text:
. 2010 Feb;159(2):217-23. doi: 10.1111/j.1365-2249.2009.04054.x. Epub 2009 Nov 12.},
   abstract = {Anti-transglutaminase antibodies are the diagnostic markers of coeliac disease. A role is suggested for infectious agents in the production of anti-transglutaminase antibodies. The aim was to measure positive anti-transglutaminase antibody levels in children with infectious diseases and to compare immunological and biological characteristics of the anti-transglutaminase antibodies derived from these children with that from coeliac patients. Two hundred and twenty-two children suffering from infectious diseases were enrolled prospectively along with seven biopsy-proven coeliacs. Serum samples were tested for anti-transglutaminase antibodies and anti-endomysium antibodies; positive samples were tested for coeliac-related human leucocyte antigen (HLA)-DQ2/8 and anti-viral antibodies. Purified anti-transglutaminase antibodies from the two study groups were tested for urea-dependent avidity, and their ability to induce cytoskeletal rearrangement and to modulate cell-cycle in Caco-2 cells, using phalloidin staining and bromodeoxyuridine incorporation assays, respectively. Nine of 222 children (4%) tested positive to anti-transglutaminase, one of whom also tested positive for anti-endomysium antibodies. This patient was positive for HLA-DQ2 and was diagnosed as coeliac following intestinal biopsy. Of the eight remaining children, two were positive for HLA-DQ8. Levels of anti-transglutaminase returned to normal in all subjects, despite a gluten-containing diet. Purified anti-transglutaminase of the two study groups induced actin rearrangements and cell-cycle progression. During an infectious disease, anti-transglutaminase antibodies can be produced temporarily and independently of gluten. The infection-triggered anti-transglutaminase antibodies have the same biological properties as that of the coeliacs, with the same in-vivo potential for damage.},
   keywords = {Actins/metabolism
Adolescent
Antibodies/pharmacology
Autoantibodies/blood/*immunology
Caco-2 Cells
Celiac Disease/blood/diagnosis/*immunology
Cell Cycle/drug effects
Child
Child, Preschool
Communicable Diseases/blood/diagnosis/*immunology
Cytoskeleton/drug effects/metabolism
Enzyme-Linked Immunosorbent Assay
Female
Humans
Male
Microscopy, Fluorescence
Prospective Studies
Transglutaminases/*immunology},
   ISSN = {0009-9104},
   Accession Number = {19912255},
   DOI = {10.1111/j.1365-2249.2009.04054.x},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Ferrara, P. and Cicala, M. and Tiberi, E. and Spadaccio, C. and Marcella, L. and Gatto, A. and Calzolari, P. and Castellucci, G.},
   title = {High fat consumption in children with celiac disease},
   journal = {Acta Gastroenterol Belg},
   volume = {72},
   number = {3},
   pages = {296-300},
   note = {Ferrara, P
Cicala, M
Tiberi, E
Spadaccio, C
Marcella, L
Gatto, A
Calzolari, P
Castellucci, G
Journal Article
Belgium
Acta Gastroenterol Belg. 2009 Jul-Sep;72(3):296-300.},
   abstract = {AIM: The purpose of this study was to estimate the caloric intake and fat consumption in children with celiac disease (CD) following a gluten-free diet (GFD). PATIENTS AND METHODS: This study enrolled 100 subjects, including 50 children with CD on a gluten-free diet and a control group of 50 healthy children. Statistical analysis to compare groups was performed using one-way ANOVA. RESULTS: A significant increase in fat consumption was observed in children with CD as compared to healthy children. The daily fat intake was 72.5 +/- 37.2 g per 100 g of food in the CD group and 52.9 +/- 35.4 g per 100 g of food in the control group (p < 0.008). A significant difference in fat intake was found between celiac and healthy females (10.21 +/- 3.15 g/100 g in the celiac group vs 7.46 +/- 2.91 g/100 g in the control group), p = 0.004. CONCLUSIONS: This study describes a significantly higher fat consumption in patients with CD on GFD as compared to controls. This increase was more pronounced in females and during the puberal age. Based on these interesting preliminary results we estimate that further investigations are necessary, such as a randomized multicentre study on the long-term effects of GFD with particular attention to the imbalance in daily fat intake.},
   keywords = {Adolescent
Celiac Disease/*diet therapy
Child
*Diet, Gluten-Free
Dietary Fats/*administration & dosage
*Energy Intake
Female
Humans
Male},
   ISSN = {1784-3227 (Print)
1784-3227},
   Accession Number = {19902861},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Festen, E. A. and Szperl, A. M. and Weersma, R. K. and Wijmenga, C. and Wapenaar, M. C.},
   title = {Inflammatory bowel disease and celiac disease: overlaps in the pathology and genetics, and their potential drug targets},
   journal = {Endocr Metab Immune Disord Drug Targets},
   volume = {9},
   number = {2},
   pages = {199-218},
   note = {Festen, Eleonora A M
Szperl, Agata M
Weersma, Rinse K
Wijmenga, Cisca
Wapenaar, Martin C
Journal Article
Research Support, Non-U.S. Gov't
Review
United Arab Emirates
Endocr Metab Immune Disord Drug Targets. 2009 Jun;9(2):199-218.},
   abstract = {Inflammatory bowel disease, which covers Crohn's disease and ulcerative colitis, and celiac disease are both inflammatory diseases of the intestinal tract. In both diseases an antigen activates several inflammatory pathways, which cause extensive damage to the intestinal mucosa and lead to increased permeability of the intestinal epithelium. The causative antigen in inflammatory bowel disease is the microflora in the intestinal lumen, facilitated by an impaired innate immune system that is unable to halt the invasion of microbes into the lamina propria. These provoke T helper 1 and T helper 17 responses in Crohn's disease and a T helper 2 response in ulcerative colitis. Pro-inflammatory cytokines and interleukins produced in these processes lead to impairment of tight junctions and increased permeability of the intestinal epithelial lining. In celiac disease, inflammation is caused by dietary gluten, a peptide present in wheat, barley and rye. In genetically predisposed people, gliadin peptides (derivatives of gluten) are presented on the Human Leukocyte Antigen DQ2 or DQ-8 molecules of antigen-presenting cells to T helper cells. This provokes a T helper 1 response, which leads to the production of pro-inflammatory cytokines and subsequent damage to, and increased permeability of the intestinal epithelium. We describe the details and overlaps in the pathomechanism and genetics of inflammatory bowel disease and celiac disease, and discuss potential drug targets for intervention.},
   keywords = {Celiac Disease/*drug therapy/*genetics/immunology
Humans
Immunity, Innate
Inflammatory Bowel Diseases/*drug therapy/*genetics/immunology
Interleukin-17/physiology
Intestines/metabolism
Nod2 Signaling Adaptor Protein/physiology
Permeability
Th1 Cells/immunology
Th2 Cells/immunology},
   ISSN = {1871-5303 (Print)
1871-5303},
   Accession Number = {19519468},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Filik, L.},
   title = {High-density lipoprotein, apolipoprotein AI concentrations, and celiac disease},
   journal = {J Clin Gastroenterol},
   volume = {44},
   number = {8},
   pages = {592; author reply 592-3},
   note = {1539-2031
Filik, Levent
Comment
Letter
United States
J Clin Gastroenterol. 2010 Sep;44(8):592; author reply 592-3. doi: 10.1097/MCG.0b013e3181d03ed9.},
   keywords = {Apolipoprotein A-I/metabolism
Case-Control Studies
Celiac Disease/*diet therapy/physiopathology
Cholesterol, HDL/*blood
Diet, Gluten-Free
Dietary Supplements
Humans
Patient Selection
*Research Design},
   ISSN = {0192-0790},
   Accession Number = {20142753},
   DOI = {10.1097/MCG.0b013e3181d03ed9},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Fluge, G. and Olesen, H. V. and Gilljam, M. and Meyer, P. and Pressler, T. and Storrosten, O. T. and Karpati, F. and Hjelte, L.},
   title = {Co-morbidity of cystic fibrosis and celiac disease in Scandinavian cystic fibrosis patients},
   journal = {J Cyst Fibros},
   volume = {8},
   number = {3},
   pages = {198-202},
   note = {1873-5010
Fluge, G
Olesen, H V
Gilljam, M
Meyer, P
Pressler, T
Storrosten, O T
Karpati, F
Hjelte, L
Journal Article
Multicenter Study
Netherlands
J Cyst Fibros. 2009 May;8(3):198-202. doi: 10.1016/j.jcf.2009.02.002. Epub 2009 Mar 19.},
   abstract = {BACKGROUND: The co-morbidity of cystic fibrosis (CF) and celiac disease (CD) has been reported sporadically since the 1960s. To our knowledge, this is the first time a systematic screening is performed in a large cohort of CF patients. METHODS: Transglutaminase-IgA (TGA), endomysium-IgA (EMA) and total IgA in serum were measured in 790 CF patients (48% females, 86% with pancreatic insufficiency). Six patients were diagnosed with CD prior to the study, all receiving a gluten-free diet. Patients with elevated TGA (>50 Units/mL) and a positive EMA test were offered a gastroscopy obtaining mucosal biopsies from the duodenum. RESULTS: Four new cases of CD were diagnosed. Two additional patients had positive serological tests, but normal biopsies. In total, 10 cases of CD (1.2%, 1:83) indicate a prevalence rate about three times higher than the general prevalence of CD in Norway and Sweden. No CD patients were detected in the Danish CF cohort. Patients diagnosed with untreated CD reported symptoms typical of both CF and CD (poor weight gain, loose and/or fatty stools, fatigue, irritability, abdominal pain). They improved after introduction of a gluten-free diet. CONCLUSIONS: Systematic screening for CD in a Scandinavian cohort of CF patients revealed a higher prevalence of CD than in the general population. Clinical signs of CD are difficult to differentiate from CF with malabsorption, and patients may go undiagnosed for a long time. In a population where CD is common we recommend screening for CD in patients with CF.},
   keywords = {Adolescent
Adult
Celiac Disease/blood/*epidemiology
Child
Child, Preschool
Comorbidity
Cross-Sectional Studies
Cystic Fibrosis/blood/*epidemiology
Female
Humans
Immunoglobulin A/blood
Infant
Male
Middle Aged
Prevalence
Scandinavian and Nordic Countries/epidemiology
Young Adult},
   ISSN = {1569-1993},
   Accession Number = {19303374},
   DOI = {10.1016/j.jcf.2009.02.002},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J.},
   title = {Adult celiac disease and its malignant complications},
   journal = {Gut Liver},
   volume = {3},
   number = {4},
   pages = {237-46},
   note = {2005-1212
Freeman, Hugh J
Journal Article
Korea (South)
Gut Liver. 2009 Dec;3(4):237-46. doi: 10.5009/gnl.2009.3.4.237. Epub 2009 Dec 31.},
   abstract = {Adult celiac disease is a chronic intestinal disorder that has been estimated to affect up to 1-2% of the population in some nations. Awareness of the disease has increased, but still it remains markedly underdiagnosed. Celiac disease is a pathologically defined condition with several characteristic clinical scenarios that should lead the clinician to suspect its presence. Critical to diagnosis is a documented responsiveness to a gluten-free diet. After diagnosis and treatment, symptoms and biopsy-proven changes may recur and appear refractory to a gluten-free diet. Recurrent symptoms are most often due to poor diet compliance, a ubiquitous and unrecognized gluten source, an initially incorrect diagnosis, or an associated disease or complication of celiac disease. Some patients with persistent symptoms and biopsy-proven changes may not have celiac disease at all, instead suffering from a sprue-like intestinal disease, so-called unclassified sprue, which is a specific entity that does not appear to respond to a gluten-free diet. Some of these patients eventually prove to have an underlying malignant cause, particularly lymphoma. The risk of developing lymphoma and other malignancies is increased in celiac disease, especially if initially diagnosed in the elderly, or late in the clinical course of the disease. However, recent studies suggest that the risk of gastric and colon cancer is low. This has led to the hypothesis that untreated celiac disease may be protective, possibly due to impaired absorption and more rapid excretion of fat or fat-soluble agents, including hydrocarbons and other putative cocarcinogens, which are implicated in the pathogenesis of colorectal cancer.},
   keywords = {Adult celiac disease
Colonic neoplasms
Lymphoma
Malignancy in celiac disease
Small intestinal cancer},
   ISSN = {1976-2283},
   Accession Number = {20431755},
   DOI = {10.5009/gnl.2009.3.4.237},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J.},
   title = {Selected luminal mucosal complications of adult celiac disease},
   journal = {Clin Exp Gastroenterol},
   volume = {2},
   pages = {9-12},
   note = {Freeman, Hugh J
Journal Article
New Zealand
Clin Exp Gastroenterol. 2009;2:9-12. Epub 2009 Feb 4.},
   abstract = {Celiac disease is a gluten-dependent intestinal disorder that appears to be associated with several clinical conditions. Some involve the luminal mucosa of the stomach and intestinal tract and may, occasionally, complicate the course of celiac disease. Collagenous colitis has been associated with celiac disease and may lead to chronic diarrhea. Conversely, some of these clinical disorders that involve the luminal mucosa of the stomach and intestine may represent the initial clinical presentation of celiac disease. These disorders should be considered in patients with celiac disease who develop recurrent or refractory symptoms despite adherence to a strict gluten-free diet. Detection of collagenous disorders that affect the luminal mucosa of the stomach or intestinal tract may result in recognition of underlying celiac disease.},
