Jump to content
  • Sign Up

Search the Community

Showing results for tags 'mucosa'.



More search options

  • Search By Tags

    Type tags separated by commas.
  • Search By Author

Content Type


Forums

  • Celiac Disease: Diagnosis, Recovery, Related Disorders & Research
    • Gluten-Free and Celiac Disease Calendar of Events
    • Celiac Disease - Pre-Diagnosis, Testing & Symptoms
    • Celiac Disease - Post Diagnosis, Recovery/Treatment(s)
    • Celiac Disease - Related Disorders & Research
    • Dermatitis Herpetiformis
    • Gluten Intolerance and Behavior
  • Celiac Disease Support & Help
    • Celiac Disease - Coping With
    • Celiac Disease - Parents of Kids or Babies With Celiac Disease
    • Gab/Chat Room - To Discuss Anything BUT Celiac Disease / Gluten-Free Diet
    • Celiac Disease - Doctors
    • Celiac Disease - Teenagers & Young Adults Only
    • Celiac Disease - Pregnancy
    • Celiac Disease - Friends and Loved Ones of Celiacs
    • Celiac Meeting Room
    • Celiac Disease - Sleep
    • Celiac Disease - Support Groups
  • Gluten-Free Lifestyle
    • Gluten-Free Foods, Products, Shopping & Medications
    • Gluten-Free Recipes - Baking & Cooking Tips
    • Gluten-Free Restaurants
    • Gluten-Free Ingredients & Food Labeling Issues
    • Celiac Disease - Publications & Publicity
    • Gluten-Free Travel
    • Gluten-Free Diet & Weight Issues
    • Gluten-Free International Room (Outside USA)
    • Gluten-Free Sports and Fitness
  • When A Gluten-Free Diet Just Isn't Enough
    • Other Food Intolerance and Leaky Gut Issues
    • Super Sensitive Celiacs & Gluten Sensitive
    • Alternative Diets
  • Forum Technical Assistance
    • Board/Forum Technical Help
  • DFW/Central Texas Celiacs's Events
  • DFW/Central Texas Celiacs's Groups/Organizations in the DFW area

Blogs

There are no results to display.

There are no results to display.

