether, 710 patients responded: 423 (73%) with celiac disease and 70 (55%) with dermatitis herpetiformis were currently consuming oats. Patients appreciated the taste, the ease of use, and the low costs; 94% believed that oats diversified the gluten-free diet; 15% of celiac disease and 28% of dermatitis herpetiformis patients had stopped eating oats. The most common reasons for avoiding oats were fear of adverse effects or contamination. There is a market demand for oats, and celiac societies and dietitians should make efforts to promote the development of products free of wheat contamination.},
   keywords = {Adolescent
Adult
Aged
Aged, 80 and over
*Avena
Celiac Disease/*diet therapy/immunology
Child
Child, Preschool
Dermatitis Herpetiformis/*diet therapy/immunology
Female
Food Contamination
Glutens/*administration & dosage
Humans
Male
Middle Aged
Quality of Life
Treatment Outcome},
   ISSN = {0002-8223 (Print)
0002-8223},
   Accession Number = {15215774},
   DOI = {10.1016/j.jada.2004.04.025},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Peracchi, M. and Conte, D. and Terrani, C. and Pizzinelli, S. and Gebbia, C. and Cappiello, V. and Spada, A. and Bardella, M. T.},
   title = {Circulating ghrelin levels in celiac patients},
   journal = {Am J Gastroenterol},
   volume = {98},
   number = {11},
   pages = {2474-8},
   note = {Peracchi, Maddalena
Conte, Dario
Terrani, Claudia
Pizzinelli, Simona
Gebbia, Carlotta
Cappiello, Vincenzo
Spada, Anna
Bardella, Maria Teresa
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
United States
Am J Gastroenterol. 2003 Nov;98(11):2474-8.},
   abstract = {OBJECTIVE: Ghrelin, the gut-brain peptide, recently identified as the natural endogenous ligand for growth hormone secretagogue receptors, exerts various endocrine and nonendocrine effects, including the control of energy homeostasis and food intake, but its possible relevance in malabsorption syndromes is unknown. Therefore, the aim of this study was to evaluate circulating ghrelin levels in adults with untreated and treated celiac disease (CD) and, for comparison, in healthy subjects. METHODS: Fasting serum ghrelin levels were measured in 30 consecutive patients with newly diagnosed CD, 13 celiac patients successfully treated with a gluten-free diet (GFD), and 30 healthy controls. RESULTS: Ghrelin levels were abnormally high in patients with active CD compared with controls (297 +/- 17.6 vs 218 +/- 15.2 pmol/L, p<0.01) and correlated positively with intestinal mucosal lesion severity (rs=0.444, p<0.02). In the successfully GFD-treated patients, ghrelin values were normal compared with controls (233 +/- 22.0 vs 218 +/- 15.2 pmol/L, ns) and, moreover, correlated negatively with body mass index (r=-0.632, p=0.02), unlike in the untreated patient group (r=-0.263, ns). CONCLUSION: High ghrelin levels characterized our series of adult patients with newly diagnosed CD and correlated significantly with the degree of severity of intestinal mucosal lesions. This is the first evidence of a relationship between ghrelin and inflammatory processes, but the mechanisms involved are still unclear. Furthermore, our findings suggest that an interplay of hormonal, metabolic, and nutritional factors could influence ghrelin secretion under pathophysiological circumstances.},
   keywords = {Adolescent
Adult
Aged
Biomarkers/blood
Case-Control Studies
Celiac Disease/*diagnosis/diet therapy
Diet Therapy/methods
Female
Ghrelin
Humans
Linear Models
Male
Middle Aged
Peptide Hormones/*blood/metabolism
Probability
Prognosis
Reference Values
Sensitivity and Specificity
Severity of Illness Index},
   ISSN = {0002-9270 (Print)
0002-9270},
   Accession Number = {14638351},
   DOI = {10.1111/j.1572-0241.2003.07709.x},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Perez-Machado, M. A. and Ashwood, P. and Thomson, M. A. and Latcham, F. and Sim, R. and Walker-Smith, J. A. and Murch, S. H.},
   title = {Reduced transforming growth factor-beta1-producing T cells in the duodenal mucosa of children with food allergy},
   journal = {Eur J Immunol},
   volume = {33},
   number = {8},
   pages = {2307-15},
   note = {Perez-Machado, Miguel A
Ashwood, Paul
Thomson, Michael A
Latcham, Frances
Sim, Rosalind
Walker-Smith, John A
Murch, Simon H
Journal Article
Research Support, Non-U.S. Gov't
Germany
Eur J Immunol. 2003 Aug;33(8):2307-15.},
   abstract = {Infant food allergies are increasing, and many breast-fed infants now sensitize to maternally-ingested antigens. As low-dose oral tolerance requires generation of suppressor lymphocytes producing TGF-beta1 (Th3 cells), we studied these cells in duodenal biopsies after diagnostic endoscopy. Spontaneous production of Th1, Th2 and Th3 cytokines by duodenal lymphocytes was studied using flow cytometry in 20 children with no eventual clinico-pathological diagnosis (controls), 30 children with multiple food allergy, nine with celiac disease and six with inflammatory enteropathies. Immunohistochemistry and in situ hybridization were used to localize TGF-beta1 protein and mRNA in matched biopsies. We found no significant Th1/Th2 skewing amongst mucosal lymphocytes in allergic children compared to controls, although celiac and inflammatory enteropathy patients showed increased Th1 responses. By contrast, the allergic children showed reduction of TGF-beta1(+) lymphocytes in both epithelial and lamina propria compartments. Reduction of TGF-beta1 expression was also seen in mononuclear cells and epithelium in food allergy by immunohistochemistry and in situ hybridization. The dominant mucosal abnormality in food allergic children was, thus, not Th2 deviation but impaired generation of Th3 cells. As generation of these cells requires innate immune response to enteric bacteria, we suggest that changing infectious exposures may inhibit primary establishment of basic oral tolerance mechanisms.},
   keywords = {Administration, Oral
Antigens/administration & dosage
Case-Control Studies
Child
Cytokines/biosynthesis
Duodenum/*immunology/pathology
Food Hypersensitivity/genetics/*immunology/pathology
Humans
Immune Tolerance
Immunohistochemistry
In Situ Hybridization
In Vitro Techniques
Infant
Infant, Newborn
Intestinal Mucosa/immunology/pathology
Prospective Studies
RNA, Messenger/genetics/metabolism
T-Lymphocytes, Regulatory/*immunology
Transforming Growth Factor beta/*biosynthesis/genetics
Transforming Growth Factor beta1},
   ISSN = {0014-2980 (Print)
0014-2980},
   Accession Number = {12884306},
   DOI = {10.1002/eji.200323308},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Perr, H. A.},
   title = {Novel foods to treat food allergy and gastrointestinal infection},
   journal = {Curr Gastroenterol Rep},
   volume = {6},
   number = {3},
   pages = {254-60},
   note = {Perr, Hilary A
Journal Article
Review
United States
Curr Gastroenterol Rep. 2004 Jun;6(3):254-60.},
   abstract = {The gastrointestinal tract communicates directly with the external environment. Necessary nutrients must be absorbed and commensal bacteria tolerated, and foreign proteins, antigens, and pathogens must be simultaneously excluded or destroyed. Immaturity or disruption of the mucosal immune defenses increases vulnerability to food allergy, intolerance, and infectious disease. Diseases resulting from ingested foreign proteins and organisms are increasing and cause morbidity and mortality worldwide. There is no specific treatment for food allergy other than avoidance. Vaccination for infectious disease is limited by the cost and logistics of distribution and administration, particularly in developing countries. Novel strategies are being explored to modulate the gut mucosal immune system by altering protein expression in food. Crops are being developed to remove deleterious allergens to prevent immunogenic exposure while preserving nutritional quality. Local food plants that express protein fragments of pathogens might provide an effective means to stimulate gut mucosal immunity while increasing vaccine accessibility.},
   keywords = {Autoimmunity
Celiac Disease/immunology
Food Hypersensitivity/immunology/*therapy
Gastric Mucosa/immunology
Gastrointestinal Diseases/immunology/*therapy
Helicobacter Infections/immunology
Helicobacter pylori/immunology
Humans
Intestinal Mucosa/immunology
Peanut Hypersensitivity/immunology
Soybeans/immunology
Triticum/immunology
Wheat Hypersensitivity/immunology/therapy},
   ISSN = {1522-8037 (Print)
1522-8037},
   Accession Number = {15128494},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Peters, J. H. and McKay, B. M. and Simasko, S. M. and Ritter, R. C.},
   title = {Leptin-induced satiation mediated by abdominal vagal afferents},
   journal = {Am J Physiol Regul Integr Comp Physiol},
   volume = {288},
   number = {4},
   pages = {R879-84},
   note = {Peters, J H
McKay, B M
Simasko, S M
Ritter, R C
R01 NS-20561/NS/NINDS NIH HHS/United States
Journal Article
Research Support, U.S. Gov't, P.H.S.