   keywords = {celiac disease
collagenous colitis
collagenous gastritis
collagenous sprue
gluten-free diet},
   ISSN = {1178-7023 (Print)
1178-7023},
   Accession Number = {21694821},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J.},
   title = {Celiac disease (gluten-sensitive enteropathy)},
   journal = {Minerva Gastroenterol Dietol},
   volume = {56},
   number = {2},
   pages = {245-9},
   note = {Freeman, H J
Journal Article
Italy
Minerva Gastroenterol Dietol. 2010 Jun;56(2):245-9.},
   abstract = {Celiac disease may be initially detected in either children or adults, even in the elderly. This small intestinal mucosal disorder is gluten-dependent and causes nutrient malabsorption, often with diarrhea and weight loss. Diagnosis depends on detection of typical biopsy changes in the proximal small bowel along with an unequivocal response to a gluten-free diet. Recurrent changes usually result from poor adherence to the gluten-free diet, sometimes intentional, or from consumption of unsuspected gluten sources. In others, the original diagnosis may not be correct (e.g., duodenal involvement with Crohn's disease) or another cause for symptoms may have supervened (e.g., collagenous colitis, functional bowel disease). Rarely, a complication may occur (e.g., collagenous sprue, lymphoma). In some, the gluten-dependent nature of the small bowel disorder was not initially documented and biopsy changes continued despite a gluten-free diet. These have a sprue-like intestinal disorder, also labeled unclassified sprue. This represents a small, but likely, heterogeneous group, and in these, intractable symptoms may be present and, in some, lymphoma is eventually diagnosed.},
   keywords = {Biopsy
Celiac Disease/*diagnosis/*diet therapy
Diet, Gluten-Free
Humans
Intestine, Small/*pathology
Treatment Outcome},
   ISSN = {1121-421X (Print)
1121-421x},
   Accession Number = {20485260},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J.},
   title = {Hepatic manifestations of celiac disease},
   journal = {Clin Exp Gastroenterol},
   volume = {3},
   pages = {33-9},
   note = {1178-7023
Freeman, Hugh James
Journal Article
New Zealand
Clin Exp Gastroenterol. 2010;3:33-9. Epub 2010 May 3.},
   abstract = {Different hepatic and biliary tract disorders may occur with celiac disease. Some have been hypothesized to share genetic or immunopathogenetic factors, such as primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis. Other hepatic changes in celiac disease may occur with malnutrition resulting from impaired nutrient absorption, including hepatic steatosis. In addition, celiac disease may be associated with rare hepatic complications, such as hepatic T-cell lymphoma.},
   keywords = {autoimmune liver disease
celiac disease
fatty liver
gluten-free diet
primary biliary cirrhosis},
   ISSN = {1178-7023},
   Accession Number = {21694844},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J.},
   title = {Mesenteric lymph node cavitation syndrome},
   journal = {World J Gastroenterol},
   volume = {16},
   number = {24},
   pages = {2991-3},
   note = {2219-2840
Freeman, Hugh James
Journal Article
United States
World J Gastroenterol. 2010 Jun 28;16(24):2991-3.},
   abstract = {The mesenteric lymph node cavitation syndrome consists of central necrosis of mesenteric lymph nodes and may occur with either celiac disease or a sprue-like intestinal disease that fails to respond to a gluten-free diet. Splenic hypofunction may also be present. The cause is not known but its development during the clinical course of celiac disease is usually indicative of a poor prognosis for the intestinal disorder, a potential for significant complications including sepsis and malignancy, particularly T-cell lymphoma, and significant mortality. Modern abdominal imaging modalities may permit earlier detection in celiac disease so that earlier diagnosis and improved understanding of its pathogenesis may result.},
   keywords = {Celiac Disease/*complications/diet therapy/pathology
Diet, Gluten-Free
Humans
Lymph Nodes/*pathology
Mesentery/*anatomy & histology
*Necrosis/etiology/pathology
Syndrome},
   ISSN = {1007-9327},
   Accession Number = {20572301},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J.},
   title = {Reproductive changes associated with celiac disease},
   journal = {World J Gastroenterol},
   volume = {16},
   number = {46},
   pages = {5810-4},
   note = {2219-2840
Freeman, Hugh-James
Journal Article
United States
World J Gastroenterol. 2010 Dec 14;16(46):5810-4.},
   abstract = {Celiac disease is a mucosal disorder of the small intestine that may be triggered by dietary exposure to gluten in genetically-susceptible individuals. The disorder is often associated with diarrhea, malabsorption and weight loss along with other extra-intestinal complications. Reproductive changes have been described, including impaired fertility and adverse pregnancy outcomes possibly related to immune-mediated mechanisms or nutrient deficiency. Other possible pathogenetic factors that may alter placental function include maternal celiac disease autoantibodies binding to placental transglutaminase, and genetic mutations that may facilitate microthrombus formation. Reports noting activation during pregnancy or the puerperium may be important, and suggest that celiac disease may also be hypothetically precipitated by maternal exposure to one or more fetal antigens.},
   keywords = {Celiac Disease/*complications
Female
Fertility
Humans
Male
Pregnancy
Pregnancy Complications/*etiology
*Pregnancy Outcome
*Reproduction},
   ISSN = {1007-9327},
   Accession Number = {21155001},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J.},
   title = {Update on collagenous sprue},
   journal = {World J Gastroenterol},
   volume = {16},
   number = {3},
   pages = {296-8},
   note = {2219-2840
Freeman, Hugh James
Journal Article
United States
World J Gastroenterol. 2010 Jan 21;16(3):296-8.},
   abstract = {Collagenous sprue has traditionally been defined as a small intestinal mucosal disorder characterized by persistent diarrhea, severe malabsorption with multiple nutrient deficiencies and progressive weight loss. Pathologically, a severe to variably severe "flattened" mucosal biopsy lesion with distinctive sub-epithelial deposits in the lamina propria region is detected. Histochemical stains and ultrastructural studies have confirmed that these deposits contain collagens. Often, an initial diagnosis of celiac disease is considered but no continued response to treatment with a gluten-free diet occurs. Recent reports indicate an intimate relationship between collagenous sprue and celiac disease, sometimes with concomitant T-cell enteropathy. In addition, permanent disappearance of these deposits after resection of a localized colon cancer suggested that this disorder could actually represent a paraneoplastic morphologic marker of an occult malignancy. Studies showing either gastric or colonic involvement (or both) with this unusual collagenous inflammatory mucosal process may also reflect a far more extensive and heterogeneous process than previously appreciated.},
   keywords = {*Celiac Disease/drug therapy/metabolism/pathology
Collagen/metabolism
Humans
Immunosuppressive Agents/therapeutic use
Steroids/therapeutic use},
   ISSN = {1007-9327},
   Accession Number = {20082473},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J. and Gillett, H. R. and Gillett, P. M. and Oger, J.},
   title = {Adult celiac disease with acetylcholine receptor antibody positive myasthenia gravis},
   journal = {World J Gastroenterol},
   volume = {15},
   number = {38},
   pages = {4741-4},
   note = {2219-2840
Freeman, Hugh J
Gillett, Helen R
Gillett, Peter M
Oger, Joel
Case Reports
Journal Article
United States
World J Gastroenterol. 2009 Oct 14;15(38):4741-4.},
   abstract = {Celiac disease has been associated with some autoimmune disorders. A 40-year-old competitive strongman with celiac disease responded to a gluten-free diet, but developed profound and generalized motor weakness with acetylcholine receptor antibody positive myasthenia gravis, a disorder reported to occur in about 1 in 5000. This possible relationship between myasthenia gravis and celiac disease was further explored in serological studies. Frozen stored serum samples from 23 acetylcholine receptor antibody positive myasthenia gravis patients with no intestinal symptoms were used to screen for celiac disease. Both endomysial and tissue transglutaminase antibodies were examined. One of 23 (or, about 4.3%) was positive for both IgA-endomysial and IgA tissue transglutaminase antibodies. Endoscopic studies subsequently showed duodenal mucosal scalloping and biopsies confirmed the histopathological changes of celiac disease. Celiac disease and myasthenia gravis may occur together more often than is currently appreciated. The presence of motor weakness in celiac disease may be a clue to occult myasthenia gravis, even in the absence of intestinal symptoms.},
   keywords = {Adult
Antibodies/chemistry
Biopsy
Celiac Disease/complications/*immunology
Humans
Immunoglobulin A/metabolism
Male
Myasthenia Gravis/complications/*immunology
Nervous System Diseases/diagnosis
Receptors, Cholinergic/chemistry/*immunology
Treatment Outcome},
   ISSN = {1007-9327},
   Accession Number = {19824105},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Freeman, H. J. and Webber, D. L.},
   title = {Free perforation of the small intestine in collagenous sprue},
   journal = {World J Gastroenterol},
   volume = {15},
   number = {35},
   pages = {4446-8},
   note = {2219-2840
Freeman, Hugh J
Webber, Douglas L
Case Reports
Journal Article
United States
World J Gastroenterol. 2009 Sep 21;15(35):4446-8.},
   abstract = {A 67-year-old man with celiac disease developed recurrent diarrhea, profound weakness and weight loss, with evidence of marked protein depletion. His clinical course was refractory to a strict gluten-free diet and steroid therapy. Postmortem studies led to definition of unrecognized collagenous sprue that caused ulceration and small intestinal perforation. Although PCR showed identical monoclonal T-cell populations in antemortem duodenal biopsies and postmortem jejunum, careful pathological evaluation demonstrated no frank lymphoma. Rarely, overt or even cryptic T-cell lymphoma may complicate collagenous sprue, however, small intestinal ulcers and perforation may also develop independently. The dramatic findings here may reflect an underlying or early molecular event in the eventual clinical appearance of overt T-cell lymphoma.},
   keywords = {Aged
Celiac Disease/*complications/diet therapy/pathology
Diagnosis, Differential
Diarrhea/complications/pathology
Diet, Gluten-Free
Fatal Outcome
Humans
Intestinal Mucosa/*pathology
Intestinal Perforation/*etiology/pathology
Male
Weight Loss},
   ISSN = {1007-9327},
   Accession Number = {19764099},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Freitag, T. L. and Rietdijk, S. and Junker, Y. and Popov, Y. and Bhan, A. K. and Kelly, C. P. and Terhorst, C. and Schuppan, D.},
   title = {Gliadin-primed CD4+CD45RBlowCD25- T cells drive gluten-dependent small intestinal damage after adoptive transfer into lymphopenic mice},
   journal = {Gut},
   volume = {58},
   number = {12},
   pages = {1597-605},
   note = {1468-3288
Freitag, T L
Rietdijk, S
Junker, Y
Popov, Y
Bhan, A K
Kelly, C P
Terhorst, C
Schuppan, D
P30 DK040561/DK/NIDDK NIH HHS/United States
P30 DK043351/DK/NIDDK NIH HHS/United States
R21 DK073254/DK/NIDDK NIH HHS/United States
P30 DK040561-14/DK/NIDDK NIH HHS/United States
1 R21 DKO73254-01/PHS HHS/United States
Journal Article
Research Support, N.I.H., Extramural
England
Gut. 2009 Dec;58(12):1597-605. doi: 10.1136/gut.2009.186361. Epub 2009 Aug 10.},
   abstract = {BACKGROUND AND AIMS: Coeliac disease is a common small intestinal inflammatory disorder that results from a breach of intestinal tolerance to dietary gluten proteins, driven by gluten-reactive effector T cells. We aimed to assess the pathogenic role of gluten-reactive T cells and to generate a model of gluten-induced enteropathy. METHODS: CD4+CD25- T cell fractions were adoptively transferred into lymphopenic mice, leading to "baseline" small intestinal inflammation. RESULTS: Rag1-/- recipients of gliadin-presensitised CD4+CD45RBlowCD25- T cells, but not CD4+CD45RBhigh naive T cells, gained less weight and suffered from more severe duodenitis when challenged with oral gluten than recipients on gluten-free diet, or recipients of control (ovalbumin)-presensitised T cells. This was accompanied by deterioration of mucosal histological features characteristic of coeliac disease, and increased Th1/Th17 cell polarisation in the duodenum and the periphery. Interestingly, reintroduction of a gluten-free diet led to weight gain, improvement of histological duodenitis, and a decrease in duodenal interferon gamma and interleukin 17 transcripts. Moreover, B cell-competent nude recipients of gliadin-presensitised CD4+CD45RBlowCD25- T cells produced high levels of serum anti-gliadin immunoglobulin A (IgA) and IgG1/IgG2c only when challenged with oral gluten. CONCLUSIONS: CD4+ T cell immunity to gluten leads to a breach of oral gluten tolerance and small intestinal pathology in lymphopenic mice, similar to human coeliac disease. This model will be useful for the study of coeliac disease pathogenesis, and also for testing novel non-dietary therapies for coeliac disease.},
   keywords = {Adoptive Transfer
Animals
Antigens, CD45/analysis
CD4-Positive T-Lymphocytes/*immunology
Celiac Disease/*immunology/pathology
Diet, Gluten-Free
Disease Models, Animal