Categories

  • Celiac.com Sponsors
  • Celiac Disease
  • Safe Gluten-Free Food List / Unsafe Foods & Ingredients
  • Gluten-Free Food & Product Reviews
  • Gluten-Free Recipes
    • Gluten-Free Recipes: American & International Foods
    • Gluten-Free Recipes: Biscuits, Rolls & Buns
    • Gluten-Free Recipes: Noodles & Dumplings
    • Gluten-Free Dessert Recipes: Pastries, Cakes, Cookies, etc.
    • Gluten-Free Bread Recipes
    • Gluten-Free Flour Mixes
    • Gluten-Free Kids Recipes
    • Gluten-Free Recipes: Snacks & Appetizers
    • Gluten-Free Muffin Recipes
    • Gluten-Free Pancake Recipes
    • Gluten-Free Pizza Recipes
    • Gluten-Free Recipes: Soups, Sauces, Dressings & Chowders
    • Gluten-Free Recipes: Cooking Tips
    • Gluten-Free Scone Recipes
    • Gluten-Free Waffle Recipes
  • Celiac Disease Diagnosis, Testing & Treatment
  • Miscellaneous Information on Celiac Disease
    • Additional Celiac Disease Concerns
    • Celiac Disease Research Projects, Fundraising, Epidemiology, Etc.
    • Conferences, Publicity, Pregnancy, Church, Bread Machines, Distillation & Beer
    • Gluten-Free Diet, Celiac Disease & Codex Alimentarius Wheat Starch
    • Gluten-Free Food Ingredient Labeling Regulations
    • Celiac.com Podcast Edition
  • Celiac Disease & Gluten Intolerance Research
  • Celiac Disease & Related Diseases and Disorders
    • Lists of Diseases and Disorders Associated with Celiac Disease
    • Addison's Disease and Celiac Disease
    • Anemia and Celiac Disease
    • Anorexia Nervosa, Bulimia and Celiac Disease
    • Arthritis and Celiac Disease
    • Asthma and Celiac Disease
    • Ataxia, Nerve Disease, Neuropathy, Brain Damage and Celiac Disease
    • Attention Deficit Disorder and Celiac Disease
    • Autism and Celiac Disease
    • Bacterial Overgrowth and Celiac Disease
    • Cancer, Lymphoma and Celiac Disease
    • Candida Albicans and Celiac Disease
    • Canker Sores (Aphthous Stomatitis) & Celiac Disease
    • Casein / Cows Milk Intolerance and Celiac Disease
    • Chronic Fatigue Syndrome and Celiac Disease
    • Cognitive Impairment and Celiac Disease
    • Crohn's Disease and Celiac Disease
    • Depression and Celiac Disease
    • Dermatitis Herpetiformis: Skin Condition Associated with Celiac Disease
    • Diabetes and Celiac Disease
    • Down Syndrome and Celiac Disease
    • Dyspepsia, Acid Reflux and Celiac Disease
    • Epilepsy and Celiac Disease
    • Eye Problems, Cataract and Celiac Disease
    • Fertility, Pregnancy, Miscarriage and Celiac Disease
    • Fibromyalgia and Celiac Disease
    • Flatulence (Gas) and Celiac Disease
    • Gall Bladder Disease and Celiac Disease
    • Gastrointestinal Bleeding and Celiac Disease
    • Geographic Tongue (Glossitis) and Celiac Disease
    • Growth Hormone Deficiency and Celiac Disease
    • Heart Failure and Celiac Disease
    • Infertility, Impotency and Celiac Disease
    • Inflammatory Bowel Disease and Celiac Disease
    • Intestinal Permeability and Celiac Disease
    • Irritable Bowel Syndrome and Celiac Disease
    • Kidney Disease and Celiac Disease
    • Liver Disease and Celiac Disease
    • Lupus and Celiac Disease
    • Malnutrition, Body Mass Index and Celiac Disease