United States
Am J Physiol Regul Integr Comp Physiol. 2005 Apr;288(4):R879-84. Epub 2004 Dec 9.},
   abstract = {Leptin is a hormone secreted into the systemic blood primarily by white adipose tissue. However, leptin also is synthesized and stored by cells in the gastric mucosa. Because gastric mucosal leptin is secreted in response to ingestion of a meal, we hypothesized that it might contribute to satiation (meal termination) by acting on gastrointestinal vagal afferent neurons. To test whether leptin is capable of acutely reducing short-term food intake, we measured consumption of a liquid meal (15% sucrose) following low-dose leptin administration via the celiac artery, which perfuses the upper gastrointestinal tract. Leptin (1, 3, 10 mug) was infused via a chronically implanted, nonocclusive celiac arterial catheter or via a jugular vein catheter with its tip in the right cardiac atrium. Fifteen percent sucrose intake was then measured for 30 min. We found that leptin dose dependently inhibited sucrose intake when infused through the celiac catheter but not when infused into the general circulation via a jugular catheter. Plasma leptin concentrations in the general circulation following celiac arterial or jugular leptin infusions were not significantly different. Celiac arterial leptin infusion did not reduce meal size in vagotomized or capsaicin-treated rats. Finally, we also found that reduction of meal size by celiac leptin infusion was markedly enhanced when coinfused with cholecystokinin, a gastrointestinal satiety peptide whose action depends on vagal afferent neurons. Our results support the hypothesis that leptin contributes to satiation by a mechanism dependent on gastrointestinal vagal afferent innervation of the upper gastrointestinal tract.},
   keywords = {Abdomen/*innervation
Afferent Pathways/*physiology
Angiography
Animals
Capsaicin/pharmacology
Celiac Artery
Eating/drug effects
Infusions, Intra-Arterial
Infusions, Intravenous
Jugular Veins
Leptin/administration & dosage/blood/*pharmacology
Male
Rats
Rats, Sprague-Dawley
Satiation/*physiology
Sucrose/pharmacology
Vagotomy
Vagus Nerve/*physiology},
   ISSN = {0363-6119 (Print)
0363-6119},
   Accession Number = {15591156},
   DOI = {10.1152/ajpregu.00716.2004},
   year = {2005},
   type = {Ref–rence Type}
}

@article{
   author = {Petukhov, A. B. and Lysikov Iu, A. and Ishkova, VIu},
   title = {[Digestive pathology and digestive function of small intestine mucous layer]},
   journal = {Vopr Pitan},
   volume = {73},
   number = {6},
   pages = {21-4},
   note = {Petukhov, A B
Lysikov, Iu A
Ishkova, V Iu
English Abstract
Journal Article
Russia (Federation)
Vopr Pitan. 2004;73(6):21-4.},
   abstract = {The research of small intestine mucous layer at children and adults is carried out. It is revealed high meanings enzyme distribution in human small intestine mucous layer and their change at celiac disease, food allergy, short-bowel syndrome.},
   keywords = {Adolescent
Adult
Alkaline Phosphatase/metabolism
Celiac Disease/enzymology/physiopathology
Child
Child, Preschool
*Digestion
Digestive System Diseases/enzymology/*physiopathology
Endoscopy, Gastrointestinal
Enteritis/enzymology/physiopathology
Food Hypersensitivity/enzymology/physiopathology
Humans
Intestinal Mucosa/enzymology/*physiopathology
Intestine, Small/enzymology/*physiopathology
Lactase/metabolism
Short Bowel Syndrome/enzymology/physiopathology
beta-Fructofuranosidase/metabolism},
   ISSN = {0042-8833 (Print)
0042-8833},
   Accession Number = {15685855},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Pozler, O. and Neumann, D.},
   title = {[Diabetes and celiac disease]},
   journal = {Vnitr Lek},
   volume = {50},
   number = {5},
   pages = {412-4},
   note = {Pozler, O
Neumann, D
English Abstract
Journal Article
Review
Czech Republic
Vnitr Lek. 2004 May;50(5):412-4.},
   abstract = {Celiac sprue is permanent lifelong intolerance of gluten which in some sensitive individuals leads to an inflammation of various grades followed by atrophy of jejunum mucosa. Diagnosis of celiac sprue is based on proof of histopathological changes in jejunum mucosa as a result of presence of gluten in food. In recent years, serum endogenous myosin and tissue transglutaminase antibodies were used in a diagnostic algorithm. We distinguish active, silent, latent, and potential celiac sprue. Simultaneous incidence of type I diabetes mellitus and celiac sprue has been documented in a range of studies. Both diseases have common immunology and genetic characters. Prevalence of celiac sprue in patients with type I diabetes is several times higher compared to prevalence of this disease in the population. There is the prevalence of celiac sprue 3.6-5.1% in children with type I diabetes mellitus in the Czech Republic, silent form of the disease is the most frequent one. An effect of a strict gluten free diet on a metabolic control of diabetes has not been proved. It is necessary to assess (at least once per two years) actively and on regular basis endogenous myosin and/or tissue transglutaminase antibodies in patients with type I diabetes.},
   keywords = {Celiac Disease/*complications/diagnosis/physiopathology
Diabetes Mellitus, Type 1/*complications
Humans},
   ISSN = {0042-773X (Print)
0042-773x},
   Accession Number = {15305643},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Rostami, K. and Malekzadeh, R. and Shahbazkhani, B. and Akbari, M. R. and Catassi, C.},
   title = {Coeliac disease in Middle Eastern countries: a challenge for the evolutionary history of this complex disorder?},
   journal = {Dig Liver Dis},
   volume = {36},
   number = {10},
   pages = {694-7},
   note = {Rostami, K
Malekzadeh, R
Shahbazkhani, B
Akbari, M R
Catassi, C
Journal Article
Netherlands
Dig Liver Dis. 2004 Oct;36(10):694-7.},
   abstract = {About 10,000 years ago domestication and farming of wheat and other cereals developed in the 'Fertile Crescent', an area including modern Turkey, Iraq and Iran. Agriculture then slowly spread from Middle East to Europe. Coeliac disease is the permanent intolerance to dietary gluten, the major protein component of wheat. It has been until relatively recently hypothesised that wheat consumption exerted a negative selective pressure on genes predisposing to coeliac disease, eventually leading to higher coeliac disease frequency in Northeastern Europe because of lack of exposure to cereals. This theory is at variance with recent studies showing that coeliac disease is as common in Middle Eastern countries as in Europe. High prevalence of coeliac disease has been found in Iran, in both the general population and at-risk groups, e.g. patients with irritable bowel syndrome or type 1 diabetes. Clinical manifestations of coeliac disease vary markedly with the age of the patient, the duration and the extent of disease. Clinical studies showed that presentation with non-specific symptoms or no symptoms is as common in the Middle East as in Europe. Wheat represented a major component of the Iranian diet for many centuries and it may be argued that the continuous and high level of exposure to wheat proteins has induced some degree of immune tolerance, leading to milder symptoms that may be misdiagnosed as irritable bowel syndrome or unexplained gastrointestinal disorders. The gluten-free diet represents a real challenge to both patients and clinicians in this area. This is particularly difficult in the absence of any supply for gluten-free diet in Middle Eastern countries.},
   keywords = {Celiac Disease/*epidemiology/etiology
Diet
Food
Humans
India/epidemiology
Iran/epidemiology
Iraq/epidemiology
Kuwait/epidemiology
Libya/epidemiology
Middle East/epidemiology
Prevalence
Saudi Arabia/epidemiology
Triticum/adverse effects},
   ISSN = {1590-8658 (Print)
1590-8658},
   Accession Number = {15506671},
   DOI = {10.1016/j.dld.2004.05.010},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Rousset, H.},
   title = {[A great imitator for the allergologist: intolerance to gluten]},
   journal = {Eur Ann Allergy Clin Immunol},
   volume = {36},
   number = {3},
   pages = {96-100},
   note = {Rousset, H
English Abstract
Journal Article
Review
Italy
Eur Ann Allergy Clin Immunol. 2004 Mar;36(3):96-100.},
   abstract = {Intolerance of gluten, resposible for Coeliac disease, is essentially shown by an auto-immune enteropathy, even if the cutaneous manifestation (herpetiform dermatitis) and perhaps certain neurological signs (cerebral syndrome, peripheral neuropathy) may be independent as well as associated with the intestinal illness. This affection is of immunological nature, occuring in a genetic field that predisposes to the illness (familial form: concordance of 70% in homozygote twins; 90% of patients show an HLA molecule of type DQ2, DQ8 in almost all the other cases. The exogenous factor is the gluten content contained in wheat, rye and barley, more precisely by the intermediary "the prolamines" which are the "reactive" element that induces a the same time an inflammatory reaction of type TH11 locally (expressed by the histological aspect of a duodenal biopsy evolving as villous atrophy) and a humoral response with production of anti-gliadine and anti-transglutaminase antibodies (the role of the latter enzyme is intervention in the local transformation of antigens to make them antigenic). It is an illness of adults as well as children and this point must now be emphasized. Recent epidemiological studies insist on a high prevalence (1/300 in Europe). Clinical expression, at the start very polymorphic and so misleading, before the appearance of the more classical signs of malabsorption and development, always feared, towards a lymphoma. These signs are haematological (anemia of various types, hyper platelets by hyposplenism, haemorrhagic signs) cutaneous (herpetiform dermatitis, cutaneous vasculitis) mucosal (aphtose), hepatic (cytolysis), neurophysical (fatigue, troubles of behaviour, cerebral syndrome, neuropathy) and osteo-articulitis (osteopenia, arthralgias, diffuse pains). The association of certain auto-immune illnesses must be emphasized (diabetes, Hashimoto thyroiditis, Gougerot disease, primitive biliary cirrhosis). To think early of the possibility of intolerance to gluten, is to give the means of a very easy diagnosis (measurement of anti-gliadin, anti-endomysium and anti-transglutaminase, and secondarily duodenal biopsy if necessary), and it is early elimination of gluten food which will make the various clinical manifestations disappear and so prevent the risk of evolution to a tumoral pathology.},
   keywords = {Adolescent
Adult
Allergens/*adverse effects/immunology
Anemia/etiology
Autoimmune Diseases/*diagnosis/epidemiology/etiology/immunology
Bone Diseases/etiology
Celiac Disease/*diagnosis/epidemiology/etiology/immunology
Child
Child, Preschool
Dermatitis Herpetiformis/etiology
Diabetes Mellitus, Type 1/complications
Diagnosis, Differential
Female
Glutens/*adverse effects/immunology
Hemorrhage/etiology
Humans
Infant
Intestinal Mucosa/immunology
Male
Middle Aged
Nervous System Diseases/etiology},
   ISSN = {1764-1489 (Print)
1764-1489},
   Accession Number = {15137480},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Rujner, J. and Socha, J. and Syczewska, M. and Wojtasik, A. and Kunachowicz, H. and Stolarczyk, A.},