Duodenitis/immunology/pathology
Gliadin/*immunology
Glutens/immunology
Immune Tolerance
Immunoglobulin A/biosynthesis
Immunoglobulin G/biosynthesis
Interleukin-2 Receptor alpha Subunit/analysis
Lymphopenia/*immunology
Male
Mice
Mice, Inbred C57BL
Mice, Nude
T-Lymphocyte Subsets/immunology
Th1 Cells/immunology
Weight Gain},
   ISSN = {0017-5749},
   Accession Number = {19671544},
   DOI = {10.1136/gut.2009.186361},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Frisullo, G. and Nociti, V. and Iorio, R. and Patanella, A. K. and Marti, A. and Assunta, B. and Plantone, D. and Cammarota, G. and Tonali, P. A. and Batocchi, A. P.},
   title = {Increased CD4+CD25+Foxp3+ T cells in peripheral blood of celiac disease patients: correlation with dietary treatment},
   journal = {Hum Immunol},
   volume = {70},
   number = {6},
   pages = {430-5},
   note = {1879-1166
Frisullo, Giovanni
Nociti, Viviana
Iorio, Raffaele
Patanella, Agata Katia
Marti, Alessandro
Assunta, Bianco
Plantone, Domenico
Cammarota, Giovanni
Tonali, Pietro Attilio
Batocchi, Anna Paola
Journal Article
United States
Hum Immunol. 2009 Jun;70(6):430-5. doi: 10.1016/j.humimm.2009.04.006. Epub 2009 Apr 11.},
   abstract = {Regulatory CD4+ CD25+Foxp3+ T cells are involved in the regulation of immune response and inhibit protective antitumor immunity. Celiac disease (CD), a food gluten-sensitive enteropathy, is considered a T-cell-mediated autoimmune disease and is generally associated with an overall increased risk of cancer in CD patients. We observed a higher percentage of circulating CD4+CD25+Foxp3+ T cells and an increased Foxp3 expression in CD4+CD25+ T cells from untreated than from treated CD patients. In co-culture, CD4+CD25+ T cells from both treated and untreated CD patients significantly suppressed the proliferation of autologous CD4+CD25(-) T cells similarly to values in healthy subjects. Our study suggests that Treg proportion and Foxp3 expression in circulating CD4+CD25+ T cells could justify the increased global risk of malignancy in CD population and support the efficacy of lifelong gluten-free diet in the reduction of the cancer risk.},
   keywords = {Adolescent
Adult
Antigens, CD4/*blood/immunology
CD4-Positive T-Lymphocytes/immunology/pathology
Celiac Disease/*diet therapy/immunology/pathology
Cell Proliferation
Cells, Cultured
*Diet, Gluten-Free
Female
Forkhead Transcription Factors/*blood/immunology
Humans
Interleukin-2 Receptor alpha Subunit/*blood/immunology
Longitudinal Studies
Male
Middle Aged
T-Lymphocytes/*immunology/pathology
T-Lymphocytes, Regulatory/immunology/pathology
Young Adult},
   ISSN = {0198-8859},
   Accession Number = {19364517},
   DOI = {10.1016/j.humimm.2009.04.006},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Frisullo, G. and Nociti, V. and Iorio, R. and Patanella, A. K. and Plantone, D. and Bianco, A. and Marti, A. and Cammarota, G. and Tonali, P. A. and Batocchi, A. P.},
   title = {T-bet and pSTAT-1 expression in PBMC from coeliac disease patients: new markers of disease activity},
   journal = {Clin Exp Immunol},
   volume = {158},
   number = {1},
   pages = {106-14},
   note = {1365-2249
Frisullo, G
Nociti, V
Iorio, R
Patanella, A K
Plantone, D
Bianco, A
Marti, A
Cammarota, G
Tonali, P A
Batocchi, A P
Comparative Study
Journal Article
England
Clin Exp Immunol. 2009 Oct;158(1):106-14. doi: 10.1111/j.1365-2249.2009.03999.x.},
   abstract = {Coeliac disease (CD) is considered a T cell-mediated autoimmune disease, and up-regulation of T-bet and phosphorylated signal transducers and activators of transcription (pSTAT)1, key transcription factors for the development of T helper type 1 (Th1) cells, has been described in the mucosa of patients with untreated CD. Using transcription factor analysis, we investigated whether T-bet and pSTAT1 expressions are up-regulated in the peripheral blood of CD patients and correlate with disease activity. Using flow cytometry, we analysed T-bet, pSTAT1 and pSTAT3 expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes from peripheral blood of 15 untreated and 15 treated CD patients and 30 controls, and longitudinally in five coeliac patients before and after dietary treatment. We evaluated using enzyme-linked immunosorbent assay (ELISA), interferon (FN)-gamma, interleukin (IL)-17 and IL-10 production by peripheral blood mononuclear cell (PBMC) cultures. T-bet expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes and IFN-gamma production by PBMC was higher in untreated than in treated CD patients and controls. pSTAT1 expression was higher in CD4(+)T cells, B cells and monocytes from untreated than from treated CD patients and controls. pSTAT3 was increased only in monocytes from untreated patients compared with CD-treated patients and controls. The data obtained from the longitudinal evaluation of transcription factors confirmed these results. Flow cytometric analysis of pSTAT1 and T-bet protein expression in peripheral blood mononuclear cells could be useful and sensible markers in the follow-up of CD patients to evaluate disease activity and response to dietary treatment.},
   keywords = {Acute Disease
Adult
Analysis of Variance
Antigens, CD19/immunology
B-Lymphocytes/immunology/metabolism
Biomarkers/blood
CD4-Positive T-Lymphocytes/metabolism
CD8-Positive T-Lymphocytes/metabolism
Case-Control Studies
Celiac Disease/*blood/diet therapy
Diet, Gluten-Free
Female
Flow Cytometry/methods
Humans
Interferon-gamma/analysis
Interleukin-10/analysis
Interleukin-17/analysis
Leukocytes, Mononuclear/*metabolism
Male
Middle Aged
STAT1 Transcription Factor/*analysis
STAT3 Transcription Factor/blood
T-Box Domain Proteins/*analysis},
   ISSN = {0009-9104},
   Accession Number = {19737237},
   DOI = {10.1111/j.1365-2249.2009.03999.x},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Fundia, A. F. and Larripa, I. and Slavutsky, I.},
   title = {[Genetic alterations, genomic instability and cancer in celiac disease]},
   journal = {Acta Gastroenterol Latinoam},
   volume = {39},
   number = {1},
   pages = {55-62},
   note = {Fundia, Ariela F
Larripa, Irene
Slavutsky, Irma
English Abstract
Journal Article
Review
Argentina
Acta Gastroenterol Latinoam. 2009 Mar;39(1):55-62.},
   abstract = {Celiac disease (CD) is a common autoimmune disorder characterized by intestinal inflammation and mucosal atrophy triggered by dietary gluten in genetically predisposed individuals. Although, most patients improve with a gluten-free diet, a small percentage (2-5%) develops refractoriness or pre- and malignant complications. Malignancies are the most serious complications of CD, including gastrointestinal carcinomas and non-Hodgkin lymphoma, particularly Enteropathy-type T-cell lymphoma, a rare high-grade T-cell non-Hodgkin lymphoma of the small intestine, almost exclusively observed in CD patients. The molecular basis behind cancer development in CD is not known. To really understand CD-cancer biology it is important to known all of its genetic and genomic alterations. Carcinogenesis involves the acquisition of multiple genetic changes that create a background of genetic instability which accelerate the accumulation of subsequent mutations. Two major modes of genome destabilization have been recognized: microsatellite instability and chromosome instability (CIN). A review of genetic abnormalities reported in CD, refractory sprue or CD-associated tumors, suggests that a CIN phenotype is implied in malignant transformation in CD. Moreover, our recent findings showing that a group of untreated CD patients exhibits genomic instability at nucleotide level, affecting specific microsatellite loci, provides evidence of molecular alterations in non-malignant CD cells. In conclusion, most genetic studies, point to the role of chronic inflammation in the induction of genomic instability and malignant emergence in at-risk individuals.},
   keywords = {Autoimmune Diseases/*complications/genetics
Celiac Disease/*complications/diet therapy/genetics
Diet, Gluten-Free
Genetic Predisposition to Disease
*Genomic Instability
Humans
Neoplasms/*genetics},
   ISSN = {0300-9033 (Print)
0300-9033},
   Accession Number = {19408741},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Galicka-Latala, D. and Zwolinska-Wcislo, M. and Sosin-Rudnicka, L. and Rozpondek, P.},
   title = {[The role of celiac disease and type 1 diabetes coexistance. Is celiac disease responsible for diabetic status?]},
   journal = {Przegl Lek},
   volume = {66},
   number = {4},
   pages = {170-5},
   note = {Galicka-Latala, Danuta
Zwolinska-Wcislo, Malgorzata
Sosin-Rudnicka, Lucyna
Rozpondek, Piotr
English Abstract
Journal Article
Poland
Przegl Lek. 2009;66(4):170-5.},
   abstract = {Celiac disease is the status of the autoimmune answer provoked by gluten ingestion in genetically predisposed people. Recently gluten entheropathy was considered as a rare clinical problem in adults. Celiac disease is an autoimmune disorder that can coexist with other diseases, such as diabetes mellitus type 1 (DMID), thyroid gland diseases. The aim of our study was evaluation of the frequency of coexistence of celiac disease with DMID using the level of anti tissue transglutaminase antibodies (IgA- tTG) and mucosal biopsy from the distal part of the duodenum. An attempt was made to estimate the influence of celiac disease on the intensity of clinical symptoms and metabolic balance in patients with DMID. Our study included 109 patients with DMID, aged 18-52 years. The frequency of the incidence of celiac disease in DMID patients was 9.71%. Gastric symptoms, such as diarrhea, abdominal pain were more frequent in patients with villous atrophy in the intestine. Hyperglycemia and problems with glucose balance in the serum were observed. Introduction of the gluten free diet led to improvement quality of life, less frequent hypoglycemic episodes and disappearance of diarrhea, increase of serum iron and decrease of IgA-tTG level in the serum. It is necessary to measure the level of IgA- tTG in patients with DMID. Diagnosis of celiac disease in patients with DMID and its treatment with gluten free diet causes the clinical, histological and biochemical improvement in these patients.},
   keywords = {Adolescent
Adult
Causality
Celiac Disease/diet therapy/*epidemiology
Child
Comorbidity
Diabetes Mellitus, Type 1/*epidemiology
Diet, Gluten-Free
Female
Humans
Immunoglobulin A/metabolism
Male
Middle Aged
Transglutaminases/immunology
Young Adult},
   ISSN = {0033-2240 (Print)
0033-2240},
   Accession Number = {19708505},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Galvan, J. A. and Lemos, G. and Fernandez de Cossio, M. E. and Ruenes, C. and Martinez, Y. and Tejeda, Y. and Roca, J. and Palenzuela, D. O. and Novoa, L. I. and Nazabal, M.},
   title = {Silent celiac disease in a cohort of healthy adults},
   journal = {Autoimmunity},
   volume = {42},
   number = {8},
   pages = {705-8},
   note = {1607-842x
Galvan, Jose A
Lemos, Gilda
Fernandez de Cossio, Maria E
Ruenes, Caridad
Martinez, Yadina
Tejeda, Yelaine
Roca, Juan
Palenzuela, Daniel O
Novoa, Lidia I
Nazabal, Marcelo
Journal Article
England
Autoimmunity. 2009;42(8):705-8. doi: 10.3109/08916930903214009.},
   abstract = {BACKGROUND: Recent studies suggest that celiac disease (CD) is common in many developing countries. Because the disease may be under diagnosed in Cuba, we studied the presence of the disease in a group of apparently healthy adult. AIMS/HYPOTHESIS: It was to assess for the first time, the presence of silent CD in a cohort of healthy Cuban adults individuals and to evaluate the tools for diagnosis of CD in this group. METHODS: A total of 200 healthy Cuban adult from Havana City were evaluated. Tissue transglutaminase antibodies (tTGA) were determined by one-step immunochromatographic assay and by commercial ELISA kit. CD specific human leukocyte antigen (HLA) typing was performed by polymerase chain reaction amplification, using sequence-specific primers. In the subject positive for tTGA, the CD was confirmed by intestinal biopsy. RESULTS: From the 200 studied individuals, only one subject was identified as positive by both assays, being submitted to duodenal biopsy. Morphological changes consistent with CD were found and also supported by HLA-DQ2 (HLA-DQA1*0501-DQB1*02). In the follow-up after one year, histological recovery was assessed by a second intestinal biopsy and the serological marker became negative. CONCLUSIONS: This study confirms the existence of silent CD among healthy adult in Cuba and highlights the importance of mass screening for this disease among them. The one-step immunochromatographic assay is a good tool for this purpose.},
   keywords = {Adolescent
Adult
Aged
Antibodies/blood/immunology
Celiac Disease/*diagnosis/diet therapy/*epidemiology/immunology
Cohort Studies
Cuba/epidemiology
Diet, Gluten-Free
Duodenum/pathology
Female
GTP-Binding Proteins/immunology
HLA-DQ Antigens/immunology
HLA-DQ alpha-Chains
HLA-DQ beta-Chains
*Health
Humans
Immunoglobulin A/blood/immunology
Male
Middle Aged
Transglutaminases/immunology
Young Adult},
   ISSN = {0891-6934},
   Accession Number = {19886741},
   DOI = {10.3109/08916930903214009},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Garrido, A. and Luque, A. and Vazquez, A. and Hernandez, J. M. and Alcantara, F. and Marquez, J. L.},
   title = {[Primary small bowel neoplasms as a complication of celiac disease]},
   journal = {Gastroenterol Hepatol},
   volume = {32},
   number = {9},
   pages = {618-21},
   note = {Garrido, Antonio
Luque, Angel
Vazquez, Antonio
Hernandez, Jose Maria
Alcantara, Federico
Marquez, Jose Luis
Case Reports
English Abstract
Journal Article
Spain
Gastroenterol Hepatol. 2009 Nov;32(9):618-21. doi: 10.1016/j.gastrohep.2009.05.003. Epub 2009 Jul 21.},