    • Migraine Headaches and Celiac Disease
    • Multiple Sclerosis and Celiac Disease
    • Myasthenia Gravis Celiac Disease
    • Obesity, Overweight & Celiac Disease
    • Osteoporosis, Osteomalacia, Bone Density and Celiac Disease
    • Psoriasis and Celiac Disease
    • Refractory Celiac Disease & Collagenous Sprue
    • Sarcoidosis and Celiac Disease
    • Scleroderma and Celiac Disease
    • Schizophrenia / Mental Problems and Celiac Disease
    • Sepsis and Celiac Disease
    • Sjogrens Syndrome and Celiac Disease
    • Skin Problems and Celiac Disease
    • Sleep Disorders and Celiac Disease
    • Thrombocytopenic Purpura and Celiac Disease
    • Thyroid & Pancreatic Disorders and Celiac Disease
    • Tuberculosis and Celiac Disease
  • The Origins of Celiac Disease
  • Gluten-Free Grains and Flours
  • Oats and Celiac Disease: Are They Gluten-Free?
  • Frequently Asked Questions
  • Journal of Gluten Sensitivity
    • Journal of Gluten Sensitivity Autumn 2018 Issue
    • Journal of Gluten Sensitivity Summer 2018 Issue
    • Journal of Gluten Sensitivity Spring 2018 Issue
    • Journal of Gluten Sensitivity Winter 2018 Issue
    • Journal of Gluten Sensitivity Autumn 2017 Issue
    • Journal of Gluten Sensitivity Summer 2017 Issue
    • Journal of Gluten Sensitivity Spring 2017 Issue
    • Journal of Gluten Sensitivity Winter 2017 Issue
    • Journal of Gluten Sensitivity Autumn 2016 Issue
    • Journal of Gluten Sensitivity Summer 2016 Issue
    • Journal of Gluten Sensitivity Spring 2016 Issue
    • Journal of Gluten Sensitivity Winter 2016 Issue
    • Journal of Gluten Sensitivity Autumn 2015 Issue
    • Journal of Gluten Sensitivity Summer 2015 Issue
    • Journal of Gluten Sensitivity Spring 2015 Issue
    • Journal of Gluten Sensitivity Winter 2015 Issue
    • Journal of Gluten Sensitivity Autumn 2014 Issue
    • Journal of Gluten Sensitivity Summer 2014 Issue
    • Journal of Gluten Sensitivity Spring 2014 Issue
    • Journal of Gluten Sensitivity Winter 2014 Issue
    • Journal of Gluten Sensitivity Autumn 2013 Issue
    • Journal of Gluten Sensitivity Summer 2013 Issue
    • Journal of Gluten Sensitivity Spring 2013 Issue
    • Journal of Gluten Sensitivity Winter 2013 Issue
    • Journal of Gluten Sensitivity Autumn 2012 Issue
    • Journal of Gluten Sensitivity Summer 2012 Issue
    • Journal of Gluten Sensitivity Spring 2012 Issue
    • Journal of Gluten Sensitivity Winter 2012 Issue
    • Journal of Gluten Sensitivity Autumn 2011 Issue
    • Journal of Gluten Sensitivity Summer 2011 Issue
    • Journal of Gluten Sensitivity Spring 2006 Issue
    • Journal of Gluten Sensitivity Summer 2005 Issue
  • Celiac Disease Support Groups
    • United States of America: Celiac Disease Support Groups and Organizations
    • Outside the USA: Celiac Disease Support Groups and Contacts
  • Celiac Disease Doctor Listing
  • Kids and Celiac Disease
  • Gluten-Free Travel
  • Gluten-Free Cooking
  • Gluten-Free
  • Allergy vs. Intolerance
  • Tax Deductions for Gluten-Free Food
  • Gluten-Free Newsletters & Magazines
  • Gluten-Free & Celiac Disease Links
  • History of Celiac.com
    • History of Celiac.com Updates Through October 2007
    • Your E-mail in Support of Celiac.com 1996 to 2006