   title = {Magnesium status in children and adolescents with coeliac disease without malabsorption symptoms},
   journal = {Clin Nutr},
   volume = {23},
   number = {5},
   pages = {1074-9},
   note = {Rujner, Jolanta
Socha, Jerzy
Syczewska, Malgorzata
Wojtasik, Anna
Kunachowicz, Hanna
Stolarczyk, Anna
Clinical Trial
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
England
Clin Nutr. 2004 Oct;23(5):1074-9.},
   abstract = {BACKGROUND & AIMS: Magnesium deficiency has been reported in coeliac disease (CD) with clinical symptoms. The aim of this study was to evaluate magnesium status in CD without malabsorption symptoms in patients aged 5-18 years. In the study participated 41 coeliac patients on a gluten-free diet (GFD) for a mean 11 years with IgAEmA (-) and normal villi, 28 patients with untreated subclinical (atypical) CD with IgAEmA (+) and villous atrophy, and 8 healthy subjects as a control group. METHOD: Magnesium status was examined by an intravenous Mg loading test, determination of serum and erythrocyte Mg concentrations, and urinary excretion. Steatorrhea was assessed by fecal fat excretion. Magnesium, calcium, protein, and fat intake were evaluated by a food frequency questionnaire. RESULTS: The frequency of magnesium deficiency as assessed by the magnesium loading test was: 19.6% in treated, 21.4% in untreated CD patients, and 25% in control group, similar in both sexes, sporadic in small towns (3.8%), frequent in large cities and rural villages (23.5% vs. 32.3%). Fat excretion was within normal limits. The following results were found, respectively: decreased serum magnesium concentration, 7.3% vs. 3.6% vs. 0%, decreased erythrocyte Mg concentration, 14.6% vs. 25% vs. 12.5%; decreased intake of magnesium, 29% vs. 32% vs. 0%. CONCLUSIONS: The frequency of magnesium deficiency was similar in pediatric patients who were treated for CD or in patients with subclinical CD, and in control group; magnesium deficiency in patients participating in our study depended on an imbalanced diet.},
   keywords = {Adolescent
Celiac Disease/complications/*metabolism
Child
Child, Preschool
Diet
Erythrocytes/chemistry
Feces/chemistry
Female
Glutens/administration & dosage/metabolism
Humans
Magnesium/*administration & dosage/blood/*metabolism/urine
Magnesium Deficiency/complications/*epidemiology
Male
Nutrition Policy
Nutritional Requirements
Nutritional Status},
   ISSN = {0261-5614 (Print)
0261-5614},
   Accession Number = {15380898},
   DOI = {10.1016/j.clnu.2003.10.018},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Saalman, R. and Dahlgren, U. I. and Fallstrom, S. P. and Hanson, L. A. and Ahlstedt, S. and Wold, A. E.},
   title = {Avidity progression of dietary antibodies in healthy and coeliac children},
   journal = {Clin Exp Immunol},
   volume = {134},
   number = {2},
   pages = {328-34},
   note = {Saalman, R
Dahlgren, U I
Fallstrom, S P
Hanson, L A
Ahlstedt, S
Wold, A E
Journal Article
Research Support, Non-U.S. Gov't
England
Clin Exp Immunol. 2003 Nov;134(2):328-34.},
   abstract = {In most individuals minute amounts of food proteins pass undegraded across the intestinal mucosa and trigger antibody formation. Children with coeliac disease have enhanced antibody production against gliadin as well as other dietary antigens, e.g. beta-lactoglobulin, in cow's milk. Antibody avidity, i.e. the binding strength between antibody and antigen, often increases during antibody responses and may be related to the biological effectiveness of antibodies. The aim of the present study was to determine the avidity of serum IgG antibodies against beta-lactoglobulin and gliadin in healthy children during early childhood and compare these avidities to those found in children with coeliac disease. The average antibody avidity was analysed using a thiocyanate elution assay, whereas the antibody activity of the corresponding sera was assayed by ELISA. The avidity of serum IgG antibodies against beta-lactoglobulin as well as gliadin increased with age in healthy children, even in the face of falling antibody titres to the same antigens. Children with untreated coeliac disease had IgG anti-beta-lactoglobulin antibodies of significantly higher avidity than healthy children of the same age, and the same trend was observed for IgG antigliadin antibodies. The present data suggest that the avidities of antibodies against dietary antigens increase progressively during early childhood, and that this process seems to be accelerated during active coeliac disease.},
   keywords = {Aging/immunology
*Antibody Affinity
Celiac Disease/*immunology
Child, Preschool
Dietary Proteins/*immunology
Follow-Up Studies
Gliadin/immunology
Humans
Immunoglobulin G/immunology
Infant
Lactoglobulins/immunology},
   ISSN = {0009-9104 (Print)
0009-9104},
   Accession Number = {14616795},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Sabra, A. and Bellanti, J. A. and Rais, J. M. and Castro, H. J. and de Inocencio, J. M. and Sabra, S.},
   title = {IgE and non-IgE food allergy},
   journal = {Ann Allergy Asthma Immunol},
   volume = {90},
   number = {6 Suppl 3},
   pages = {71-6},
   note = {Sabra, Aderbal
Bellanti, Joseph A
Rais, Jonathan Malka
Castro, Henry J
de Inocencio, Julia Mendez
Sabra, Selma
Journal Article
Review
United States
Ann Allergy Asthma Immunol. 2003 Jun;90(6 Suppl 3):71-6.},
   abstract = {BACKGROUND: Food allergy (FA) is characterized by an abnormal immunologic reactivity to food proteins. The gastro-intestinal tract serves not only a nutritive function but also is a major immunologic organ. Although previously thought to be triggered primarily by an IgE-mediated mechanism of injury, considerable evidence now suggests that non-IgE mechanisms may also be involved in the pathogenesis of FA. OBJECTIVE: To review the immunologic disturbances that occur in FA and to correlate these with the clinical manifestations expressed in affected target organs based upon a classification of IgE and non-IgE mechanisms. METHODS: Data collected from a computerized MEDLINE search were used for the analysis of the following topics: immediate GI hypersensitivity, oral allergy syndrome, acute urticaria and angioedema, acute bronchospasm, celiac disease, cow's milk enteropathy, dietary protein enterocolitis, breast milk colitis, proctolitis, proctitis, dermatitis herpetiformis, Heiner syndrome, eosinophilic gastroenteritis, atopic dermatitis, asthma, attention-deficit-hyperactivity disorder and behavioral disorders, as well as systems affected by mucosal associated lymphoid tissue-mediated injury of associated lymphoid tissues and the immunologic deviation to Th1 or Th2 mechanisms of FA. CONCLUSIONS: The results of this review allow the construction of a central, unifying hypothesis for a new classification of FA as follows: the clinical manifestations of FA, expressed in affected target organs, may be the result of immunologic injury mediated by interaction of food antigens with contiguous elements of mucosal associated lymphoid tissue. These appear to be modulated by relative imbalances of the Th1/Th2 paradigm, which may be the ultimate determinant governing the expression of FA as IgE-mediated, non--IgE-mediated, or mixed forms of IgE/non-IgE mechanisms of FA.},
   keywords = {Dietary Proteins/*adverse effects/*immunology
Food Hypersensitivity/classification/*immunology
Humans
Hypersensitivity, Immediate/classification/*etiology/immunology
Immune System/immunology
Immune Tolerance/immunology
Immunity, Mucosal/immunology
Incidence},
   ISSN = {1081-1206 (Print)
1081-1206},
   Accession Number = {12839117},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Salvati, V. M. and MacDonald, T. T. and del Vecchio Blanco, G. and Mazzarella, G. and Monteleone, I. and Vavassori, P. and Auricchio, S. and Pallone, F. and Troncone, R. and Monteleone, G.},
   title = {Enhanced expression of interferon regulatory factor-1 in the mucosa of children with celiac disease},
   journal = {Pediatr Res},
   volume = {54},
   number = {3},
   pages = {312-8},
   note = {Salvati, Virginia M
MacDonald, Thomas T
del Vecchio Blanco, Giovanna
Mazzarella, Giuseppe
Monteleone, Ivan
Vavassori, Piero
Auricchio, Salvatore
Pallone, Francesco
Troncone, Riccardo
Monteleone, Giovanni
Journal Article
Research Support, Non-U.S. Gov't
United States
Pediatr Res. 2003 Sep;54(3):312-8. Epub 2003 Jun 4.},
   abstract = {Celiac disease (CD) is an enteropathy characterized by a Th1-type immune response to the dietary gluten. The transcriptional mechanisms or factors that control Th1 cell development in this condition remain to be elucidated. The aim of this study was to analyze in CD the expression of interferon (IFN) regulatory factor (IRF)-1, a transcription factor that regulates the differentiation and function of Th1 cells. Duodenal biopsies were taken from children with untreated CD and control children, and analyzed for IRF-1 by Southern blotting of reverse-transcriptase PCR products and Western blotting. IRF-1 DNA-binding activity was assessed by electrophoretic shift mobility assay. The effect of gliadin stimulation on IRF-1 induction was investigated in an ex vivo organ culture of treated CD biopsies. Enhanced IRF-1 was seen in untreated CD in comparison with controls. This was evident at both the RNA and protein level. Furthermore, untreated CD samples exhibited stronger nuclear accumulation and DNA-binding activity of IRF-1 than controls. In contrast, IRF-2, a transcriptional repressor that binds the same DNA element and competes with IRF-1, was expressed at the same level in nuclear proteins extracted from both untreated CD and control patients. In explant cultures of treated CD biopsies, gliadin enhanced both IRF-1 RNA and protein. This effect was prevented by a neutralizing IFN-gamma antibody. Furthermore, stimulation of normal duodenal biopsies with IFN-gamma enhanced IRF-1. These data indicate that IRF-1 is a hallmark of the gliadin-mediated inflammation in CD and suggest that IFN-gamma/IRF-1 signaling pathway can play a key role in maintaining and expanding the local Th1 inflammatory response in this disease.},
   keywords = {Adolescent
Celiac Disease/immunology/*metabolism/pathology
Cells, Cultured
Child
DNA/metabolism
DNA-Binding Proteins/genetics/immunology/*metabolism
Duodenum/metabolism/pathology
Gliadin/metabolism
Humans
Interferon Regulatory Factor-1
Interferon-gamma/metabolism
Intestinal Mucosa/immunology/*metabolism/pathology
Phosphoproteins/genetics/immunology/*metabolism
Transcription Factors/genetics/metabolism},
   ISSN = {0031-3998 (Print)
0031-3998},
   Accession Number = {12788988},
   DOI = {10.1203/01.pdr.0000079184.70237.9c},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Sclafani, A. and Ackroff, K. and Schwartz, G. J.},
   title = {Selective effects of vagal deafferentation and celiac-superior mesenteric ganglionectomy on the reinforcing and satiating action of intestinal nutrients},
   journal = {Physiol Behav},
   volume = {78},
   number = {2},
   pages = {285-94},
   note = {Sclafani, Anthony
Ackroff, Karen
Schwartz, Gary J
R01 DK031135/DK/NIDDK NIH HHS/United States
DK-31135/DK/NIDDK NIH HHS/United States
DK-47208/DK/NIDDK NIH HHS/United States
Journal Article
Research Support, U.S. Gov't, P.H.S.