   abstract = {Celiac disease is produced by gluten intake in genetically susceptible children and adults and is the most common severe food intolerance in western countries. Eliminating gluten from the diet is essential in these patients, since most of the complications that can occur are more frequent if there is lack of treatment adherence. The most serious complication in these patients is the development of neoplasms, the most frequent being enteropathy-associated T-cell lymphoma; however, an increase in the incidence of small bowel adenocarcinoma has also been described. We present two cases of small bowel carcinoma in patients with celiac disease, which were diagnosed at the onset of the disease.},
   keywords = {Adenocarcinoma/*etiology
Aged
Celiac Disease/*complications
Duodenal Neoplasms/*etiology
Female
Humans
Ileal Neoplasms/*etiology
Middle Aged},
   ISSN = {0210-5705 (Print)
0210-5705},
   Accession Number = {19625106},
   DOI = {10.1016/j.gastrohep.2009.05.003},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Genuis, S. J. and Bouchard, T. P.},
   title = {Celiac disease presenting as autism},
   journal = {J Child Neurol},
   volume = {25},
   number = {1},
   pages = {114-9},
   note = {1708-8283
Genuis, Stephen J
Bouchard, Thomas P
Case Reports
Journal Article
United States
J Child Neurol. 2010 Jan;25(1):114-9. doi: 10.1177/0883073809336127. Epub 2009 Jun 29.},
   abstract = {Gluten-restricted diets have become increasingly popular among parents seeking treatment for children diagnosed with autism. Some of the reported response to celiac diets in children with autism may be related to amelioration of nutritional deficiency resulting from undiagnosed gluten sensitivity and consequent malabsorption. A case is presented of a 5-year-old boy diagnosed with severe autism at a specialty clinic for autistic spectrum disorders. After initial investigation suggested underlying celiac disease and varied nutrient deficiencies, a gluten-free diet was instituted along with dietary and supplemental measures to secure nutritional sufficiency. The patient's gastrointestinal symptoms rapidly resolved, and signs and symptoms suggestive of autism progressively abated. This case is an example of a common malabsorption syndrome associated with central nervous system dysfunction and suggests that in some contexts, nutritional deficiency may be a determinant of developmental delay. It is recommended that all children with neurodevelopmental problems be assessed for nutritional deficiency and malabsorption syndromes.},
   keywords = {Autistic Disorder/*diagnosis
Celiac Disease/*diagnosis/diet therapy
Child, Preschool
Diagnosis, Differential
Humans
Male
Treatment Outcome},
   ISSN = {0883-0738},
   Accession Number = {19564647},
   DOI = {10.1177/0883073809336127},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Gessendorfer, B. and Koehler, P. and Wieser, H.},
   title = {Preparation and characterization of enzymatically hydrolyzed prolamins from wheat, rye, and barley as references for the immunochemical quantitation of partially hydrolyzed gluten},
   journal = {Anal Bioanal Chem},
   volume = {395},
   number = {6},
   pages = {1721-8},
   note = {1618-2650
Gessendorfer, Benedict
Koehler, Peter
Wieser, Herbert
Journal Article
Research Support, Non-U.S. Gov't
Germany
Anal Bioanal Chem. 2009 Nov;395(6):1721-8. doi: 10.1007/s00216-009-3080-6.},
   abstract = {Celiac disease (CD) is a permanent gastrointestinal disorder characterized by the intolerance to a group of proteins called gluten present in wheat, rye, barley, and possibly oats. The only therapy is a strict lifelong gluten-free diet. The standard method for gluten determination in foods produced for CD patients is the R5-enzyme-linked immunosorbent assay (ELISA) as proposed by the recent Codex Alimentarius Draft Revised Standard. This test is based on the determination of prolamins, the alcohol-soluble proteins of gluten, and is available as a sandwich ELISA for intact proteins and as a competitive ELISA for gluten-derived peptides. While the suitability of the sandwich ELISA including a wheat prolamin (gliadin) reference for calibration has been shown by various studies and a ring test, the competitive ELISA still lacks a convenient reference for the quantitation of gluten peptides in fermented cereal foods (e.g., sourdough products, starch syrup, malt extracts, beer). Therefore, the aim of the present study was to prepare a suitable reference for the quantitation of partially hydrolyzed gluten in fermented wheat, rye, and barley products. The prolamin fractions from barley (hordein) and rye (secalin) were isolated from corresponding flours by means of a modified preparative Osborne fractionation. The prolamin fraction from wheat was obtained as reference gliadin from the Prolamin Working Group. The prolamin fractions were successively digested by pepsin and trypsin or pepsin and chymotrypsin procedures, which have been used for CD-specific toxicity tests on cereal storage proteins for many years. The protein/peptide content (N x 5.7) of the prolamin fractions and digests, which was the basis for the calculation of the gluten content by means of ELISA, varied between 67.1% and 96.0%. The prolamin fractions and enzymatic digests were then tested for their response in both sandwich and competitive assays. Intact prolamins responded similarly in both ELISA showing no important differences between the cereals. In the case of digested proteins, however, the sandwich ELISA was considerably less sensitive than the competitive ELISA. The former provided approximately 40% and the latter 70% of the signal intensity obtained with the intact prolamins. Thus, the combination of the competitive ELISA and the enzymatic digests of prolamin fractions as reference was considered to be an adequate system for the analysis of partially hydrolyzed gluten. The limit of detection using a peptic-tryptic hordein digest as reference was 2.3 microg prolamin equivalent per milliliter, and the limit of quantitation was 6.7 microg prolamin equivalent per milliliter. This system was applied for the determination of gluten equivalents in five commercial beverages based on fermented cereals.},
   keywords = {Calibration
Chemical Fractionation
Enzyme-Linked Immunosorbent Assay/methods/*standards
Glutens/*analysis
Hordeum/*chemistry
Hydrolysis
Peptide Hydrolases/chemistry
Prolamins/*chemistry/isolation & purification
Reference Standards
Secale/*chemistry
Triticum/*chemistry},
   ISSN = {1618-2642},
   Accession Number = {19763549},
   DOI = {10.1007/s00216-009-3080-6},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Ghimpu, S. and Bozomitu, L. and Cardei, E. and Oltean, C. and Burlacu, M. and Anton, D. and Trandafir, L. and Mihaila, D. and Moraru, D.},
   title = {[Helicobacter pylori infection in children with celiac disease]},
   journal = {Rev Med Chir Soc Med Nat Iasi},
   volume = {113},
   number = {4},
   pages = {1093-8},
   note = {Ghimpu, Silvia
Bozomitu, Laura
Cardei, E
Oltean, Carmen
Burlacu, M
Anton, Dana
Trandafir, Laura
Mihaila, Doina
Moraru, D
English Abstract
Journal Article
Romania
Rev Med Chir Soc Med Nat Iasi. 2009 Oct-Dec;113(4):1093-8.},
   abstract = {UNLABELLED: The purpose of this study is to evaluate symptomatology, endoscopic and histopathologic changes of Helicobacter pylori infection and gastritis lesions without Helicobacter pylori infection on children diagnosed with celiac disease. MATERIAL AND METHOD: 15 children under gluten-free diet were selected and, because of the recurrence of the dyspeptic syndrome, an upper digestive endoscopy associated with histopathologic exam was performed. Considering the histopathologic result we made two groups: first group (8 children with celiac disease and Helicobacter pylori infection) and second group (7 children with celiac disease without Helicobacter pylori infection, but associated with gastritis lesions). RESULTS: The main symptom was diffuse abdominal pain in both groups. The endoscopic antrum aspects were congestive with striped aspect (first group--12.5%, second group--42.9%) and congestive with nodulation (first group--25%, second group--14.3%). The histopathologic diagnosis were: moderate active chronic pangastritis (first group--25%, second group--14.3%) moderate active chronic gastritis (first group--25%,second group--14.3%), lymphocytic gastritis (first group--12.5%, second group--14.3%). CONCLUSION: The histopathologic exam remains the gold standard for celiac disease, gastritis lesions and Helicobacter pylori infection.},
   keywords = {Abdominal Pain/microbiology
Adolescent
Celiac Disease/*complications/diagnosis/microbiology/*pathology
Child
Child, Preschool
Diet, Gluten-Free
Endoscopy, Gastrointestinal
Female
Gastritis/microbiology/pathology
Helicobacter Infections/complications/diagnosis/*pathology
*Helicobacter pylori/isolation & purification
Humans
Male
Retrospective Studies
Risk Factors
Severity of Illness Index},
   ISSN = {0048-7848 (Print)
0048-7848},
   Accession Number = {20191880},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Gibson, P. R.},
   title = {Overview of inflammatory bowel disease in Australia in the last 50 years},
   journal = {J Gastroenterol Hepatol},
   volume = {24 Suppl 3},
   pages = {S63-8},
   note = {1440-1746
Gibson, Peter R
Historical Article
Journal Article
Review
Australia
J Gastroenterol Hepatol. 2009 Oct;24 Suppl 3:S63-8. doi: 10.1111/j.1440-1746.2009.06073.x.},
   abstract = {Inflammatory diseases of the intestine, including Crohn's disease, ulcerative colitis, and celiac disease are now very common in Australia and remain major challenges for clinicians. Australian (and New Zealand) clinicians and scientists have made considerable contributions to our current understanding of these diseases over the last 50 years, including pathogenesis (such as the 'butyrate hypothesis', 'endoplasmic reticulum (ER) stress', and the identification of the peptide sequences that incite celiac disease), true population epidemiology (albeit in New Zealand), precise clinical observation, new investigative tools, innovative new potential therapies, influential clinical drug trials (such as triple antibiotics for Crohn's disease), and a dietary approach with efficacy for functional gut symptoms (the low FODMAP diet). Underpinning the success has been clinical excellence and adaptation of clinicians to the changing landscape of disease severity and therapeutic options. The future is indeed bright if such trends continue.},
   keywords = {Australia/epidemiology
Gastroenterology/*history/trends
History, 20th Century
History, 21st Century
Humans
Inflammatory Bowel Diseases/diagnosis/epidemiology/etiology/*history/therapy
New Zealand/epidemiology
Predictive Value of Tests
Risk Factors
Treatment Outcome},
   ISSN = {0815-9319},
   Accession Number = {19799701},
   DOI = {10.1111/j.1440-1746.2009.06073.x},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Gil-Humanes, J. and Piston, F. and Tollefsen, S. and Sollid, L. M. and Barro, F.},
   title = {Effective shutdown in the expression of celiac disease-related wheat gliadin T-cell epitopes by RNA interference},
   journal = {Proc Natl Acad Sci U S A},
   volume = {107},
   number = {39},
   pages = {17023-8},
   note = {1091-6490
Gil-Humanes, Javier
Piston, Fernando
Tollefsen, Stig
Sollid, Ludvig M
Barro, Francisco
Journal Article
Research Support, Non-U.S. Gov't
United States
Proc Natl Acad Sci U S A. 2010 Sep 28;107(39):17023-8. doi: 10.1073/pnas.1007773107. Epub 2010 Sep 9.},
   abstract = {Celiac disease (CD) is an enteropathy triggered by the ingestion of gluten proteins from wheat and similar proteins from barley and rye. The inflammatory reaction is controlled by T cells that recognize gluten peptides in the context of human leukocyte antigen (HLA) DQ2 or HLA-DQ8 molecules. The only available treatment for the disease is a lifelong gluten-exclusion diet. We have used RNAi to down-regulate the expression of gliadins in bread wheat. A set of hairpin constructs were designed and expressed in the endosperm of bread wheat. The expression of gliadins was strongly down-regulated in the transgenic lines. Total gluten protein was extracted from transgenic lines and tested for ability to stimulate four different T-cell clones derived from the intestinal lesion of CD patients and specific for the DQ2-alpha-II, DQ2-gamma-VII, DQ8-alpha-I, and DQ8-gamma-I epitopes. For five of the transgenic lines, there was a 1.5-2 log reduction in the amount of the DQ2-alpha-II and DQ2-gamma-VII epitopes and at least 1 log reduction in the amount of the DQ8-alpha-I and DQ8-gamma-I epitopes. Furthermore, transgenic lines were also tested with two T-cell lines that are reactive with omega-gliadin epitopes. The total gluten extracts were unable to elicit T-cell responses for three of the transgenic wheat lines, and there were reduced responses for six of the transgenic lines. This work shows that the down-regulation of gliadins by RNAi can be used to obtain wheat lines with very low levels of toxicity for CD patients.},
   keywords = {Base Sequence
Celiac Disease/*immunology
Cell Line
Epitopes, T-Lymphocyte/*genetics/immunology
Gliadin/*genetics/immunology
HLA-DQ Antigens/immunology
Humans
Molecular Sequence Data
Nucleic Acid Conformation
Plants, Genetically Modified/genetics/*immunology
*RNA Interference
RNA, Small Interfering/chemistry/genetics
T-Lymphocytes/immunology
Triticum/genetics/*immunology},
   ISSN = {0027-8424},
   Accession Number = {20829492},
   DOI = {10.1073/pnas.1007773107},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Giuca, M. R. and Cei, G. and Gigli, F. and Gandini, P.},
   title = {Oral signs in the diagnosis of celiac disease: review of the literature},