Find results in...

Find results that contain...


Date Created

  • Start

    End


Last Updated

  • Start

    End


Filter by number of...

Joined

  • Start

    End


Group


AIM


MSN


Website URL


ICQ


Yahoo


Jabber


Skype


Interests


Location

Found 9 results

  1. Celiac.com 12/03/2018 - Biomarkers in blood samples are not effective indicators for diagnosis or monitoring of celiac disease. A team of researchers recently set out to assess biomarkers of celiac disease derived from neoepitopes of deamidated gliadin peptides (DGP) and tTG fragments, and to assess their usefulness in identifying patients with celiac disease with mucosal healing. The research team included RS Choung, SK Rostamkolaei, JM Ju, EV Marietta, CT Van Dyke, JJ Rajasekaran, V Jayaraman, T Wang, K Bei, KE Rajasekaran, K Krishna, HK Krishnamurthy, and JA Murray. They are variously affiliated with the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA; Vibrant Sciences LLC, San Carlos, CA, USA; and with the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA. The team began by analyzing serum samples from 90 patients with biopsy-proven celiac disease, along with 79 healthy control subjects for immune reactivity against the tTG-DGP complex. They used a fluorescent peptide microarray platform to estimate the antibody binding intensity of each synthesized tTG-DGP epitope. They validated results in 82 patients with newly diagnosed celiac disease, and in 217 control subjects. They assessed the ability of the peptide panel to spot patients with mucosal healing based on histologic results and using serum samples from 85 patients with treated and healed celiac disease; 81 patients with treated but unhealed celiac disease who showed villous atrophy despite adhering to a gluten-free diet; 82 patients with untreated celiac disease; 27 disease control subjects who showed villous atrophy without celiac disease; and 217 healthy control subjects. To assess their data, they relied on principal component analysis followed by machine learning and support vector machine modeling. In all, the team found 172 immunogenic epitopes of the tTG-DGP complex. Compared with control subjects, celiac patients showed substantially higher immune reactivity against these epitopes. In the test group, neoepitopes derived from the tTG-DGP complex identified people with celiac disease with a remarkable 99% sensitivity and 100% specificity. Blood samples from untreated celiac patients showed the greatest average antibody-binding intensity against the tTG-DGP complex. Blood from patients with treated but unhealed CeD mucosa (15.1 ± 7.5) showed significantly higher average antibody-binding intensity than blood from patients with treated and healed CeD mucosa (5.5±3.4) (P<.001). The test spotted celiac patients with healing mucosa with 84% sensitivity and 95% specificity. The research team discovered immunogenic epitopes of the tTG-DGP complex, and found that a test that measures immune response to epitopes accurately identified both celiac patients and patients with mucosal healing. From this study, the team concludes that the biomarker method for celiac testing could be useful in both the detection and monitoring of celiac disease. Read more at: Gastroenterology.
  2. Celiac.com 07/18/2016 - Researchers still don't have a very good understanding about what triggers non-celiac wheat sensitivity. To get a better idea, a team of researchers recently set out to examine the inflammatory response in the rectal mucosa of patients with well-defined non-celiac wheat sensitivity. Specifically, they wanted to look at type 1 innate lymphoid cells in the rectal mucosa of those patients. The research team included Diana Di Liberto, Pasquale Mansueto, Alberto D'Alcamo, Marianna Lo Pizzo, Elena Lo Presti1, Girolamo Geraci, Francesca Fayer, Giuliana Guggino, Giuseppe Iacono, Francesco Dieli, and Antonio Carroccio. They are variously affiliated with the Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), University of Palermo, Palermo, Italy, the Dipartimento di Biopatologia e Biotecnologie Mediche (DIBIMED), University of Palermo, Palermo, Italy, the Dipartimento Biomedico di Medicina Interna e Specialistica (DIBIMIS), University of Palermo, Palermo, Italy, the Surgery Department at the University of Palermo in Palermo, Italy, and with the Pediatric Gastroenterology, ARNAS Di Cristina Hospital, Palermo, Italy 6Internal Medicine, Giovanni Paolo II Hospital, Sciacca (ASP Agrigento), Palermo, Italy. For their study, the team included 22 patients with irritable bowel syndrome (IBS)-like clinical presentation, diagnosed with non-celiac wheat sensitivity by double-blind placebo-controlled challenge. As control subjects, they used eight IBS patients who were not improving on wheat-free diet. Two weeks after each of the subjects consumed 80 grams of wheat daily as part of an oral challenge, the researchers isolated cells from rectal biopsies and thoroughly characterized them using fluorescence-activated cell sorting analysis for intracellular cytokines and surface markers. Analysis of the rectal biopsies of wheat-challenged non-celiac wheat sensitivity patients showed that a significant mucosal CD45+ infiltrate consisted of CD3+ and CD3− lymphocytes, with the latter spontaneously producing more interferon (IFN)-γ than IBS controls. About 30% of IFN-γ-producing CD45+ cells were T-bet+, CD56−, NKP44−, and CD117−, defining them as a type-1 innate lymphoid cells (ILC1). IFN-γ-producing ILC1 cells significantly decreased in 10 patients analyzed 2 weeks after they resumed a wheat-free diet. This study shows that IFN-γ-producing ILC1 cells infiltrate rectal mucosa, promoting the lymphoid cell population, which gives rise to non-celiac wheat sensitivity. Source: Clinical and Translational Gastroenterology, 2016 doi:10.1038/ctg.2016.35