United States
Physiol Behav. 2003 Feb;78(2):285-94.},
   abstract = {The role of vagal afferents and splanchnic fibers in nutrient-induced flavor conditioning and feeding suppression was determined. Male rats were fitted with intraduodenal (ID) catheters and given subdiaphragmatic vagal deafferentation (SDA), celiac-superior mesenteric ganglionectomy (CGX), combined (COM) treatments, or sham surgery. In separate conditioning trials, they were trained to drink (30 min/day) flavored saccharin solutions paired with concurrent ID infusions of 8% maltodextrin or water and 3.55% corn oil or water. Experiment 1 revealed that SDA and sham rats showed equal preferences for the nutrient-paired flavors over the water-paired flavors. In contrast, SDA rats, unlike sham rats, failed to suppress their intake of a palatable fluid when infused intraduodenally with maltodextrin or corn oil. Experiment 2 revealed that CGX, COM and sham rats all developed preferences for the maltodextrin-paired flavor, although CGX alone or COM attenuated the conditioned preference. CGX and COM treatments also attenuated or blocked the feeding inhibitory actions of ID nutrient infusions. These findings along with prior data indicate that gut vagal afferents and splanchnic nerves are not essential for flavor-nutrient preference conditioning, whereas both vagal afferents and splanchnic nerves are implicated in carbohydrate- and fat-induced satiation.},
   keywords = {Afferent Pathways/physiology
*Animal Nutritional Physiological Phenomena
Animals
Choice Behavior
Conditioning (Psychology)
Corn Oil/administration & dosage
Duodenum
Food Preferences
Ganglia, Sympathetic/*physiology
Ganglionectomy
Intestines/*physiology
Male
Polysaccharides/administration & dosage
Rats
Rats, Sprague-Dawley
*Reinforcement (Psychology)
*Satiety Response
Vagotomy
Vagus Nerve/*physiology},
   ISSN = {0031-9384 (Print)
0031-9384},
   Accession Number = {12576127},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Sdepanian, V. L. and de Miranda Carvalho, C. N. and de Morais, M. B. and Colugnati, F. A. and Fagundes-Neto, U.},
   title = {Bone mineral density of the lumbar spine in children and adolescents with celiac disease on a gluten-free diet in Sao Paulo, Brazil},
   journal = {J Pediatr Gastroenterol Nutr},
   volume = {37},
   number = {5},
   pages = {571-6},
   note = {Sdepanian, Vera Lucia
de Miranda Carvalho, Cecilia Noronha
de Morais, Mauro Batista
Colugnati, Fernando Antonio Basile
Fagundes-Neto, Ulysses
Journal Article
United States
J Pediatr Gastroenterol Nutr. 2003 Nov;37(5):571-6.},
   abstract = {BACKGROUND: To compare bone mineral density (BMD) in children and adolescents with celiac disease (CD) and control subjects and to evaluate diet adequacy and calcium metabolism in patients with CD. METHODS: Thirty patients with asymptomatic CD (17 children, 13 adolescents), on a gluten-free diet, and 23 healthy subjects were studied. BMD of the lumbar spine (dual energy x-ray absorptiometry) was performed on all patients and control subjects. In patients, food diaries for nine nonconsecutive days were obtained and analyzed. In patients, laboratory tests pertaining to calcium balance were obtained. RESULTS: The mean weight and height of the adolescents with CD were lower than those of control subjects (weight: 45.8 +/- 10.5 kg v 55.3 +/- 10.5 kg, P = 0.037; height: 153.0 +/- 11.0 cm v 167 +/- 12.0 cm, P = 0.007). The mean BMD in adolescents with CD was significantly lower than that of the control subjects (0.917 +/- 0.116 g/cm2 v 1.060 +/- 0.158 g/cm2, P = 0.015), whereas no significant difference was found between children with CD and control subjects (P = 0.595). A multiple-regression model shows that increases in BMD relative to height were lower in adolescents with CD than in control subjects. The proportion of adolescents who had started a gluten-free diet after 2 years of age was higher than that of children with CD (P < 0.001). High percentages of magnesium, calcium, and phosphorous deficiencies were present in CD patients' diets. The serum levels of ionized and total calcium and parathormone were normal. CONCLUSIONS: The BMD of adolescents with CD was lower than that of the control subjects, whereas no difference was found between the BMD of children with CD and that of control subjects.},
   keywords = {Adolescent
Body Height
Body Mass Index
Body Weight
*Bone Density
Brazil
Calcium, Dietary/administration & dosage
Celiac Disease/*diet therapy/*physiopathology
Child
Diet
Glutens/*administration & dosage
Humans
*Lumbar Vertebrae
Magnesium/administration & dosage
Phosphorus, Dietary/administration & dosage
Regression Analysis},
   ISSN = {0277-2116 (Print)
0277-2116},
   Accession Number = {14581799},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Sicherer, S. H.},
   title = {Clinical aspects of gastrointestinal food allergy in childhood},
   journal = {Pediatrics},
   volume = {111},
   number = {6 Pt 3},
   pages = {1609-16},
   note = {1098-4275
Sicherer, Scott H
Journal Article
Review
United States
Pediatrics. 2003 Jun;111(6 Pt 3):1609-16.},
   abstract = {Gastrointestinal food allergies are a spectrum of disorders that result from adverse immune responses to dietary antigens. The named disorders include immediate gastrointestinal hypersensitivity (anaphylaxis), oral allergy syndrome, allergic eosinophilic esophagitis, gastritis, and gastroenterocolitis; dietary protein enterocolitis, proctitis, and enteropathy; and celiac disease. Additional disorders sometimes attributed to food allergy include colic, gastroesophageal reflux, and constipation. The pediatrician faces several challenges in dealing with these disorders because diagnosis requires differentiating allergic disorders from many other causes of similar symptoms, and therapy requires identification of causal foods, application of therapeutic diets and/or medications, and monitoring for resolution of these disorders. This review catalogs the spectrum of gastrointestinal food allergies that affect children and provides a framework for a rational approach to diagnosis and management.},
   keywords = {Child
Food Hypersensitivity/*complications/*diagnosis/therapy
Gastrointestinal Diseases/*etiology/therapy
Humans
Infant},
   ISSN = {0031-4005},
   Accession Number = {12777600},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Spaenij-Dekking, E. H. and Kooy-Winkelaar, E. M. and Nieuwenhuizen, W. F. and Drijfhout, J. W. and Koning, F.},
   title = {A novel and sensitive method for the detection of T cell stimulatory epitopes of alpha/beta- and gamma-gliadin},
   journal = {Gut},
   volume = {53},
   number = {9},
   pages = {1267-73},
   note = {Spaenij-Dekking, E H A
Kooy-Winkelaar, E M C
Nieuwenhuizen, W F
Drijfhout, J W
Koning, F
Journal Article
Research Support, Non-U.S. Gov't
England
Gut. 2004 Sep;53(9):1267-73.},
   abstract = {BACKGROUND: It is now generally accepted that coeliac disease (CD) is caused by inflammatory T cell responses to gluten peptides bound to HLA-DQ2 or -DQ8 molecules. There is overwhelming evidence that CD patients can mount T cell responses to peptides found in both alpha-gliadin and gamma-gliadin molecules. Assays that would detect the presence or absence of such peptides in food would thus be accurate indicators of safety for consumption by CD patients. AIMS: The development of a sensitive method to detect T cell stimulatory epitopes of alpha-gliadin and gamma-gliadin molecules in food products. METHODS: Monoclonal antibodies (mAb) were raised against peptides encoding the T cell stimulatory epitopes of alpha-gliadin (amino acids (aa) 59-71) and aa gamma-gliadin (aa 142-153 and aa 147-159). These mAb competition assays were developed that quantitatively detect T cell stimulatory epitopes present on both intact proteins and peptides of sizes recognisable by CD4(+) T cells. RESULTS: With the mAb based competition assays, T cell epitopes were detected in pepsin/trypsin digests of wheat proteins and ethanol extracts of various food products, with detection levels lower than those reached with gluten specific T cells. Moreover, the presence of T cell stimulatory epitopes was also detected in preparations of barley, rye, and triticale, other cereals known to be toxic for CD patients. CONCLUSIONS: A new antibody based method has been developed, detecting the presence of T cell stimulatory gluten peptides. This can be used to further ensure the safety of food consumed by CD patients.},
   keywords = {Animals
Antibodies, Monoclonal/immunology
Binding, Competitive
Cell Division/immunology
Edible Grain/immunology
Enzyme-Linked Immunosorbent Assay/methods
Epitopes, T-Lymphocyte/*analysis/immunology
Food
Food Analysis/methods
Gliadin/*immunology
Humans
Lymphocyte Activation
Mice
Mice, Inbred BALB C
Peptide Fragments/immunology
T-Lymphocytes/immunology},
   ISSN = {0017-5749 (Print)
0017-5749},
   Accession Number = {15306583},
   DOI = {10.1136/gut.2003.037952},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Stenhammar, L. and Falth-Magnusson, K. and Grodzinsky, E. and Hallert, C. and Hogberg, L. and Magnusson, K. E.},
   title = {[From ear to bread loaf. Several Swedish contributions to celiac disease research]},
   journal = {Lakartidningen},
   volume = {101},
   number = {48},
   pages = {3932-4, 3937},
   note = {Stenhammar, Lars
Falth-Magnusson, Karin
Grodzinsky, Ewa
Hallert, Claes
Hogberg, Lotta
Magnusson, Karl-Eric
Journal Article
Sweden
Lakartidningen. 2004 Nov 25;101(48):3932-4, 3937.},
   keywords = {Bread/adverse effects
*Celiac Disease/epidemiology/genetics/prevention & control
Edible Grain/adverse effects
Humans
Incidence
Primary Prevention
*Research
Sweden/epidemiology},
   ISSN = {0023-7205 (Print)