   journal = {Minerva Stomatol},
   volume = {59},
   number = {1-2},
   pages = {33-43},
   note = {Giuca, M R
Cei, G
Gigli, F
Gandini, P
Journal Article
Review
Italy
Minerva Stomatol. 2010 Jan-Feb;59(1-2):33-43.},
   abstract = {This study explores the possibility that the celiac disease (CD) may be correlated with the insurgence of some oral signs, as based on a systematic review of the literature. Should this correlation be proven, any dentistry's screening would then be important to diagnose early celiac sprue pathogenesis. A literature survey was accomplished by using the Medline database (Entrez PubMed). The survey, which covered the period from the year 1972 to 2009, provided 382 published articles. Of these, 29 articles were selected according to inclusionary/exclusionary criteria, and consequently qualified for the final review analysis. Manual searching through the reference lists of the selected articles allowed the obtainment of others 17 articles. Findings gathered through this literature's review corroborate the significance of a causal relationship between some oral signs and CD. There are enough evidence making the correlation between CD and oral defects scientifically sustainable. This recognition should lead dentists to play more significant roles in screening for CD, as otherwise, if not properly diagnosed and not treated with a gluten-free diet, may eventually cause some malignancies.},
   keywords = {Adult
Atrophy
Avitaminosis/etiology
Bibliometrics
Celiac Disease/complications/*diagnosis/epidemiology
Child
Clinical Trials as Topic
Dental Enamel Hypoplasia/epidemiology/etiology
Glossitis/epidemiology/etiology
Humans
Malabsorption Syndromes/etiology
Recurrence
Stomatitis, Aphthous/epidemiology/etiology
Tongue/pathology
Tooth Eruption},
   ISSN = {0026-4970 (Print)
0026-4970},
   Accession Number = {20212408},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Goh, V. L. and Estrada, D. E. and Lerer, T. and Balarezo, F. and Sylvester, F. A.},
   title = {Effect of gluten-free diet on growth and glycemic control in children with type 1 diabetes and asymptomatic celiac disease},
   journal = {J Pediatr Endocrinol Metab},
   volume = {23},
   number = {11},
   pages = {1169-73},
   note = {Goh, Vi Lier
Estrada, D Elizabeth
Lerer, Trudy
Balarezo, Fabiola
Sylvester, Francisco A
Journal Article
Germany
J Pediatr Endocrinol Metab. 2010 Nov;23(11):1169-73.},
   abstract = {We aimed to evaluate the effects of a gluten-free diet on growth and glycemic control in children with type 1 diabetes mellitus (DM) and asymptomatic, biopsy-proven celiac disease (CD). Each case of CD was compared to two children with DM and no CD. We studied weight, height, and hemoglobin A1c (HgbAlc) up to 12 months pre- and post- CD diagnosis in 29 cases and 58 controls. The change in body mass index (deltaBMI Z-score) over 2 years was significantly higher in CD cases vs. controls (mean +/- SD 0.33 +/- 0.74 vs. +/- 0.08 +/- 0.46; p = 0.023). However, BMI Z-score did not change in CD patients diagnosed with DM for > 1 year. Mean HgbA1c was similar between groups throughout the study. In conclusion, children with asymptomatic CD and DM do not have significant changes in BMI, height Z-score or metabolic control 1 year post-diagnosis.},
   keywords = {Adolescent
Blood Glucose/*analysis
Body Mass Index
Celiac Disease/blood/*diet therapy/physiopathology
Child
Diabetes Mellitus, Type 1/blood/*physiopathology
*Diet, Gluten-Free
Female
Growth
Hemoglobin A, Glycosylated/analysis
Humans
Male},
   ISSN = {0334-018X (Print)
0334-018x},
   Accession Number = {21284331},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Gomes, S. P. and Nyengaard, J. R. and Misawa, R. and Girotti, P. A. and Castelucci, P. and Blazquez, F. H. and de Melo, M. P. and Ribeiro, A. A.},
   title = {Atrophy and neuron loss: effects of a protein-deficient diet on sympathetic neurons},
   journal = {J Neurosci Res},
   volume = {87},
   number = {16},
   pages = {3568-75},
   note = {1097-4547
Gomes, Silvio Pires
Nyengaard, Jens Randel
Misawa, Rubia
Girotti, Priscila Azevedo
Castelucci, Patricia
Blazquez, Francisco Hernandez Javier
de Melo, Mariana Pereira
Ribeiro, Antonio Augusto Coppi
Journal Article
Research Support, Non-U.S. Gov't
United States
J Neurosci Res. 2009 Dec;87(16):3568-75. doi: 10.1002/jnr.22167.},
   abstract = {Protein deficiency is one of the biggest public health problems in the world, accounting for about 30-40% of hospital admissions in developing countries. Nutritional deficiencies lead to alterations in the peripheral nervous system and in the digestive system. Most studies have focused on the effects of protein-deficient diets on the enteric neurons, but not on sympathetic ganglia, which supply extrinsic sympathetic input to the digestive system. Hence, in this study, we investigated whether a protein-restricted diet would affect the quantitative structure of rat coeliac ganglion neurons. Five male Wistar rats (undernourished group) were given a pre- and postnatal hypoproteinic diet receiving 5% casein, whereas the nourished group (n = 5) was fed with 20% casein (normoproteinic diet). Blood tests were carried out on the animals, e.g., glucose, leptin, and triglyceride plasma concentrations. The main structural findings in this study were that a protein-deficient diet (5% casein) caused coeliac ganglion (78%) and coeliac ganglion neurons (24%) to atrophy and led to neuron loss (63%). Therefore, the fall in the total number of coeliac ganglion neurons in protein-restricted rats contrasts strongly with no neuron losses previously described for the enteric neurons of animals subjected to similar protein-restriction diets. Discrepancies between our figures and the data for enteric neurons (using very similar protein-restriction protocols) may be attributable to the counting method used. In light of this, further systematic investigations comparing 2-D and 3-D quantitative methods are warranted to provide even more advanced data on the effects that a protein-deficient diet may exert on sympathetic neurons. (c) 2009 Wiley-Liss, Inc.},
   keywords = {Analysis of Variance
Animals
Animals, Newborn
Atrophy/metabolism/pathology
Blood Glucose/metabolism
Cell Count
Cell Size
Female
Ganglia, Sympathetic/metabolism/*pathology
Leptin/blood
Male
Maternal-Fetal Exchange/*physiology
Nerve Degeneration/metabolism
Neurons/metabolism/*pathology
Organ Size
Pregnancy
Protein Deficiency/metabolism/*pathology
Rats
Rats, Wistar
Triglycerides/blood},
   ISSN = {0360-4012},
   Accession Number = {19598252},
   DOI = {10.1002/jnr.22167},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Gonda, T. A. and Khan, S. U. and Cheng, J. and Lewis, S. K. and Rubin, M. and Green, P. H.},
   title = {Association of intussusception and celiac disease in adults},
   journal = {Dig Dis Sci},
   volume = {55},
   number = {10},
   pages = {2899-903},
   note = {1573-2568
Gonda, Tamas A
Khan, Sharif-Uz-Zaman
Cheng, Jian
Lewis, Suzanne K
Rubin, Moshe
Green, Peter H R
Journal Article
United States
Dig Dis Sci. 2010 Oct;55(10):2899-903. doi: 10.1007/s10620-009-1086-8. Epub 2009 Dec 24.},
   abstract = {INTRODUCTION: Intussusception (IS) is rare in adults. However, the more frequent use of cross-sectional imaging has resulted in an increase in its detection. Because of the reported association with celiac disease, we determined the prevalence of IS among a cohort with celiac disease. METHODS: An anonymized prospectively maintained celiac disease database and radiological database were reviewed. RESULTS: Of a total of 880 patients, 14 (age 47 +/- 17.5 years; 50% female) had IS that was detected by CT in 10, capsule endoscopy in three, and barium studies in two. The reason for evaluation was abdominal pain in 78% (11/14), whereas in the remainder (3/14) were incidental. IS was the initial manifestation of celiac disease in 57% (8/14). Two patients were found to have lead-point intussusceptions and both had small-bowel adenocarcinoma, and 10/14 had severe villous atrophy (subtotal or total). Among those with established celiac disease, IS was detected early, within 3 years of diagnosis. Follow-up was available for 11 patients, 9 of who adhered strictly to a gluten-free diet, and six had no recurrence. Among all the patients diagnosed with IS on radiologic studies at our institution, 45 were considered to have idiopathic IS. Only two of these patients had evaluation for celiac disease. CONCLUSION: IS occurs in celiac disease. It may be the initial presentation and is associated with abdominal pain. Adenocarcinoma needs to be excluded. The majority of patients do not have recurrent symptoms after adherence to a gluten-free diet. Celiac disease should be considered more frequently when IS is encountered.},
   keywords = {Abdominal Pain/epidemiology/pathology
Adenocarcinoma/epidemiology/pathology
Adult
Atrophy
Biopsy
Capsule Endoscopy
Celiac Disease/*epidemiology/*pathology
Chi-Square Distribution
Databases, Factual
Female
Follow-Up Studies
Humans
Incidental Findings
Intestinal Neoplasms/epidemiology/pathology
Intussusception/*epidemiology/*pathology
Male
Middle Aged},
   ISSN = {0163-2116},
   Accession Number = {20033844},
   DOI = {10.1007/s10620-009-1086-8},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Goodman, B. P. and Mistry, D. H. and Pasha, S. F. and Bosch, P. E.},
   title = {Copper deficiency myeloneuropathy due to occult celiac disease},
   journal = {Neurologist},
   volume = {15},
   number = {6},
   pages = {355-6},
   note = {2331-2637
Goodman, Brent P
Mistry, Deven H
Pasha, Shabana F
Bosch, Peter E
Case Reports
Journal Article
United States
Neurologist. 2009 Nov;15(6):355-6. doi: 10.1097/NRL.0b013e31819428a8.},
   abstract = {INTRODUCTION: Copper deficiency is an increasingly recognized cause of gait unsteadiness. Recognized causes of copper deficiency include excess zinc ingestion, and malabsorption. Although hematologic abnormalities have been attributed to copper deficiency in patients with celiac disease, myeloneuropathy due to copper deficiency has not been well described in patients with celiac disease. CASE REPORT: A 69-year-old woman was evaluated for a 5-year history of progressive gait unsteadiness and weight loss. She had no other gastrointestinal symptoms. Her neurologic examination revealed a sensory ataxia, and electrodiagnostic testing confirmed a myeloneuropathy. She had decreased serum copper levels and markedly elevated gliadin and tissue transglutaminase antibodies. Subsequent duodenal biopsy showed findings consistent with celiac disease. The patient was diagnosed with copper deficiency myeloneuropathy due to celiac disease. Adoption of a gluten-free diet along with copper supplementation resulted in significant clinical improvement, including improvement on electrodiagnostic testing. CONCLUSIONS: Celiac disease should be considered in patients found to have copper deficiency, even in patients without gastrointestinal symptoms. Furthermore, the authors suggest that some cases of ataxia associated with celiac disease are likely due to copper deficiency myeloneuropathy.},
   keywords = {Aged
Antibodies/blood
Celiac Disease/*complications
Copper/*deficiency
Female
Gait Disorders, Neurologic/*complications
Humans
Neurologic Examination/methods
Spinal Cord Diseases/*etiology/*metabolism
Transglutaminases/immunology},
   ISSN = {1074-7931},
   Accession Number = {19901719},
   DOI = {10.1097/NRL.0b013e31819428a8},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Gopal, M. and Nour, S. and Hoskyns, W.},
   title = {Coeliac disease in a child with anorectal malformation: The importance of considering other causes of diarrhea},
   journal = {J Indian Assoc Pediatr Surg},
   volume = {15},
   number = {1},
   pages = {30-1},
   note = {1998-3891
Gopal, Milan
Nour, Shawqui
Hoskyns, Wren
Journal Article
India
J Indian Assoc Pediatr Surg. 2010 Jan;15(1):30-1. doi: 10.4103/0971-9261.69140.},
   abstract = {We present the case of an Indian child with a high anorectal malformation (ARM) who postoperatively had troublesome fecal incontinence. Based on a dietary history, weight loss, and diarrhea, a duodenal biopsy was performed that revealed coeliac disease. Since being on a gluten-free diet, her symptoms have improved dramatically. To the best of our knowledge this is the first report in the English literature of such an association between ARMs and coeliac disease. Dietary modification alone can dramatically improve symptoms in these children.},
   keywords = {Anorectal malformation
coeliac disease
fecal incontinence},
   ISSN = {0971-9261},
   Accession Number = {21180503},
   DOI = {10.4103/0971-9261.69140},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Gorgun, J. and Portyanko, A. and Marakhouski, Y. and Cherstvoy, E.},
   title = {Tissue transglutaminase expression in celiac mucosa: an immunohistochemical study},
   journal = {Virchows Arch},
   volume = {455},
   number = {4},
   pages = {363-73},
   note = {1432-2307
Gorgun, Julia
Portyanko, Anna
Marakhouski, Yuri
Cherstvoy, Eugeni
Journal Article
Research Support, Non-U.S. Gov't
Germany
Virchows Arch. 2009 Oct;455(4):363-73. doi: 10.1007/s00428-009-0832-9. Epub 2009 Sep 12.},