  3. Celiac.com 06/08/2016 - Sometimes, certain cases can stand out and grab the attention of clinicians or researchers. Such is the case of a 62-year-old woman who was suffering from severe malabsorption, and diagnosed with celiac disease based on the findings of flat, small intestinal mucosa and HLA-DQ2 positivity, although celiac blood tests were negative. A team of researchers questioned the diagnosis, because the woman showed no clinical or histological improvement after a long period of strict gluten-free diet. The research team included U Volta, MG Mumolo, G Caio, E Boschetti, R Latorre, F Giancola, P Paterini, and R De Giorgio. They variously are affiliated with the Department of Medical and Surgical Sciences at the University of Bologna, and with the Gastroenterology Unit in the Department of Gastroenterology at the University of Pisa in Italy. Based on the detection of enterocyte autoantibodies, the team found that the correct diagnosis for the woman was autoimmune enteropathy. After appropriate immunosuppressive treatment, the woman experienced the disappearance of all symptoms, and a complete recovery. Based on this case, the team notes that doctors should consider autoimmune enteropathy in the differential diagnosis of malabsorption with severe villous atrophy, including those cases with negative celiac-related serology. Source: Gastroenterol Hepatol Bed Bench. 2016 Spring;9(2):140-5.
  4. Celiac.com 07/31/2014 - Although the adverse mucosal reaction in celiac disease occurs mainly in the small intestine, other mucosal surfaces in the gastrointestinal tract and the gut-associated lymphoid tissue are also affected. To better understand the impact, a research team recently set out to examine histopathological findings in the oral mucosa of celiac disease patients. Specifically, based on the assumption that the oral mucosa could reflect the histopathological intestinal inflammation seen in celiac disease patients, they wanted to determine the pattern of T-cell subsets in the oral mucosa of young adults with celiac disease. The research team included E. Bardellini, F. Amadori, A. Ravelli, M. Salemme, S. Lonardi, V. Villanacci, and A. Majorana. For their study, they enrolled a group of 37 patients with celiac disease, ranging in age from 20-38 years. Twenty-eight were female, nine male. The team broke the 37 subjects into two groups. The nineteen patients of group A were following a gluten free diet (GFD); two patients for less than one year; 6 patients between 1 and 5 years; 11 patients more than 5 years. The 18 patients (group remained untreated. Meanwhile, fifteen healthy volunteers (age range 18-35 years, 11 females and 4 males served as controls. Because the study involved observing untreated celiac patients, the team sought and received ethical approval for the research from the Ethics Committee. The team took biopsy specimens from normal looking oral mucosa. They conducted immunohistochemical investigation with monoclonal antibodies to CD3, CD4, CD8, and gamma/delta-chains T cell receptor (TCR). They found T-lymphocytic inflammatory infiltrate significantly higher in group B (p < 0.0001); as compared with group A and with the control group. Their results confirm that the oral cavity is involved with adverse reactions to celiac disease triggers, and might offer potential for celiac diagnosis. Source: Rev Esp Enferm Dig. 2014 Feb;106(2):86-91.
  5. Celiac.com 11/28/2011 - Celiac disease often results in "leaky" intestinal mucosa. This development may involve changes in hydrophobicity of the mucus surface barrier along with changes of the epithelial barrier. A team of researchers recently compared bio-physical aspects of gastrointestinal mucosa of celiac patients with control subjects, along with the effects of gluten free diet on each group. The research team included Stefania Bertolazzi, Francesco Lanzarotto, Barbara Zanini, Chiara Ricci, Vincenzo Villanacci, and Alberto Lanzini. The team set out to compare duodenal hydrophobicity as an index of mucus barrier integrity in 38 patients studied before and 68 patients during gluten-free diet, and in 90 control subjects. They also checked for regional differences of hydrophobicity in the gastro-intestinal tract. The team gauged hydrophobicity by measuring the contact angle (CA) (Rame Hart 100/10 goniometer) created by a single drop of water applied to intestinal mucosal biopsies. Once the team pooled the results and evaluated the control groups, patients with histologically normal duodenal biopsies showed significantly higher CA (620 + 90) than patients with biopsies showing Marsh 1-2 (580 + 100; p<0.02) and Marsh 3 lesions (570+ 100; p<0.02). Among the control group, the action sequence of hydrofobicity along the gastrointestinal tract follows the pattern: gastric antrum> corpus> rectum> duodenum> oesophagus> ileum. From these results, the team concludes that people with celiac disease experience reduced hydrophobicity of duodenal mucous layer, and a reduced ability to repel luminal contents. This may may contribute to the increased intestinal permeability seen in celiac disease. This change in hydrofobicity corresponds to the severity of the mucosal lesions in the patient, and is not completely reversed by gluten-free diet. Source: BMC Gastroenterology 2011, 11:119 doi:10.1186/1471-230X-11-119