0023-7205},
   Accession Number = {15631228},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Stenhammar, L. and Hogberg, L. and Saalman, R.},
   title = {[The Pediatric Association recommends: Oats can be implemented in the gluten-free diet]},
   journal = {Lakartidningen},
   volume = {101},
   number = {18},
   pages = {1610-1},
   note = {Stenhammar, Lars
Hogberg, Lotta
Saalman, Robert
Journal Article
Sweden
Lakartidningen. 2004 Apr 29;101(18):1610-1.},
   keywords = {Adolescent
*Avena/adverse effects/toxicity
Celiac Disease/*diet therapy/psychology
Child
*Edible Grain/adverse effects/toxicity
Humans
Practice Guidelines as Topic
Quality of Life},
   ISSN = {0023-7205 (Print)
0023-7205},
   Accession Number = {15185537},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Storsrud, S. and Hulthen, L. R. and Lenner, R. A.},
   title = {Beneficial effects of oats in the gluten-free diet of adults with special reference to nutrient status, symptoms and subjective experiences},
   journal = {Br J Nutr},
   volume = {90},
   number = {1},
   pages = {101-7},
   note = {Storsrud, Stine
Hulthen, Lena R
Lenner, Ragnhild A
Journal Article
Research Support, Non-U.S. Gov't
England
Br J Nutr. 2003 Jul;90(1):101-7.},
   abstract = {In several studies oats have been reported to be tolerated by coeliac patients. The aim of the present study was to investigate the nutritional and symptomatic effects of including oats in the gluten-free diet, as well as the patients' subjective experiences. Twenty adult coeliac patients included large amounts of oats in their diet. Food intake, gastrointestinal symptoms, blood samples and body weight were examined and compared with examination at baseline. Diet compliance was checked monthly. The results are based on fifteen patients eating oats for 2 years plus three with only 6-months consumption. The median daily intake of oats was 93 (range 27-137) g/d, and the compliance was good. The mean intakes of Fe and dietary fibre increased (P<0.001) with the oat diet, as well as the intakes of thiamin and Zn (P<0.02). The bioavailability of Fe tended to decrease; this seems not to have influenced the Fe status. Temporary increased flatulence was experienced the first few weeks, as well as improved bowel function with oats in the diet. All patients who carried out the whole study period wanted to continue eating oats after the study, as they found that addition of oats in the gluten-free diet gave more variation, better taste and satiety. Oats improved the nutritional value of the gluten-free diet, had no negative effects on nutritional status and were appreciated by the subjects. Including oats can help coeliac patients following a strict gluten-free diet.},
   keywords = {Adult
*Avena
Biological Availability
Celiac Disease/*diet therapy
Dietary Fiber/*administration & dosage
Humans
Iron/metabolism
Nutritional Status
Patient Satisfaction
Statistics, Nonparametric},
   ISSN = {0007-1145 (Print)
0007-1145},
   Accession Number = {12844381},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Tanabe, S.},
   title = {IgE-binding abilities of pentapeptides, QQPFP and PQQPF, in wheat gliadin},
   journal = {J Nutr Sci Vitaminol (Tokyo)},
   volume = {50},
   number = {5},
   pages = {367-70},
   note = {Tanabe, Soichi
Comparative Study
Journal Article
Japan
J Nutr Sci Vitaminol (Tokyo). 2004 Oct;50(5):367-70.},
   abstract = {Wheat gliadin is known mainly as the causative substance for enteropathy accompanied by diarrhea (celiac disease) and food-dependent exercise-induced anaphylaxis. However, little is known in regards to the allergenicity of gliadin in atopic dermatitis. In this study, the allergenicity of gliadin was demonstrated using sera of wheat-allergic patients with atopic dermatitis. Since there are many repeated sequences in gliadin, peptides containing each motif were synthesized to evaluate their IgE-binding abilities. As a result, QQPFP and PQQPF were found to be epitopes (minimum structures for the IgE-binding). Gliadin might crosslink patient's IgE-antibodies via these epitopes and trigger subsequent allergic reactions.},
   keywords = {Allergens/chemistry/immunology
Amino Acid Sequence
Dermatitis, Atopic/immunology
Enzyme-Linked Immunosorbent Assay
Epitopes/chemistry/immunology
Food Hypersensitivity/immunology
Gliadin/chemistry/*immunology
Glutens/*analogs & derivatives/immunology
Humans
Immunoglobulin E/blood/*metabolism
Oligopeptides/chemistry/*immunology
Peptide Fragments/chemistry/immunology
Triticum/*immunology},
   ISSN = {0301-4800 (Print)
0301-4800},
   Accession Number = {15754499},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Thompson, T.},
   title = {Oats and the gluten-free diet},
   journal = {J Am Diet Assoc},
   volume = {103},
   number = {3},
   pages = {376-9},
   note = {Thompson, Tricia
Journal Article
Review
United States
J Am Diet Assoc. 2003 Mar;103(3):376-9.},
   abstract = {Whether oats should be included in a gluten-free diet has been debated for half a century. In 1995, the largest and most scientifically rigorous study on the safety of oats was published. Investigators concluded that the consumption of oats was safe for adults with celiac disease. Since 1995, several additional studies have been published. Without exception, these investigations found no adverse effects associated with the regular consumption of moderate amounts of oats. However, there are concerns among some authorities on celiac disease that even if oats themselves are safe, they nonetheless may be contaminated with wheat, rye, or barley. Unfortunately, the extent to which contamination of commercial oat products occurs is not known. Ideally, if a patient appears likely to use oats, they should be advised to consume only those products tested and found to be free of contamination.},
   keywords = {*Avena
Celiac Disease/*diet therapy
Diet, Protein-Restricted
Dietary Proteins/administration & dosage/adverse effects
Food Contamination/analysis
Food Handling/methods
Glutens/*administration & dosage/*adverse effects
Humans
Safety},
   ISSN = {0002-8223 (Print)
0002-8223},
   Accession Number = {12616264},
   DOI = {10.1053/jada.2003.50044},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Thompson, T.},
   title = {Gluten contamination of commercial oat products in the United States},
   journal = {N Engl J Med},
   volume = {351},
   number = {19},
   pages = {2021-2},
   note = {1533-4406
Thompson, Tricia
Letter
Research Support, Non-U.S. Gov't
United States
N Engl J Med. 2004 Nov 4;351(19):2021-2.},
   keywords = {Avena/*chemistry
Celiac Disease/diet therapy
Edible Grain/chemistry
*Food Contamination
Glutens/*analysis
Humans
United States},
   ISSN = {0028-4793},
   Accession Number = {15525734},
   DOI = {10.1056/nejm200411043511924},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Troncone, R. and Auricchio, R. and Paparo, F. and Maglio, M. and Borrelli, M. and Esposito, C.},
   title = {Coeliac disease and extraintestinal autoimmunity},
   journal = {J Pediatr Gastroenterol Nutr},
   volume = {39 Suppl 3},
   pages = {S740-1},
   note = {Troncone, Riccardo
Auricchio, Renata
Paparo, Franco
Maglio, Maria
Borrelli, Melissa
Esposito, Carla
Journal Article
Review
United States
J Pediatr Gastroenterol Nutr. 2004 Jun;39 Suppl 3:S740-1.},
   keywords = {Autoimmune Diseases/*immunology
Celiac Disease/*immunology
Humans},
   ISSN = {0277-2116 (Print)
0277-2116},
   Accession Number = {15167369},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Troncone, R. and Bhatnagar, S. and Butzner, D. and Cameron, D. and Hill, I. and Hoffenberg, E. and Maki, M. and Mendez, V. and de Jimenez, M. Z.},
   title = {Celiac disease and other immunologically mediated disorders of the gastrointestinal tract: Working Group report of the second World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition},
   journal = {J Pediatr Gastroenterol Nutr},
   volume = {39 Suppl 2},
   pages = {S601-10},
   note = {Troncone, Riccardo
Bhatnagar, Shinjini
Butzner, Decker
Cameron, Don
Hill, Ivor
Hoffenberg, Edward
Maki, Markku
Mendez, Virginia
de Jimenez, Mabel Zacur
European Society for Paediatric Gastroenterology, Hepatology and Nutrition
Journal Article
Review
United States
J Pediatr Gastroenterol Nutr. 2004 Jun;39 Suppl 2:S601-10.},
   keywords = {*Autoimmune Diseases/diagnosis/prevention & control/therapy
*Celiac Disease/diagnosis/prevention & control/therapy
Child
*Child Nutrition Disorders/prevention & control
Child Nutritional Physiological Phenomena
*Food Hypersensitivity/diagnosis/prevention & control/therapy
Gastroenterology
Humans
Practice Guidelines as Topic
Research
Societies, Medical},
   ISSN = {0277-2116 (Print)
0277-2116},
   Accession Number = {15184759},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Troncone, R. and Franzese, A. and Mazzarella, G. and Paparo, F. and Auricchio, R. and Coto, I. and Mayer, M. and Greco, L.},
   title = {Gluten sensitivity in a subset of children with insulin dependent diabetes mellitus},
   journal = {Am J Gastroenterol},
   volume = {98},
   number = {3},
   pages = {590-5},
   note = {Troncone, Riccardo
Franzese, Adriana
Mazzarella, Giuseppe
Paparo, Francesco
Auricchio, Renata
Coto, Iolanda
Mayer, Marina
Greco, Luigi
Journal Article
Research Support, Non-U.S. Gov't
United States
Am J Gastroenterol. 2003 Mar;98(3):590-5.},