   abstract = {Tissue transglutaminase (tTG) constitutes the main autoantigen in celiac disease (CD). The aim of the study was to clarify weather celiac disease is associated with changes in tTG expression in duodenal mucosa. Tissue transglutaminase was assessed immunohistochemically (clone CUB 7402) in duodenal biopsy specimens from 22 untreated CD patients, ten normal controls (NC) with unremarkable duodenal mucosa, and nine disease nonceliac controls (DC). In 15 CD patients duodenal biopsy specimens were repeatedly assessed after these patients had been prescribed gluten-free diet. Positive pixel count algorithm of ImageScope was used for quantitative evaluation of immunohistochemistry. Tissue transglutaminase expression in superficial epithelium differed significantly between the three groups (p < 0.001). It was increased in DC in relation to NC (p < 0.001) and in CD--in relation to NC (p < 0.001) and DC (p = 0.003). In CD and DC, cryptal epithelium was stained more intensively than in NC (p < 0.001), but there was no difference between CD and DC (p = 0.507). The same pattern was seen in lamina propria. A significant decrease in tTG expression in all the compartments was seen in repeatedly assessed samples. Untreated CD is associated with tTG overexpression, which is reversible. Tissue transglutaminase up-regulation does not seem to be specific for CD and can appear in other pathological conditions.},
   keywords = {Adolescent
Adult
Aged
Celiac Disease/*enzymology/pathology
Diet, Gluten-Free
Duodenum/*enzymology
Female
GTP-Binding Proteins
Humans
Immunohistochemistry
Intestinal Diseases/enzymology/pathology
Intestinal Mucosa/*enzymology
Middle Aged
Transglutaminases/*biosynthesis
Up-Regulation},
   ISSN = {0945-6317},
   Accession Number = {19756726},
   DOI = {10.1007/s00428-009-0832-9},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Greco, L. and Gobbetti, M. and Auricchio, R. and Di Mase, R. and Landolfo, F. and Paparo, F. and Di Cagno, R. and De Angelis, M. and Rizzello, C. G. and Cassone, A. and Terrone, G. and Timpone, L. and D'Aniello, M. and Maglio, M. and Troncone, R. and Auricchio, S.},
   title = {Safety for patients with celiac disease of baked goods made of wheat flour hydrolyzed during food processing},
   journal = {Clin Gastroenterol Hepatol},
   volume = {9},
   number = {1},
   pages = {24-9},
   note = {1542-7714
Greco, Luigi
Gobbetti, Marco
Auricchio, Renata
Di Mase, Raffaella
Landolfo, Francesca
Paparo, Francesco
Di Cagno, Raffaella
De Angelis, Maria
Rizzello, Carlo Giuseppe
Cassone, Angela
Terrone, Gaetano
Timpone, Laura
D'Aniello, Martina
Maglio, Maria
Troncone, Riccardo
Auricchio, Salvatore
Journal Article
Randomized Controlled Trial
United States
Clin Gastroenterol Hepatol. 2011 Jan;9(1):24-9. doi: 10.1016/j.cgh.2010.09.025. Epub 2010 Oct 15.},
   abstract = {BACKGROUND & AIMS: Celiac disease (CD) is characterized by an inflammatory response to wheat gluten, rye, and barley proteins. Fermentation of wheat flour with sourdough lactobacilli and fungal proteases decreases the concentration of gluten. We evaluated the safety of daily administration of baked goods made from this hydrolyzed form of wheat flour to patients with CD. METHODS: Patients were randomly assigned to consumption of 200 g per day of natural flour baked goods (NFBG) (80,127 ppm gluten; n = 6), extensively hydrolyzed flour baked goods (S1BG) (2480 ppm residual gluten; n = 2), or fully hydrolyzed baked goods (S2BG) (8 ppm residual gluten; n = 5) for 60 days. RESULTS: Two of the 6 patients who consumed NFBG discontinued the challenge because of symptoms; all had increased levels of anti-tissue transglutaminase (tTG) antibodies and small bowel deterioration. The 2 patients who ate the S1BG goods had no clinical complaints but developed subtotal atrophy. The 5 patients who ate the S2BG had no clinical complaints; their levels of anti-tTG antibodies did not increase, and their Marsh grades of small intestinal mucosa did not change. CONCLUSIONS: A 60-day diet of baked goods made from hydrolyzed wheat flour, manufactured with sourdough lactobacilli and fungal proteases, was not toxic to patients with CD. A combined analysis of serologic, morphometric, and immunohistochemical parameters is the most accurate method to assess new therapies for this disorder.},
   keywords = {Adolescent
Antibodies/blood
Celiac Disease/*therapy
Child
Diet Therapy/*adverse effects
Enzyme-Linked Immunosorbent Assay
Flour
Food Handling/*methods
Food Technology/*methods
Fungi/metabolism
Glutens/*metabolism
Humans
Hydrolysis
Immunoglobulin A/blood
Immunohistochemistry
Lactobacillus/metabolism
Peptide Hydrolases/metabolism
Triticum/*chemistry
Young Adult},
   ISSN = {1542-3565},
   Accession Number = {20951830},
   DOI = {10.1016/j.cgh.2010.09.025},
   year = {2011},
   type = {Ref–rence Type}
}

@article{
   author = {Gudjonsdottir, A. H. and Nilsson, S. and Naluai, A. T. and Ek, J. and Amundsen, S. S. and Wahlstrom, J. and Ascher, H.},
   title = {Association between genotypes and phenotypes in coeliac disease},
   journal = {J Pediatr Gastroenterol Nutr},
   volume = {49},
   number = {2},
   pages = {165-9},
   note = {1536-4801
Gudjonsdottir, Audur H
Nilsson, Staffan
Naluai, Asa Torinsson
Ek, Johan
Amundsen, Silja S
Wahlstrom, Jan
Ascher, Henry
Journal Article
Research Support, Non-U.S. Gov't
United States
J Pediatr Gastroenterol Nutr. 2009 Aug;49(2):165-9. doi: 10.1097/MPG.0b013e318196c362.},
   abstract = {BACKGROUND: Coeliac disease (CD) is a genetically driven immunological intolerance to dietary gluten with a wide range of clinical presentations. The aim of this study was to investigate the heritability of the phenotype in CD and the influence on the phenotype of different genes associated with the disease. PATIENTS AND METHODS: One hundred and seven families with at least 2 siblings with CD were collected. The patients were grouped in symptom grades on the basis of the clinical presentation, the age at diagnosis, and sex. Stratification analyses of the human leucocyte antigen-DQA1 and human leucocyte antigen-DQB1 genotypes, the CTLA4 +49A/G polymorphism, the CTLA4 haplotype MH30*G:-1147*T:+49*A:CT60*G:CT61*A, and the 5q31-33 loci were done. RESULTS: The heritability of the phenotype was estimated to be 0.45. Significant association and linkage was found between the clinical presentation and the CTLA4 +49A/G polymorphism but not for the other genotypes. No correlation was found between genotypes and age at diagnosis or sex. CONCLUSIONS: Our results indicate that the heritability is determiner of the phenotype in CD. The CTLA4 +49A/G polymorphism is correlated to the clinical presentation: the AA genotype is associated with clinically silent disease.},
   keywords = {Antigens/*genetics
Antigens, CD/*genetics
CTLA-4 Antigen
Celiac Disease/*genetics/immunology
Child
Female
*Genetic Predisposition to Disease
*Genotype
Haplotypes
Humans
Inheritance Patterns
Leukocytes/immunology
Male
*Phenotype
*Polymorphism, Single Nucleotide
Siblings},
   ISSN = {0277-2116},
   Accession Number = {19543113},
   DOI = {10.1097/MPG.0b013e318196c362},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Gunther, U. and Daum, S. and Heller, F. and Schumann, M. and Loddenkemper, C. and Grunbaum, M. and Zeitz, M. and Bojarski, C.},
   title = {Diagnostic value of confocal endomicroscopy in celiac disease},
   journal = {Endoscopy},
   volume = {42},
   number = {3},
   pages = {197-202},
   note = {1438-8812
Gunther, U
Daum, S
Heller, F
Schumann, M
Loddenkemper, C
Grunbaum, M
Zeitz, M
Bojarski, C
Journal Article
Research Support, Non-U.S. Gov't
Germany
Endoscopy. 2010 Mar;42(3):197-202. doi: 10.1055/s-0029-1243937. Epub 2010 Mar 1.},
   abstract = {BACKGROUND: Improved endoscopic screening with targeted biopsies might enhance diagnostic yield in celiac disease. Confocal endomicroscopy (CEM) allows high-resolution in vivo histological analysis. We compared the endomicroscopic findings during ongoing endoscopy with the histological findings graded according to the Marsh classification. METHODS: Twenty-four patients with celiac disease and six patients with celiac disease that was refractory on a gluten-free diet were examined using CEM. The duodenal mucosa was evaluated by CEM and by conventional histological analysis in respect of villous atrophy, crypt hyperplasia, and increased numbers of intraepithelial lymphocytes (IELs > 40 / 100 enterocytes). The CEM results were assessed as to sensitivity, specificity, and interobserver variability. A Marsh classification score determined by CEM was compared to that obtained by histology. Thirty patients undergoing routine upper gastrointestinal endoscopy were used as controls. RESULTS: Conventional histology showed villous atrophy and crypt hyperplasia in 23 and increased numbers of IELs in 27 of the 30 patients with celiac disease. With CEM, villous atrophy, crypt hyperplasia, and increased IELs were respectively identified in 17, 12, and 22 of the 30 patients. The agreement of the findings on CEM with those of conventional histology was good in relation to villous atrophy (sensitivity 74 %) and increased numbers of IELs (sensitivity 81 %), but inadequate in relation to crypt hyperplasia (sensitivity 52 %). The kappa values for determination of interobserver variability were 0.90 for villous atrophy, 1.00 for crypt hyperplasia, and 0.84 for IEL detection. In the 30 control patients, normal duodenal architecture was found by both histology and endomicroscopy, indicating an overall specificity of 100 %. CONCLUSION: The assessment of duodenal histology by CEM in patients with celiac disease is sensitive and specific in determining increased numbers of IELs and villous atrophy, but insufficient in respect of crypt hyperplasia. For routine use of CEM in patients with celiac disease, the technique would need to be improved.},
   keywords = {Atrophy/pathology
Biopsy
Celiac Disease/*diagnosis/pathology
Duodenoscopy/*methods
Duodenum/pathology
Female
Humans
Hyperplasia/pathology
Lymphocyte Count
Male
Microscopy, Confocal/*methods
Middle Aged
Sensitivity and Specificity},
   ISSN = {0013-726x},
   Accession Number = {20195989},
   DOI = {10.1055/s-0029-1243937},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Gupta, R. and Reddy, D. N. and Makharia, G. K. and Sood, A. and Ramakrishna, B. S. and Yachha, S. K. and Thapa, B. R. and Banerjee, R. and Anuradha, S. and Dutta, U. and Puri, A. S. and Jain, A. K. and Mulder, C. J. and Kumar, A. and Boindala, S.},
   title = {Indian task force for celiac disease: current status},
   journal = {World J Gastroenterol},
   volume = {15},
   number = {48},
   pages = {6028-33},
   note = {2219-2840
Gupta, Rajesh
Reddy, Duvvuru Nageshwar
Makharia, Govind K
Sood, Ajit
Ramakrishna, Balakrishnan S
Yachha, Surender Kumar
Thapa, Babu Ram
Banerjee, Rupa
Anuradha, Sekaran
Dutta, Usha
Puri, Amarender Singh
Jain, Ajay Kumar
Mulder, Chris Jj
Kumar, Ajay
Boindala, Sesikeran
Editorial
United States
World J Gastroenterol. 2009 Dec 28;15(48):6028-33.},
   abstract = {There are limited data on celiac disease (CD) from India. The limited knowledge about CD in India might be attributed to several factors. The first meeting of the Indian Task Force for Celiac Disease was held in the Asian Institute of Gastroenterology, Hyderabad, India in December 2008. The objectives of the meeting were to focus research on prevalence of CD in the wheat-eating Northern vs the rice-eating Southern Indian population, low-budget serological assays to study the underprivileged population, to involve other medical subspecialties in CD, to suggest proper legislation regarding wheat food labeling, and to organize affordable food substitutes for patients with celiac disease.},
   keywords = {Capsule Endoscopy
Celiac Disease/diet therapy/*epidemiology/pathology
Diet
Humans
India/epidemiology
Intestinal Mucosa/pathology
Patient Compliance},
   ISSN = {1007-9327},
   Accession Number = {20027674},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Gutierrez, S. and Toro, M. and Cassar, A. and Ongay, R. and Isaguirre, J. and Lopez, C. and Benedetti, L.},
   title = {[Celiac crisis: presentation as bleeding diathesis]},
   journal = {Acta Gastroenterol Latinoam},
   volume = {39},
   number = {1},
   pages = {53-4},
   note = {Gutierrez, Sebastian
Toro, Martin
Cassar, Alejandro
Ongay, Rodrigo
Isaguirre, Jorge
Lopez, Candelaria
Benedetti, Laura
Case Reports
English Abstract
Journal Article
Argentina
Acta Gastroenterol Latinoam. 2009 Mar;39(1):53-4.},
   abstract = {Celiac crisis is a severe and potentially fatal complication of celiac disease. Unusual at present, it has been described mainly in children younger than 2-years-old, but reports in adults do exist. We report a 26-years-old lady with tetany and bleeding diathesis at presentation. In spite of it rareness, it is important to consider celiac crisis among the multiple manifestations of celiac disease.},
   keywords = {Adult
Celiac Disease/*complications/diet therapy
Female
Hemorrhagic Disorders/*etiology/therapy
Humans
Prothrombin Time
Tetany/*etiology/therapy},
   ISSN = {0300-9033 (Print)
0300-9033},
   Accession Number = {19408740},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Hadithi, M. and Mulder, C. J. and Stam, F. and Azizi, J. and Crusius, J. B. and Pena, A. S. and Stehouwer, C. D. and Smulders, Y. M.},
   title = {Effect of B vitamin supplementation on plasma homocysteine levels in celiac disease},
   journal = {World J Gastroenterol},
   volume = {15},
   number = {8},
   pages = {955-60},
   note = {2219-2840
Hadithi, Muhammed
Mulder, Chris J J
Stam, Frank
Azizi, Joshan
Crusius, J Bart A
Pena, Amado Salvador
Stehouwer, Coen D A
Smulders, Yvo M
Journal Article
United States
World J Gastroenterol. 2009 Feb 28;15(8):955-60.},