  6. Celiac.com 04/27/2006 - Liver abnormalities have been found in a high percentage of celiacs when first diagnosed, around 42% according to some studies. Gluten toxicity and increased intestinal permeability have both been suspected as a cause of liver abnormalities. Serious liver disorders, including cirrhosis, have been found in association with a number of celiac disease cases which appear to resolve upon treatment and maintaining a gluten-free diet. It is not clear whether some damage to the liver may remain long term even after maintaining a gluten-free diet. Below is an interesting study (Hepatology. 2006 Mar 23;43(4):837-846) of the effects of induced liver cirrhosis on the intestinal mucosa which results in oxidative stress and an alteration of intestinal permeability, intestinal bacteria makeup, and bacterial overgrowth. Hence not only does damage to the intestine in response to gluten often result in bacterial overgrowth, but damage to the liver by gluten may also contribute to bacterial overgrowth and mucosal alterations. Damage to the liver caused by celiac disease may also have other consequences, as the liver plays many important roles including storage and production of important compounds and proteins and the removal of fat soluble toxic substances. As we are increasingly exposed to endocrine disrupting xenobiotic environmental chemicals and toxic substances, a dysfunctional livers inability to remove fat soluble toxic substances may leave celiacs more susceptible to adverse effects from these chemicals which can accumulate in adipose (fatty) tissue. In the Winter 2006 issue of Scott Adams' Celiac.com Newsletter, I discuss in detail, in Unraveling Fibromyalgia, how a dysfunctional liver and fat soluble toxic substances accumulating in innervated and vascularlized adipose tissue in the vicinity of joints may be the cause of fibromyalgia. Bacterial overgrowth has also been found in association with fibromyalgia. But clearly, lesser degrees of fatigue, muscle and joint pain, thyroid disorders, and other symptoms could also result from liver dysfunction caused by celiac disease. The inability of the liver to remove xenobiotic chemicals may also increase the risk of breast and other cancers. Recently a new review on liver disorders and celiac disease has appeared (See below - World J Gastroenterol 2006 March 14;12(10): 1493-1502 and 1503-1508): Liver Damage and the Intestinal Mucosa. One cannot ignore the secondary effects and symptoms that liver damage may add to those symptoms caused by glutens effect on the intestinal mucosa. Those unexplained aches and pains and other symptoms and disorders which have frequently been reported by some celiacs may be a result of liver dysfunction. Some notes: Elevated liver enzymes are the result of liver enzymes released by damaged liver cells. The article cites one study stating A gluten-free diet for 1 to 10 years resulted in complete normalization of liver chemistry tests in 95% patients. Normal liver chemistry tests DO NOT necessarily mean that the liver is functioning normally and that no damage remains. See: Special Considerations in Interpreting Liver Function Tests - http://www.aafp.org/afp/990415ap/2223.html Referenced Abstracts: Hepatology. 2006 Mar 23;43(4):837-846 Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: Changes in glycosylation and luminal bacteria. Natarajan SK, Ramamoorthy P, Thomas S, Basivireddy J, Kang G, Ramachandran A, Pulimood AB, Balasubramanian KA. The Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College, Vellore, India. Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl(4)-induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis. World J Gastroenterol 2006 March 14;12(10):1503-1508 Hepatobiliary and pancreatic disorders in celiac disease Hugh James Freeman Free full text: http://www.wjgnet.com/1007-9327/12/1503.asp A variety of hepatic and biliary tract disorders may complicate the clinical course of celiac disease. Some of these have been hypothesized to share common genetic factors or have a common immunopathogenesis, such as primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune forms of hepatitis or cholangitis. Other hepatic changes in celiac disease may be associated 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. Finally, pancreatic exocrine function may be impaired in celiac disease and represent a cause of treatment failure. World J Gastroenterol 