   abstract = {OBJECTIVES: The association between celiac disease and insulin dependent diabetes mellitus (IDDM) is well established. Rectal gluten challenge has been used in patients with celiac disease and in first degree relatives as a tool to assess the mucosal immune response to gluten. The aim of this study was to assess the mucosal immune response to gluten in IDDM children by rectal gluten challenge. METHODS: Rectal biopsy specimens were obtained from 19 children with IDDM before and 6 h after rectal challenge with 2 g of a peptic tryptic digest of gliadin. A total of 16 treated celiac patients and 10 control subjects were also investigated. Epithelium and lamina propria CD3(+) and gamma delta(+) lymphocytes were counted with reference to a standard reference area of muscularis mucosae (10(4) microm(2)). RESULTS: After a local instillation of gliadin, a significant (>mean + 1 SD) percentage increment of lamina propria and epithelium CD3(+) and of lamina propria and epithelium gamma delta(+) lymphocytes was observed in five IDDM children, as compared to 11 and 13 celiac patients and one and two controls, respectively. A discriminant analysis allowed correct classification of 100% of patients with celiac disease and controls. The same analysis classified four of 19 IDDM children in the group of celiac patients. The positivity was associated with normal serology (antigliadin antibody, antiendomysial antibody, and antitissue transglutaminase antibodies) and a morphologically normal jejunal mucosa. All four patients had HLA-DQ alleles associated with celiac disease. CONCLUSIONS: Approximately 20% of IDDM children react to rectal instillation of gliadin. Long term follow-up is necessary to establish whether these subjects are at increased risk for developing celiac disease.},
   keywords = {Adolescent
Adult
Autoantibodies/*blood
Child
Diabetes Mellitus, Type 1/*immunology
Female
Gliadin/immunology
Glutens/*adverse effects/*immunology
HLA Antigens/genetics
Humans
Immunohistochemistry
Intestinal Mucosa/pathology
Jejunum/drug effects/pathology
Male
Phenotype
Rectum/drug effects/pathology},
   ISSN = {0002-9270 (Print)
0002-9270},
   Accession Number = {12650792},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Tursi, A.},
   title = {Gastrointestinal motility disturbances in celiac disease},
   journal = {J Clin Gastroenterol},
   volume = {38},
   number = {8},
   pages = {642-5},
   note = {Tursi, Antonio
Journal Article
Review
United States
J Clin Gastroenterol. 2004 Sep;38(8):642-5.},
   abstract = {It is quite frequent to recognize celiac patients who show gastrointestinal motor abnormalities in clinical practice. In fact, in 30 to 60% of patients, physical examination and dyspeptic symptoms (epigastric discomfort, early satiety) suggest a gastrointestinal motility disorder. Consistent data are now available on the presence of a disturbed motility of the esophagus, stomach, small intestine, gallbladder, and colon of untreated celiac patients. Gastrointestinal abnormalities differ in different gastrointestinal districts. In fact, esophageal transit, gastric and gallbladder emptying, and orocecal transit time are delayed, while colonic transit is faster. These findings are related to the complex interactions among reduced absorption of food constituent (in particular, fat), neurologic alteration, and hormonal derangement. Motility disorders of the gut are also a predisposing factor in the development of small intestinal bacterial overgrowth and may contribute both to development of symptoms in some untreated celiacs and to the persistence of symptoms after gluten-free diet in some of them. All these alterations fortunately disappear after gluten-free diet, and patients return to well being status. Whatever the initial event in the pathogenesis of the celiac lesions may be, we know for certain at this time that gastrointestinal disturbances play an important role in the genesis of gastrointestinal symptoms in celiac disease and that surveillance for celiac disease in patients complaining of dysmotility-like dyspeptic symptoms should be increased.},
   keywords = {Celiac Disease/*physiopathology
Food
*Gastrointestinal Motility
Hormones/physiology
Humans
Intestinal Absorption},
   ISSN = {0192-0790 (Print)
0192-0790},
   Accession Number = {15319644},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Tursi, A. and Brandimarte, G. and Giorgetti, G.},
   title = {High prevalence of small intestinal bacterial overgrowth in celiac patients with persistence of gastrointestinal symptoms after gluten withdrawal},
   journal = {Am J Gastroenterol},
   volume = {98},
   number = {4},
   pages = {839-43},
   note = {Tursi, Antonio
Brandimarte, Giovanni
Giorgetti, GianMarco
Journal Article
United States
Am J Gastroenterol. 2003 Apr;98(4):839-43.},
   abstract = {OBJECTIVE: Celiac disease is a gluten-sensitive enteropathy with a broad spectrum of clinical manifestation, and most celiac patients respond to a gluten-free diet (GFD). However, in some rare cases celiacs continue to experience GI symptoms after GFD, despite optimal adherence to diet. The aim of our study was to evaluate the causes of persistence of GI symptoms in a series of consecutive celiac patients fully compliant to GFD. METHODS: We studied 15 celiac patients (five men, 10 women, mean age 36.5 yr, range 24-59 yr) who continued to experience GI symptoms after at least 6-8 months of GFD (even if of less severity). Antigliadin antibody (AGA) test, antiendomysial antibody (EMA) test, and sorbitol H2-breath test (H2-BT), as well as esophagogastroduodenoscopy (EGD) with histological evaluation, were performed before starting GFD. Bioptic samples were obtained from the second duodenal portion during EGD, and histopathology was expressed according to the Marsh classification. To investigate the causes of persistence of GI symptoms in these patients, we performed AGA and EMA tests, stool examination, EGD with histological examination of small bowel mucosa, and sorbitol-, lactose-, and lactulose H2-breath tests. RESULTS: Histology improved in all patients after 6-8 months of GFD; therefore, refractory celiac disease could be excluded. One patient with Marsh II lesions was fully compliant to his diet but had mistakenly taken an antibiotic containing gluten. Two patients showed lactose malabsorption, one patient showed Giardia lamblia and one patient Ascaris lumbricoides infestation, and 10 patients showed small intestinal bacterial overgrowth (SIBO) by lactulose H2-BT. We prescribed a diet without milk or fresh milk-derived foods to the patient with lactose malabsorption; we treated the patients with parasite infestation with mebendazole 500 mg/day for 3 days for 2 consecutive wk; and we treated the patients with SIBO with rifaximin 800 mg/day for 1 wk. The patients were re-evaluated 1 month after the end of drug treatment (or after starting lactose-free diet); at this visit all patients were symptom-free. CONCLUSIONS: This study showed that SIBO affects most celiacs with persistence of GI symptoms after gluten withdrawal.},
   keywords = {Adult
Bacteria/*growth & development/*isolation & purification
Celiac Disease/*complications/diet therapy/*microbiology
Female
Gastrointestinal Diseases/diet therapy/*etiology/*microbiology
Glutens/*contraindications
Humans
Intestine, Small/*microbiology
Male
Middle Aged
Patient Compliance
Risk Factors
Severity of Illness Index
Treatment Failure},
   ISSN = {0002-9270 (Print)
0002-9270},
   Accession Number = {12738465},
   DOI = {10.1111/j.1572-0241.2003.07379.x},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Vader, L. W. and Stepniak, D. T. and Bunnik, E. M. and Kooy, Y. M. and de Haan, W. and Drijfhout, J. W. and Van Veelen, P. A. and Koning, F.},
   title = {Characterization of cereal toxicity for celiac disease patients based on protein homology in grains},
   journal = {Gastroenterology},
   volume = {125},
   number = {4},
   pages = {1105-13},
   note = {Vader, L Willemijn
Stepniak, Dariusz T
Bunnik, Evelien M
Kooy, Yvonne M C
de Haan, Willeke
Drijfhout, Jan Wouter
Van Veelen, Peter A
Koning, Frits
Journal Article
Research Support, Non-U.S. Gov't
United States
Gastroenterology. 2003 Oct;125(4):1105-13.},
   abstract = {BACKGROUND AND AIMS: Celiac disease is caused by T-cell responses to wheat gluten-derived peptides. The presence of such peptides in other widely consumed grains, however, has hardly been studied. METHODS: We have performed homology searches to identify regions with sequence similarity to T-cell stimulatory gluten peptides in the available gluten sequences: the hordeins of barley, secalins of rye, and avenins of oats. The identified peptides were tested for T-cell stimulatory properties. RESULTS: With 1 exception, no identical matches with T-cell stimulatory gluten peptides were found in the other grains. However, less stringent searches identified 11 homologous sequences in hordeins, secalins, and avenins located in regions similar to those in the original gluten proteins. Seven of these 11 peptides were recognized by gluten-specific T-cell lines and/or clones from patients with celiac disease. Comparison of T-cell stimulatory sequences with homologous but non-T-cell stimulatory sequences indicated key amino acids that on substitution either completely or partially abrogated the T-cell stimulatory activity of the gluten peptides. Finally, we show that single nucleotide substitutions in gluten genes will suffice to induce these effects. CONCLUSIONS: These results show that the disease-inducing properties of barley and rye can in part be explained by T-cell cross-reactivity against gluten-, secalin-, and hordein-derived peptides. Moreover, the results provide a first step toward a rational strategy for gluten detoxification via targeted mutagenesis at the genetic level.},
   keywords = {Alkaloids/adverse effects/genetics/immunology
Amino Acid Sequence
Avena/adverse effects/genetics
Celiac Disease/*chemically induced/immunology
Cross Reactions
Edible Grain/*adverse effects/*genetics