   abstract = {AIM: To investigate the effect of vitamin supplements on homocysteine levels in patients with celiac disease. METHODS: Vitamin B6, folate, vitamin B12, and fasting plasma homocysteine levels were measured in 51 consecutive adults with celiac disease [median (range) age 56 (18-63) years; 40% men, 26 (51%) had villous atrophy, and 25 (49%) used B-vitamin supplements] and 50 healthy control individuals matched for age and sex. Finally, the C677T polymorphism of 5,10-methylenetetrahydrofolate reductase (MTHFR) was evaluated in 46 patients with celiac disease and all control individuals. RESULTS: Patients with celiac disease and using vitamin supplements had higher serum vitamin B6 (P = 0.003), folate (P < 0.001), and vitamin B12 (P = 0.012) levels than patients who did not or healthy controls (P = 0.035, P < 0.001, P = 0.007, for vitamin B6, folate, and vitamin B12, respectively). Lower plasma homocysteine levels were found in patients using vitamin supplements than in patients who did not (P = 0.001) or healthy controls (P = 0.003). However, vitamin B6 and folate, not vitamin B12, were significantly and independently associated with homocysteine levels. Twenty-four (48%) of 50 controls and 23 (50%) of 46 patients with celiac disease carried the MTHFR thermolabile variant T-allele (P = 0.89). CONCLUSION: Homocysteine levels are dependent on Marsh classification and the regular use of B-vitamin supplements is effective in reduction of homocysteine levels in patients with celiac disease and should be considered in disease management.},
   keywords = {Adolescent
Adult
Celiac Disease/*blood/*drug therapy
Creatinine/metabolism
Dietary Supplements
Female
Folic Acid/blood
Homocysteine/*blood
Humans
Male
Methylenetetrahydrofolate Reductase (NADPH2)/genetics
Middle Aged
Pantothenic Acid/blood
Polymorphism, Single Nucleotide
Vitamin B 12/blood
Vitamin B Complex/*therapeutic use
Young Adult},
   ISSN = {1007-9327},
   Accession Number = {19248194},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Hadithi, M. and Pena, A. S.},
   title = {Current methods to diagnose the unresponsive and complicated forms of coeliac disease},
   journal = {Eur J Intern Med},
   volume = {21},
   number = {4},
   pages = {247-53},
   note = {1879-0828
Hadithi, M
Pena, A S
Journal Article
Review
Netherlands
Eur J Intern Med. 2010 Aug;21(4):247-53. doi: 10.1016/j.ejim.2010.01.015. Epub 2010 Feb 26.},
   abstract = {Coeliac disease is a common disorder. Due to the protean manifestations of the disease and the often mild but indolent course, the diagnosis is often missed. The method to diagnose this in principle reversible disease after the introduction of a gluten-free diet has attracted the attention of several scientific disciplines to find the simplest and most patient-friendly test. This has resulted in a noticeable impact on the clinical practice next to a general increased awareness of its existence, its pathogenesis, its course and recent evidence of increased mortality. Amendments made in the diagnostic criteria of coeliac disease over the last half century have simplified the diagnosis. However, the aspect most relevant to the specialist in internal medicine is related to its grave consequences when the disease fails to respond to a gluten-free diet. These refractory cases may culminate in severe complications with sombre endings and malignancy. Fortunately, current technology can offer the specialist in internal medicine more facilities to diagnose the cause of the complicated cases in order to attempt to intervene in the course of disease and hopefully save these patients. We review the available tools that now exist and their indications that can be practiced in a modern clinical setting for the diagnosis of the complicated forms of this disease.},
   keywords = {Celiac Disease/*diagnosis/diet therapy/pathology
Diet, Gluten-Free
Duodenum
Endoscopy, Gastrointestinal
Histocompatibility Testing
Humans},
   ISSN = {0953-6205},
   Accession Number = {20603030},
   DOI = {10.1016/j.ejim.2010.01.015},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Hadjivassiliou, M. and Rao, D. G. and Wharton, S. B. and Sanders, D. S. and Grunewald, R. A. and Davies-Jones, A. G.},
   title = {Sensory ganglionopathy due to gluten sensitivity},
   journal = {Neurology},
   volume = {75},
   number = {11},
   pages = {1003-8},
   note = {1526-632x
Hadjivassiliou, M
Rao, D G
Wharton, S B
Sanders, D S
Grunewald, R A
Davies-Jones, A G B
Medical Research Council/United Kingdom
Journal Article
Research Support, Non-U.S. Gov't
United States
Neurology. 2010 Sep 14;75(11):1003-8. doi: 10.1212/WNL.0b013e3181f25ee0.},
   abstract = {OBJECTIVES: Gluten sensitivity can engender neurologic dysfunction, one of the two commonest presentations being peripheral neuropathy. The commonest type of neuropathy seen in the context of gluten sensitivity is sensorimotor axonal. We report 17 patients with sensory ganglionopathy associated with gluten sensitivity. METHODS: This is a retrospective observational case series of 17 patients with sensory ganglionopathy and gluten sensitivity. All patients had been followed up for a number of years in dedicated gluten sensitivity/neurology and neuropathy clinics. RESULTS: Out of a total of 409 patients with different types of peripheral neuropathies, 53 (13%) had clinical and neurophysiologic evidence of sensory ganglionopathy. Out of these 53 patients, 17 (32%) had serologic evidence of gluten sensitivity. The mean age of those with gluten sensitivity was 67 years and the mean age at onset was 58 years. Seven of those with serologic evidence of gluten sensitivity had enteropathy on biopsy. Fifteen patients went on a gluten-free diet, resulting in stabilization of the neuropathy in 11. The remaining 4 had poor adherence to the diet and progressed, as did the 2 patients who did not opt for dietary treatment. Autopsy tissue from 3 patients demonstrated inflammation in the dorsal root ganglia with degeneration of the posterior columns of the spinal cord. CONCLUSIONS: Sensory ganglionopathy can be a manifestation of gluten sensitivity and may respond to a strict gluten-free diet.},
   keywords = {Action Potentials/physiology
Aged
Aged, 80 and over
Ataxia/etiology/physiopathology
Biopsy
Celiac Disease/diet therapy/pathology
Diet
Diet, Gluten-Free
Female
Food Hypersensitivity/*complications/diet therapy/immunology
Ganglia, Sensory/*pathology
Gliadin/immunology
Glutens/*adverse effects/immunology
Humans
Immunoglobulin A/immunology
Immunoglobulin G/immunology
Male
Middle Aged
Peripheral Nervous System Diseases/*etiology/immunology/pathology},
   ISSN = {0028-3878},
   Accession Number = {20837968},
   DOI = {10.1212/WNL.0b013e3181f25ee0},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Hadjivassiliou, M. and Sanders, D. S. and Grunewald, R. A. and Woodroofe, N. and Boscolo, S. and Aeschlimann, D.},
   title = {Gluten sensitivity: from gut to brain},
   journal = {Lancet Neurol},
   volume = {9},
   number = {3},
   pages = {318-30},
   note = {1474-4465
Hadjivassiliou, Marios
Sanders, David S
Grunewald, Richard A
Woodroofe, Nicola
Boscolo, Sabrina
Aeschlimann, Daniel
Journal Article
Research Support, Non-U.S. Gov't
Review
England
Lancet Neurol. 2010 Mar;9(3):318-30. doi: 10.1016/S1474-4422(09)70290-X.},
   abstract = {Gluten sensitivity is a systemic autoimmune disease with diverse manifestations. This disorder is characterised by abnormal immunological responsiveness to ingested gluten in genetically susceptible individuals. Coeliac disease, or gluten-sensitive enteropathy, is only one aspect of a range of possible manifestations of gluten sensitivity. Although neurological manifestations in patients with established coeliac disease have been reported since 1966, it was not until 30 years later that, in some individuals, gluten sensitivity was shown to manifest solely with neurological dysfunction. Furthermore, the concept of extraintestinal presentations without enteropathy has only recently become accepted. In this Personal View, we review the range of neurological manifestations of gluten sensitivity and discuss recent advances in the diagnosis and understanding of the pathophysiological mechanisms underlying neurological dysfunction related to gluten sensitivity.},
   keywords = {Animals
Brain Diseases/diet therapy/etiology
Celiac Disease/complications/diet therapy/epidemiology
Diet, Gluten-Free
Gastrointestinal Diseases/diet therapy/etiology
Glutens/adverse effects
Humans
Nervous System Diseases/diet therapy/*etiology},
   ISSN = {1474-4422},
   Accession Number = {20170845},
   DOI = {10.1016/s1474-4422(09)70290-x},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Hall, N. J. and Rubin, G. and Charnock, A.},
   title = {Systematic review: adherence to a gluten-free diet in adult patients with coeliac disease},
   journal = {Aliment Pharmacol Ther},
   volume = {30},
   number = {4},
   pages = {315-30},
   note = {1365-2036
Hall, N J
Rubin, G
Charnock, A
Journal Article
Research Support, Non-U.S. Gov't
Review
England
Aliment Pharmacol Ther. 2009 Aug 15;30(4):315-30. doi: 10.1111/j.1365-2036.2009.04053.x. Epub 2009 May 26.},
   abstract = {BACKGROUND: Coeliac disease is increasingly diagnosed in adult patients who present with atypical symptoms or who are asymptomatic and detected by case screening. Its treatment, a gluten-free diet, can have a considerable impact on daily living. Understanding the factors associated with non-adherence is important in terms of supporting patients with their condition. AIM: To investigate factors associated with adherence to a gluten-free diet in adults with coeliac disease. METHODS: A literature search of multiple electronic databases using a pre-determined search string for literature between 1980 and November 2007 identified a possible 611 hits. After checking for relevance, 38 studies were included in this review. RESULTS: Rates for strict adherence range from 42% to 91% depending on definition and method of assessment and are the lowest among ethnic minorities and those diagnosed in childhood. Adherence is most strongly associated with cognitive, emotional and socio-cultural influences, membership of an advocacy group and regular dietetic follow-up. Screen and symptom-detected coeliac patients do not differ in their adherence to a gluten-free diet. CONCLUSIONS: The existing evidence for factors associated with non-adherence to a gluten-free diet is of variable quality. Further and more rigorous research is needed to characterize those individuals most likely to be non-adherent to assist them better with their treatment.},
   keywords = {Adult
Celiac Disease/*diet therapy/psychology
Food Labeling
Glutens/*administration & dosage
Humans
Patient Compliance
Young Adult},
   ISSN = {0269-2813},
   Accession Number = {19485977},
   DOI = {10.1111/j.1365-2036.2009.04053.x},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Hallert, C. and Svensson, M. and Tholstrup, J. and Hultberg, B.},
   title = {Clinical trial: B vitamins improve health in patients with coeliac disease living on a gluten-free diet},
   journal = {Aliment Pharmacol Ther},
   volume = {29},
   number = {8},
   pages = {811-6},
   note = {1365-2036
Hallert, C
Svensson, M
Tholstrup, J
Hultberg, B
Journal Article
Multicenter Study
Randomized Controlled Trial
England
Aliment Pharmacol Ther. 2009 Apr 15;29(8):811-6. doi: 10.1111/j.1365-2036.2009.03945.x. Epub 2008 Jan 20.},
   abstract = {BACKGROUND: Patients with coeliac disease living on a gluten-free diet show vitamin deficiency and reduced subjective health status. AIM: To study the biochemical and clinical effects of B vitamin supplementation in adults with longstanding coeliac disease. METHODS: In a double blind placebo controlled multicentre trial, 65 coeliac patients (61% women) aged 45-64 years on a strict gluten-free diet for several years were randomized to a daily dose of 0.8 mg folic acid,0.5 mg cyanocobalamin and 3 mg pyridoxine or placebo for 6 months. The outcome measures were psychological general well-being (PGWB) and the plasma total homocysteine (tHcy) level, marker of B vitamin status. RESULTS: Fifty-seven patients (88%) completed the trial. The tHcy level was baseline median 11.7 micromol/L (7.4-23.0), significantly higher than in matched population controls [10.2 micromol/L (6.7-22.6) (P < 0.01)]. Following vitamin supplementation, tHcy dropped a median of 34% (P < 0.001), accompanied by significant improvement in well-being (P < 0.01), notably Anxiety (P < 0.05) and Depressed Mood (P < 0.05) for patients with poor well-being. CONCLUSIONS: Adults with longstanding coeliac disease taking extra B vitamins for 6 months showed normalized tHcy and significant improvement in general well-being, suggesting that B vitamins should be considered in people advised to follow a gluten-free diet.},
   keywords = {Anxiety/psychology
Celiac Disease/blood/psychology/*therapy
Depressive Disorder/psychology
*Diet, Gluten-Free
Female
Folic Acid/*therapeutic use
Health Status
Homocysteine/blood
Humans
Male
Middle Aged
Pyridoxine/*therapeutic use
Surveys and Questionnaires
Vitamin B 12/*therapeutic use
Vitamin B Complex/*therapeutic use},
   ISSN = {0269-2813},
   Accession Number = {19154566},
   DOI = {10.1111/j.1365-2036.2009.03945.x},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Harris, K. M. and Fasano, A. and Mann, D. L.},
   title = {Monocytes differentiated with IL-15 support Th17 and Th1 responses to wheat gliadin: implications for celiac disease},
   journal = {Clin Immunol},
   volume = {135},
   number = {3},
   pages = {430-9},
   note = {1521-7035
Harris, Kristina M
Fasano, Alessio
Mann, Dean L
R01 DK048373/DK/NIDDK NIH HHS/United States
R21 DK078699/DK/NIDDK NIH HHS/United States
R21 DK078699-02/DK/NIDDK NIH HHS/United States
DK078699/DK/NIDDK NIH HHS/United States
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
United States
Clin Immunol. 2010 Jun;135(3):430-9. doi: 10.1016/j.clim.2010.01.003. Epub 2010 Feb 11.},