Epitopes/immunology
Gliadin/adverse effects/genetics/immunology
Glutens/*adverse effects/*analogs & derivatives/*genetics/immunology
Humans
Molecular Sequence Data
Plant Proteins/adverse effects/genetics/immunology
Prolamins
Proline/genetics
Secale/adverse effects/genetics
T-Lymphocytes/immunology
Triticum/adverse effects/genetics
Tyramine/analogs & derivatives},
   ISSN = {0016-5085 (Print)
0016-5085},
   Accession Number = {14517794},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Valdes, I. and Garcia, E. and Llorente, M. and Mendez, E.},
   title = {Innovative approach to low-level gluten determination in foods using a novel sandwich enzyme-linked immunosorbent assay protocol},
   journal = {Eur J Gastroenterol Hepatol},
   volume = {15},
   number = {5},
   pages = {465-74},
   note = {Valdes, Israel
Garcia, Enrique
Llorente, Mercedes
Mendez, Enrique
Journal Article
England
Eur J Gastroenterol Hepatol. 2003 May;15(5):465-74.},
   abstract = {OBJECTIVES: There is currently much call for a reliable enzyme-linked immunosorbent assay (ELISA) protocol for determining gluten in foods to serve as a basis for further Codex Alimentarius regulations. Given its ability to recognize the potential coeliac-toxic epitope QQPFP, which occurs repeatedly in alpha-, gamma- and omega-gliadins, hordeins and secalins, the monoclonal antibody R5 raised against a secalin extract may prove to be an essential tool for gluten analysis. This study was designed to develop a highly sensitive and specific sandwich ELISA to quantify low levels of wheat, barley and rye prolamins in foods for coeliacs. METHODS: Simple sandwich ELISA based on the use of a single monoclonal antibody (R5) as both the coating and detection was developed. A quantitative cocktail gluten-extraction procedure for heat-processed foods was also tested. RESULTS: R5-ELISA was able to identify gliadins, hordeins and secalins with assay sensitivities of 0.78, 0.39 and 0.39 ng/ml, respectively. The assay's detection limit was 1.5 ng gliadins/ml (1.56 ppm gliadins, 3.2 ppm gluten). The system proved insensitive to the non-coeliac-toxic cereals maize, rice and oats, and was non-cultivar-dependent. It was also able to detect gliadins and hordeins in unprocessed and heat-processed wheat- and barley-based products, and to estimate the gluten content of hydrolysed foods. CONCLUSION: We present a new generation of a robust sandwich R5-ELISA with good reproducibility (8.7%) and repeatability (7.7%). Its gluten-detection limit of 3.2 ppm is lower than the existing threshold of 20-200 ppm. The ELISA, which is equally sensitive to barley, wheat and rye prolamins, is compatible with the quantitative cocktail extraction procedure for heat-processed foods. Along with the cocktail procedure, the Working Group on Prolamin Analysis and Toxicity is currently evaluating an R5-ELISA system as proposed by the Codex Alimentarius Commission.},
   keywords = {Antibodies, Monoclonal/immunology
Celiac Disease/diet therapy
Edible Grain/chemistry
Enzyme-Linked Immunosorbent Assay/*methods
Food Analysis/*methods
Gliadin/analysis
Glutens/*analysis/immunology
Humans
Plant Proteins/analysis
Prolamins
Reference Standards
Reproducibility of Results
Sensitivity and Specificity},
   ISSN = {0954-691X (Print)
0954-691x},
   Accession Number = {12702901},
   DOI = {10.1097/01.meg.0000059119.41030.df},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Varadarajulu, S. and Noone, T. and Hawes, R. H. and Cotton, P. B.},
   title = {Pancreatic duct stent insertion for functional smoldering pancreatitis},
   journal = {Gastrointest Endosc},
   volume = {58},
   number = {3},
   pages = {438-41},
   note = {Varadarajulu, Shyam
Noone, Tara
Hawes, Robert H
Cotton, Peter B
Journal Article
United States
Gastrointest Endosc. 2003 Sep;58(3):438-41.},
   abstract = {BACKGROUND: Some patients with smoldering pancreatitis in the absence of necrosis, pseudocyst, and ductal disruption experience unremitting abdominal pain caused by persistent pancreatic inflammation. Experience with the use of pancreatic duct stents in this patient population was reviewed. PATIENTS AND METHODS: Data for 11 patients with smoldering pancreatitis who underwent ERCP with pancreatic duct stent placement were reviewed retrospectively. All patients had severe, daily pain that worsened with ingestion of food, had required narcotic analgesics for control of pain, had lost weight, and had persistently elevated serum levels of pancreatic enzymes as well as pancreatic inflammatory changes on CT (without necrosis or pseudocyst). Six patients were being treated with parenteral nutrition. OBSERVATIONS: The mean duration of symptoms from the onset of pancreatitis until pancreatic duct stent insertion was 74 days (range 14-151 days). Stents were placed for a mean of 7 weeks (range 2-19 weeks). Pancreatic stent placement provided permanent pain relief in 10 (91%) patients within a mean of 9 days (range 3-20 days); one patient had persistent symptoms requiring celiac plexus blockade after 5 months. Parenteral nutrition and treatment with narcotic agents were discontinued for 10 patients within a mean of 15 days (range 7-39 days) after pancreatic duct insertion. CONCLUSIONS: Smoldering pancreatitis may result from functional obstruction, possibly caused by edema or spasm, of the papillary orifice. Insertion of a stent into the pancreatic duct alleviates pain, enables early resumption of oral intake of food, and facilitates pancreatic duct drainage. It also may help to prevent complications arising from persistent pancreatic inflammation.},
   keywords = {Abdominal Pain/etiology
Acute Disease
Cholangiopancreatography, Endoscopic Retrograde
Female
Humans
Male
Middle Aged
*Pancreatic Ducts
Pancreatitis/diagnostic imaging/*therapy
Retrospective Studies
*Stents
Time Factors},
   ISSN = {0016-5107 (Print)
0016-5107},
   Accession Number = {14528225},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Veres, G. and Westerholm-Ormio, M. and Kokkonen, J. and Arato, A. and Savilahti, E.},
   title = {Cytokines and adhesion molecules in duodenal mucosa of children with delayed-type food allergy},
   journal = {J Pediatr Gastroenterol Nutr},
   volume = {37},
   number = {1},
   pages = {27-34},
   note = {Veres, Gabor
Westerholm-Ormio, Mia
Kokkonen, Jorma
Arato, Andras
Savilahti, Erkki
Journal Article
Research Support, Non-U.S. Gov't
United States
J Pediatr Gastroenterol Nutr. 2003 Jul;37(1):27-34.},
   abstract = {OBJECTIVES: The aim was to investigate the expression of cytokines, adhesion molecules, and activation and proliferation markers in duodenal biopsies from children with delayed-type food allergy (FA). METHODS: Seven children with untreated FA (uFA), seven children with treated FA (tFA) to cow milk and/or cereals, and five normal controls furnished duodenal biopsy specimens. Additionally, five pediatric patients with celiac disease were included, serving exclusively as positive controls for in situ hybridization. Interferon-gamma (IFN-gamma), interleukin-4 (IL-4), adhesion molecules, and activation markers were detected by immunohistochemistry, and expression of IFN-gamma and IL-4 messenger RNA was revealed by in situ hybridization. RESULTS: uFA patients had a higher density of IFN-gamma positive cells in the lamina propria than did tFA patients and controls (P = 0.053 and P = 0.018). Moreover, the uFA patients exhibited a higher proportion of crypt cells in mitosis than did tFA patients (P = 0.026), and stronger staining of HLA-DR in the crypts and increased density of gammadelta-T cell receptor-positive intraepithelial lymphocytes than did controls (P = 0.048 and P = 0.010). The densities of alpha(4)beta(7) positive cells in the lamina propria tended to be higher in controls than in uFA or tFA patients (P = 0.106, P = 0.073). Expression of IL-4 mRNA was significantly higher in celiac patients than in the other study groups (uFA P = 0.006, tFA P = 0.010; controls P = 0.029), and celiac patients showed higher expression of IFN-gamma mRNA than did tFA patients or controls (P = 0.017 and P = 0.016). CONCLUSIONS: As expected, Th1 dominance was present in the lamina propria of children with delayed-type FA. It may cause activation of epithelial cells and increase their turnover.},
   keywords = {Adolescent
Biopsy
Cell Adhesion Molecules/*immunology
Child
Child, Preschool
Cytokines/*immunology
Duodenum/*immunology/pathology
Endoscopy
Female
Food Hypersensitivity/*immunology
Humans
Interferon-gamma/immunology
Interleukin-4/immunology
Intestinal Mucosa/*immunology/pathology
Male
RNA, Messenger/immunology
Time Factors},
   ISSN = {0277-2116 (Print)
0277-2116},
   Accession Number = {12827002},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {von Tirpitz, C. and Reinshagen, M.},
   title = {Management of osteoporosis in patients with gastrointestinal diseases},
   journal = {Eur J Gastroenterol Hepatol},
   volume = {15},
   number = {8},
   pages = {869-76},
   note = {von Tirpitz, Christian
Reinshagen, Max
Journal Article
Review
England
Eur J Gastroenterol Hepatol. 2003 Aug;15(8):869-76.},
   abstract = {Osteoporosis is a frequent complication in the course of various gastrointestinal disorders. Since its pathogenesis is complex, and incompletely understood in comparison to the well-known pathomechanism of postmenopausal osteoporosis, adequate management is difficult. We first summarize those therapeutic options which have strong evidence in postmenopausal osteoporosis and, thereafter, we review those in the context of different gastrointestinal diseases. Treatment of the underlying intestinal disorder seems to be most important to normalise altered bone metabolism and to prevent osteoporosis in patients with coeliac disease. In patients with osteoporosis associated with Crohn's disease, various treatment strategies (such as vitamin D, sodium fluoride, bisphosphonates) are discussed. In contrast to postmenopausal osteoporosis, interventional studies in secondary osteoporosis are often limited by the small study population and data about the efficacy of any treatment in prevention of fractures are therefore lacking. Well-conducted, controlled studies with the endpoint of preventing fractures are therefore required to optimise the treatment of osteoporosis in these patients.},
   keywords = {Bone and Bones/drug effects
Calcitonin/administration & dosage
Calcium/administration & dosage
Celiac Disease/complications/drug therapy
Dietary Supplements
Diphosphonates/therapeutic use
Female
Gastrectomy/adverse effects
Gastrointestinal Diseases/*complications
Hormone Replacement Therapy/methods
Humans
Inflammatory Bowel Diseases/complications/drug therapy
Male
Osteoporosis/complications/diet therapy/*drug therapy
Sodium Fluoride/therapeutic use
Vitamin D/administration & dosage},
   ISSN = {0954-691X (Print)
0954-691x},
   Accession Number = {12867796},
   DOI = {10.1097/01.meg.0000059185.46867.8e},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Wittig, B. M. and Zeitz, M.},
   title = {The gut as an organ of immunology},
   journal = {Int J Colorectal Dis},
   volume = {18},
   number = {3},
   pages = {181-7},
   note = {Wittig, B M
Zeitz, M
Journal Article
Review
Germany
Int J Colorectal Dis. 2003 May;18(3):181-7. Epub 2002 Nov 5.},
   abstract = {BACKGROUND: In normal conditions human gut mucosa is infiltrated with a large number of mononuclear cells due to continuous stimulation by luminal antigens. This state of "physiological" inflammation is tightly controlled, as several mucosal cells interact to maintain an appropriate local immune response. Moreover, gut-associated lymphoid tissue must constantly distinguish harmless antigens that are present in food and on commensal bacteria from pathogenic microbes. INTERVENTIONS AND RESEARCH: The oral administration of soluble protein antigens induces a state of systemic immunological unresponsiveness specific to the fed protein, termed oral tolerance. The two major mechanisms to explain oral tolerance are anergy/deletion of autoreactive lymphocytes and active suppression. Changes in the pathways of immune activation are detected in chronic intestinal inflammation, such as inflammatory bowel disease or celiac disease. CONCLUSION: An appreciation of the current knowledge of the gut immune system is of importance for understanding and development of new treatment modalities in chronic intestinal inflammation.},
   keywords = {Adjuvants, Immunologic/therapeutic use
Antigens/administration & dosage/immunology
Cell Differentiation
Cytokines/antagonists & inhibitors/biosynthesis
Dendritic Cells/immunology
Humans
*Immune Tolerance
Intestinal Mucosa/cytology/*immunology
Peyer's Patches/immunology},
   ISSN = {0179-1958 (Print)
0179-1958},
   Accession Number = {12673481},
   DOI = {10.1007/s00384-002-0444-1},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Zhao, Z. and Egashira, Y. and Sanada, H.},
   title = {Ferulic acid is quickly absorbed from rat stomach as the free form and then conjugated mainly in liver},
   journal = {J Nutr},
   volume = {134},
   number = {11},
   pages = {3083-8},
   note = {Zhao, Zhaohui
Egashira, Yukari
Sanada, Hiroo
Journal Article
United States
J Nutr. 2004 Nov;134(11):3083-8.},
   abstract = {Ferulic acid (FA) is one of the most abundant phenolic antioxidants in the human diet. Many studies have documented its beneficial properties. It is therefore essential to understand the absorption and metabolism of FA in detail. The purpose of this study was to confirm the hypothesis that FA is absorbed in rat stomach and metabolized mainly in the liver. We determined the recovery of FA and its metabolites (FA sulfate/glucuronides) in rat gastric contents, gastric mucosa, portal vein plasma, celiac arterial plasma, bile, and urine after 2.25 micromol FA was administered in 0.5 mL physiological saline and incubated for 25 min in situ in the stomach of rats. Within 25 min, 74 +/- 11% of the administered FA disappeared from the stomach; later, FA was recovered in both free and conjugated forms in plasma, bile, and urine. On the other hand, only free FA was detected in the gastric contents and mucosa; it was also detected in the portal vein plasma as 49 +/- 5% of the total FA (all forms of FA). However, the proportion of free FA in the celiac arterial plasma, bile, and urine decreased to 5-8%. These results indicate that FA can be quickly absorbed from the rat stomach, and then is likely metabolized mainly in the liver. Such novel information would be helpful in the use of FA as a nutrient supplement. For example, oral administration of FA in capsule form or in a form bonded with sugar esters may provide a more appropriate concentration of FA in the circulation, which may improve its proposed efficacy in preventing chronic disease.},
   keywords = {Absorption
Animals
Bile/chemistry
Blood
Celiac Artery
Coumaric Acids/analysis/chemistry/*pharmacokinetics
Gastric Mucosa/chemistry/metabolism
Glucuronides/metabolism
Liver/*metabolism
Male
Portal Vein
Rats
Rats, Wistar
Stomach/chemistry/*metabolism
Sulfates/metabolism
Urine/chemistry},
   ISSN = {0022-3166 (Print)
0022-3166},
   Accession Number = {15514279},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Ziegler, A. G. and Schmid, S. and Huber, D. and Hummel, M. and Bonifacio, E.},
   title = {Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies},
   journal = {Jama},
   volume = {290},
   number = {13},
   pages = {1721-8},
   note = {1538-3598
Ziegler, Anette-G
Schmid, Sandra
Huber, Doris
Hummel, Michael
Bonifacio, Ezio
Journal Article
Research Support, Non-U.S. Gov't
United States
JAMA. 2003 Oct 1;290(13):1721-8.},
   abstract = {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.},
   keywords = {Autoantibodies/*blood
Child
Child, Preschool
Cohort Studies
Diabetes Mellitus, Type 1/*epidemiology/genetics/immunology
GTP-Binding Proteins/immunology
Genotype
Glutamate Decarboxylase/immunology
Glutens
HLA Antigens/genetics
Humans
Infant
*Infant Food
Infant Nutritional Physiological Phenomena/*physiology
Infant, Newborn
Insulin Antibodies/blood
Islets of Langerhans/*immunology
Milk, Human
Proportional Hazards Models
Risk Factors
Transglutaminases/immunology},
   ISSN = {0098-7484},
   Accession Number = {14519706},
   DOI = {10.1001/jama.290.13.1721},
   year = {2003},
   type = {Ref–rence Type}
}

@article{
   author = {Zoller, H. and Vogel, W.},
   title = {Iron supplementation in athletes--first do no harm},
   journal = {Nutrition},
   volume = {20},
   number = {7-8},
   pages = {615-9},
   note = {Zoller, Heinz
Vogel, Wolfgang
Journal Article
Research Support, Non-U.S. Gov't
United States
Nutrition. 2004 Jul-Aug;20(7-8):615-9.},
   abstract = {Although it generally does not improve performance, iron is often used by elite athletes. The physiologic changes induced by exercise can mimic iron deficiency and decrease hemoglobin and ferritin concentrations. Determination of serum transferrin receptor concentrations may identify true iron deficiency, which occurs particularly in young athletes. In contrast, increased iron stores in the body are a frequent finding in elite athletes who have used long-term iron supplementation. Elite runners have increased intestinal blood loss, but this usually can be compensated by enhanced absorption of dietary iron. The combination of exercise-induced hemolysis with enhanced intestinal blood loss in various endurance sports leads to severe abnormalities of routine tests, and extreme physical activity may be responsible for positive fecal occult blood determinations. Indiscriminate iron supplementation carries the risk of inducing hemochromatosis in individuals homozygous for the widespread C282Y allele of the HFE gene. This polymorphism is common and can be found in about 1% of individuals of Northern European descent; moreover, iron supplementation can modify the presentation of important underlying diseases such as celiac disease or colon carcinoma. In conclusion, iron supplements should be prescribed for athletes with iron-deficiency anemia and carefully monitored if given for prophylaxis; unless a therapeutic response occurs, investigations to establish the cause of iron deficiency should be initiated.},
   keywords = {Adaptation, Physiological
Dietary Supplements
Exercise/physiology
Ferritins/blood
Hemochromatosis/chemically induced
Hemoglobins/analysis
Humans
Intestinal Absorption
Iron/deficiency
Iron, Dietary/*administration & dosage/adverse effects/pharmacokinetics
Risk Factors
Sports/*physiology},
   ISSN = {0899-9007 (Print)
0899-9007},
   Accession Number = {15212743},
   DOI = {10.1016/j.nut.2004.04.006},
   year = {2004},
   type = {Ref–rence Type}
}

@article{
   author = {Zone, J. J. and Hull, C. M.},
   title = {Warning: bread may be harmful to your health},
   journal = {J Am Acad Dermatol},
   volume = {51},
   number = {1 Suppl},
   pages = {S27-8},
   note = {Zone, John J
Hull, Christopher M
Journal Article
Review
United States
J Am Acad Dermatol. 2004 Jul;51(1 Suppl):S27-8.},
   keywords = {Bread/*adverse effects
Celiac Disease/*complications
Dermatitis Herpetiformis/*etiology/therapy
Humans},
   ISSN = {0190-9622 (Print)
0190-9622},
   Accession Number = {15243499},
   DOI = {10.1016/j.jaad.2004.01.021},
   year = {2004},
   type = {Ref–rence Type}
}

license: MIT

license_type: permissive

branch_name: refs/heads/master

extension: bib