   abstract = {Interleukin (IL)-15 contributes to the immunopathogenesis of Celiac disease (CD). However, it is not clear how IL-15 affects APC that shape adaptive immune responses to the dietary antigen, gliadin. Using PBMC from healthy individuals, we show that monocytes differentiated with IL-15 (IL15-DC) produced IL-1beta, IL-6, IL-15, IL-23, TNFalpha and CCL20 in response to pepsin-trypsin digested gliadin (PTG) and activated contact-dependent Th17 and Th1 responses from autologous CD4(+) T cells. Lower concentrations of IL-15 augmented IFNgamma responses to PTG in PBMC from CD patients compared to controls. Thus, IL-15 supports Th17 and Th1 responses to a dietary antigen that is normally well-tolerated in healthy individuals by generating IL15-DC. These potentially pathogenic immune responses may result in CD patients and not healthy individuals as a consequence of IL-15 hypersensitivity. Therefore, genetic and/or environmental factors that control IL-15 expression and responsiveness in the intestine likely participate in the pathogenesis of CD.},
   keywords = {Celiac Disease/*immunology/metabolism
Cell Differentiation/*immunology
Cell Separation
Cells, Cultured
Dendritic Cells/immunology/metabolism
Flow Cytometry
Gene Expression Regulation/*immunology
Gliadin/*immunology
Humans
Interleukin-15/biosynthesis/genetics/*physiology
Interleukin-17/*biosynthesis
Lymphocyte Activation/immunology
Monocytes/cytology/*immunology
Th1 Cells/*immunology/metabolism},
   ISSN = {1521-6616},
   Accession Number = {20153259},
   DOI = {10.1016/j.clim.2010.01.003},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Hasosah, M. and Davidson, G. and Jacobson, K.},
   title = {Persistent elevated tissue-transglutaminase in cystic fibrosis},
   journal = {J Paediatr Child Health},
   volume = {45},
   number = {4},
   pages = {172-3},
   note = {1440-1754
Hasosah, Mohammed
Davidson, George
Jacobson, Kevan
Case Reports
Editorial
Australia
J Paediatr Child Health. 2009 Apr;45(4):172-3. doi: 10.1111/j.1440-1754.2009.01477.x.},
   keywords = {Celiac Disease/*complications/*diagnosis/diet therapy
Child
Cystic Fibrosis/*complications/*diagnosis/enzymology
Diagnosis, Differential
Endoscopy
HLA-DQ Antigens/analysis
Humans
Male
Transglutaminases/*analysis},
   ISSN = {1034-4810},
   Accession Number = {19426374},
   DOI = {10.1111/j.1440-1754.2009.01477.x},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Hatting, M. and Galm, O. and Meyer, M. and Trautwein, C. and Tischendorf, J. J.},
   title = {[Anemia and severe thrombocytopenia in celiac disease]},
   journal = {Med Klin (Munich)},
   volume = {105},
   number = {4},
   pages = {249-52},
   note = {1615-6722
Hatting, Maximilian
Galm, Oliver
Meyer, Martin
Trautwein, Christian
Tischendorf, Jens J W
Case Reports
English Abstract
Journal Article
Germany
Med Klin (Munich). 2010 Apr;105(4):249-52. doi: 10.1007/s00063-010-1035-5.},
   abstract = {BACKGROUND: The frequency of diagnosis of celiac disease has increased since the introduction of serologic testing. The number of patients in whom extraintestinal symptoms reflect the initial manifestation is rising. Common symptoms are changes in blood counts, which can arise from changes in all cell lineages. Among these, iron deficiency anemia is very common, but also thrombocytosis and thrombocytopenia have been reported to manifest themselves within the framework of celiac disease. CASE REPORT: The authors report on a patient with malnutrition, macrocytic anemia, and pronounced thrombocytopenia. Based on changes of peripheral blood smear and endoscopic result, celiac disease was suspected that could be confirmed by histology of duodenal biopsies. The thrombocytopenia was reversible after initiation of gluten-free diet and folic acid substitution. In addition, clinical symptoms resolved and hematologic reconstitution could be observed. CONCLUSION: Similar deficiencies have almost exclusively been observed in patients with increased folic acid requirements during pregnancy or intensive care. Celiac disease must be taken into consideration, if changes in blood counts occur associated with gastrointestinal symptoms.},
   keywords = {Anemia, Macrocytic/diagnosis/*etiology
Biopsy
Celiac Disease/*diagnosis/diet therapy/pathology
Diet, Gluten-Free
Female
Folic Acid/administration & dosage
Humans
Intestinal Mucosa/pathology
Middle Aged
Protein-Energy Malnutrition/diet therapy/etiology/pathology
Thrombocytopenia/diagnosis/*etiology},
   ISSN = {0723-5003},
   Accession Number = {20455043},
   DOI = {10.1007/s00063-010-1035-5},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Hauser, W. and Janke, K. H. and Klump, B. and Gregor, M. and Hinz, A.},
   title = {Anxiety and depression in adult patients with celiac disease on a gluten-free diet},
   journal = {World J Gastroenterol},
   volume = {16},
   number = {22},
   pages = {2780-7},
   note = {2219-2840
Hauser, Winfried
Janke, Karl-Heinz
Klump, Bodo
Gregor, Michael
Hinz, Andreas
Journal Article
Research Support, Non-U.S. Gov't
United States
World J Gastroenterol. 2010 Jun 14;16(22):2780-7.},
   abstract = {AIM: To compare anxiety and depression levels in adult patients with celiac disease (CD) on a gluten-free diet (GFD) with controls. METHODS: The levels of anxiety, depression and of a probable anxiety or depressive disorder were assessed by the Hospital Anxiety and Depression Scale in 441 adult patients with CD recruited by the German Celiac Society, in 235 age- and sex-matched patients with inflammatory bowel disease (IBD) in remission or with slight disease activity, and in 441 adult persons of a representative German general population sample (GP). Potential demographic (age, sex, social class, family status) and disease-related (latency to diagnosis, duration of GFD, compliance with GFD, thyroid disease) predictors of anxiety and depression in CD were tested for by regression analyses. RESULTS: The level of anxiety in CD patients was predicted (R(2) = 0.07) by female gender (P = 0.01). Female sex (OR = 3.6, 95% CI: 1.3-9.4, P = 0.01) was associated with a probable anxiety disorder. Living alone (OR = 0.5, 95% CI: 0.2-0.9, P = 0.05) was associated with a reduced risk of an anxiety disorder. The level of depression and a probable depressive disorder were not predicted by any of the demographic and medical variables tested for. The levels of anxiety in patients with CD (6.6 +/- 3.4) and with IBD (6.9 +/- 3.7) were higher than those of persons in the GP (4.6 +/- 3.3) (both P < 0.001). The levels of depression in persons with CD (4.2 +/- 3.4), IBD (4.6 +/- 3.4) and of the GP (4.2 +/- 3.8) did not differ (P = 0.3). The prevalence of a probable anxiety disorder in persons with CD (16.8%) and IBD (14.0%) was higher than that of the GP (5.7%) (P < 0.001). The prevalence of a probable depressive disorder did not differ significantly between the three groups (P = 0.1). CONCLUSION: Anxiety in adult German female celiacs on a GFD is higher than in persons of the GP. Female celiacs on a GFD should be screened for anxiety.},
   keywords = {Adaptation, Psychological
Adult
Aged
Anxiety/*etiology
Celiac Disease/*diet therapy
Depressive Disorder/*etiology
Diet, Gluten-Free/*adverse effects/*psychology
Female
Germany
Humans
Male
Middle Aged
Patient Compliance
Surveys and Questionnaires},
   ISSN = {1007-9327},
   Accession Number = {20533598},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Heap, G. A. and van Heel, D. A.},
   title = {Genetics and pathogenesis of coeliac disease},
   journal = {Semin Immunol},
   volume = {21},
   number = {6},
   pages = {346-54},
   note = {1096-3618
Heap, Graham A
van Heel, David A
Wellcome Trust/United Kingdom
Journal Article
Research Support, Non-U.S. Gov't
Review
England
Semin Immunol. 2009 Dec;21(6):346-54. doi: 10.1016/j.smim.2009.04.001. Epub 2009 May 13.},
   abstract = {Coeliac disease is a common complex disease caused by a dietary intolerance to wheat gluten. Susceptibility is determined by both environmental and genetic factors. Coeliac disease results from complex interactions between the innate immune system, an adaptive T and B cell response and the mucosal barrier where inflammation is ultimately manifested. Genetic variants within the HLA region are well established, while variants outside of the HLA region have recently been identified. These variants are beginning to enhance our understanding of the immunology of the condition. This review focuses on the immunological pathogenesis of coeliac disease with special reference to the influence of genetic susceptibility on disease development.},
   keywords = {Celiac Disease/*genetics/*immunology/physiopathology
*Genetic Predisposition to Disease
HLA Antigens/genetics
Humans
Transglutaminases/metabolism},
   ISSN = {1044-5323},
   Accession Number = {19443237},
   DOI = {10.1016/j.smim.2009.04.001},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Helmerhorst, E. J. and Zamakhchari, M. and Schuppan, D. and Oppenheim, F. G.},
   title = {Discovery of a novel and rich source of gluten-degrading microbial enzymes in the oral cavity},
   journal = {PLoS One},
   volume = {5},
   number = {10},
   pages = {e13264},
   note = {1932-6203
Helmerhorst, Eva J
Zamakhchari, Maram
Schuppan, Detlef
Oppenheim, Frank G
DE7652/DE/NIDCR NIH HHS/United States
R37 DE005672/DE/NIDCR NIH HHS/United States
R01 DE007652/DE/NIDCR NIH HHS/United States
DE05672/DE/NIDCR NIH HHS/United States
R21 DK073254/DK/NIDDK NIH HHS/United States
AI087803/AI/NIAID NIH HHS/United States
DK073254/DK/NIDDK NIH HHS/United States
F31 DE005672/DE/NIDCR NIH HHS/United States
DE18132/DE/NIDCR NIH HHS/United States
AI078385/AI/NIAID NIH HHS/United States
R21 DE018132/DE/NIDCR NIH HHS/United States
R01 DE005672/DE/NIDCR NIH HHS/United States
R01 AI087803/AI/NIAID NIH HHS/United States
R21 AI078385/AI/NIAID NIH HHS/United States
Journal Article
Research Support, N.I.H., Extramural
United States
PLoS One. 2010 Oct 11;5(10):e13264. doi: 10.1371/journal.pone.0013264.},
   abstract = {BACKGROUND: Celiac disease is a T cell mediated-inflammatory enteropathy caused by the ingestion of gluten in genetically predisposed individuals carrying HLA-DQ2 or HLA-DQ8. The immunogenic gliadin epitopes, containing multiple glutamine and proline residues, are largely resistant to degradation by gastric and intestinal proteases. Salivary microorganisms however exhibit glutamine endoprotease activity, discovered towards glutamine- and proline-rich salivary proteins. The aim was to explore if gliadins can serve as substrates for oral microbial enzymes. METHODOLOGY/PRINCIPAL FINDINGS: Proteolytic activity in suspended dental plaque was studied towards a) gliadin-derived paranitroanilide(pNA)-linked synthetic enzyme substrates b) a mixture of natural gliadins and c) synthetic highly immunogenic gliadin peptides (33-mer of alpha2-gliadin and 26-mer of gamma-gliadin). In addition, gliadin zymography was conducted to obtain the approximate molecular weights and pH activity profiles of the gliadin-degrading oral enzymes and liquid iso-electric focusing was performed to establish overall enzyme iso-electric points. Plaque bacteria efficiently hydrolyzed Z-YPQ-pNA, Z-QQP-pNA, Z-PPF-pNA and Z-PFP-pNA, with Z-YPQ-pNA being most rapidly cleaved. Gliadin immunogenic domains were extensively degraded in the presence of oral bacteria. Gliadin zymography revealed that prominent enzymes exhibit molecular weights >70 kD and are active over a broad pH range from 3 to 10. Liquid iso-electric focusing indicated that most gliadin-degrading enzymes are acidic in nature with iso-electric points between 2.5 and 4.0. CONCLUSIONS/SIGNIFICANCE: This is the first reported evidence for gluten-degrading microorganisms associated with the upper gastro-intestinal tract. Such microorganisms may play a hitherto unappreciated role in the digestion of dietary gluten and thus protection from celiac disease in subjects at risk.},
   keywords = {Amino Acid Sequence
Chromatography, High Pressure Liquid
Enzymes/chemistry/*metabolism
Gliadin/metabolism
Glutens/*metabolism
Hydrogen-Ion Concentration
Hydrolysis
Isoelectric Focusing
Molecular Sequence Data
Mouth/*microbiology
Sequence Homology, Amino Acid
Spectrometry, Mass, Electrospray Ionization
Tandem Mass Spectrometry},
   ISSN = {1932-6203},
   Accession Number = {20948997},
   DOI = {10.1371/journal.pone.0013264},
   year = {2010},
   type = {Ref–rence Type}
}

@article{
   author = {Hernandez-Lahoz, C. and Rodriguez, S. and Tunon, A. and Saiz, A. and Santamarta, E. and Rodrigo, L.},
   title = {[Sustained clinical remission in a patient with remittent-recurrent multiple sclerosis and celiac disease gluten-free diet for 6 years]},
   journal = {Neurologia},
   volume = {24},
   number = {3},
   pages = {213-5},
   note = {Hernandez-Lahoz, C
Rodriguez, S
Tunon, A
Saiz, A
Santamarta, E
Rodrigo, L
Letter
Spain
Neurologia. 2009 Apr;24(3):213-5.},
   keywords = {Adult
*Diet, Gluten-Free
Humans
Multiple Sclerosis/*diet therapy/pathology/physiopathology
Remission Induction},
   ISSN = {0213-4853 (Print)
0213-4853},
   Accession Number = {19418302},
   year = {2009},
   type = {Ref–rence Type}
}

@article{
   author = {Herrera, M. J. and Hermoso, M. A. and Quera, R.},
   title = {[An update on the pathogenesis of celiac disease]},
   journal = {Rev Med Chil},
   volume = {137},
   number = {12},
   pages = {1617-26},
   note = {Herrera, Maria Jose
Hermoso, Marcela A
Quera, Rodrigo
English Abstract
Journal Article
Research Support, Non-U.S. Gov't
Review
Chile
Rev Med Chil. 2009 Dec;137(12):1617-26. doi: /S0034-98872009001200012. Epub 2010 Mar 17.},
   abstract = {Celiac disease (CD), with a 1% worldwide prevalence, is an enteropathy caused by an autoimmune reaction to gluten in genetically susceptible individuals, which codify for histocompatibility molecules H

license: MIT

license_type: permissive

branch_name: refs/heads/master

extension: bib