2006 March 14;12(10):1493-1502 Gut flora and bacterial translocation in chronic liver disease John Almeida, Sumedha Galhenage, Jennifer Yu, Jelica Kurtovic, Stephen M Riordan Free full text: http://www.wjgnet.com/1007-9327/12/1493.asp Increasing evidence suggests that derangement of gut flora is of substantial clinical relevance to patients with cirrhosis. Intestinal bacterial overgrowth and increased bacterial translocation of gut flora from the intestinal lumen, in particular, predispose to an increased potential for bacterial infection in this group. Recent studies suggest that, in addition to their role in the pathogenesis of overt infective episodes and the clinical consequences of sepsis, gut flora contributes to the pro-inflammatory state of cirrhosis even in the absence of overt infection. Furthermore, manipulation of gut flora to augment the intestinal content of lactic acid-type bacteria at the expense of other gut flora species with more pathogenic potential may favorably influence liver function in cirrhotic patients. Here we review current concepts of the various inter-relationships between gut flora, bacterial translocation, bacterial infection, pro-inflammatory cytokine production and liver function in this group.
  7. Celiac.com 02/03/2010 - Celiac disease increases production of IL-17A by cells that also make IFN-gamma. Recently, a research team set out to characterize the expression of IL-17A-producing cells in celiac disease. The team included I. Monteleone, M. Sarra, G. Del Vecchio Blanco, O. A. Paoluzi, E. Franzè, D. Fina, A. Fabrizi, T. T. Macdonald, F. Pallone, and G. Monteleone of the Department of Internal Medicine at the University of Tor Vergata in Rome, Italy. Infiltration of the mucosa with IFN-gamma-secreting Th1 cells is one of the features associated with celiac disease. Recent studies have shown the pathogenic effects previously attributed to Th1 cells may in fact be caused by a novel subset of T cells, termed Th17 cells, and noted for expressing high levels of IL-17A. In this study, the team set out to characterize the expression of IL-17A-producing cells in celiac disease. Using real-time PCR and ELISA, the team showed that expression of IL-17A RNA and protein is greater in active celiac disease biopsy specimens than in specimens from inactive celiac disease, and normal mucosal biopsies. Through flow cytometry, the team confirmed that the mucosa of celiac disease patients overproduces IL-17A, and that the main sources for this overproduction were CD4(+) and CD4(+)CD8(+) cells. Most IL-17A-producing CD4(+) and CD4(+)CD8(+) cells co-expressed IFN-gamma but did not co-express CD161. Including a peptic-tryptic digest of gliadin to ex-vivo organ cultures of duodenal biopsy specimens taken from patients with inactive celiac disease enhanced IL-17A production by both CD4(+) and CD4(+)CD8(+) cells. Since the team showed earlier that patients with celiac disease overproduced IL-21, a T cell-derived cytokine involved in the control of Th17 cell responses, they next determined whether IL-21 was responsible for regulating IL-17A expression. Blocking IL-21 action with a neutralizing IL-21 Ab lowered total IL-17A expression in cultures of active celiac disease and peptic-tryptic digest of gliadin-treated celiac disease biopsy specimens. From the data, the team concludes that celiac disease increases IL-17A, which is produced by cells that also produce IFN-gamma. Source: Journal of Immunology, 2010 Jan 8.
  8. TI- Disaccharidasen-Aktivitaten als Beurteilungskriterium der Dunndarmschleimhaut. AU- Stern M; Plettner C JN- Monatsschr Kinderheilkd; 131 (5) p264-8 PY- May 1983 AB- Activities of lactase, sucrase, and maltase were determined in small intestinal biopsies of 125 children with Coeliac disease, cows milk protein intolerance, transient gluten intolerance, nonspecific enteropathies, and controls. Four cases of primary disaccharidase deficiencies could be identified. In the enteropathies, morphometric data were more closely correlated to the degree of the mucosal lesion (r = -0.92 for crypt depth) than were disaccharidase activities (r = 0.61 for lactase). In a stepwise discriminate analysis of the patient groups, based upon immunological, morphometric, and biochemical variables, lactase activity was a valuable secondary criterion, ranking third among the variables used.
  9. AU- Kaczmarski M; Lisiecka M; Kurpatkowska B; Jastrzebska J JN- Acta Med Pol; 30 (3-4) p129-39 PY- 1989 AB- Quantitative estimation of the infiltration by intraepithelial lymphocytes and eosinophils of the mucosa was carried out in 21 children with cows milk and 35 children with gluten intolerance. Before dietary treatment, a statistically significant increase in the infiltration by LIE in children with milk intolerance to the mean value of 34.1 cells and in children with gluten intolerance to 39.0 cells was found, what statistically significantly differed from the mean value of LIE for the control group (19.0 cells/100 epithelial cells). The eosinophilic infiltration in this phase of the disease was noted in 38% of children with cows milk intolerance (16.9 cells/mm2) and in 27% of children with gluten intolerance (28.6 cells/mm2). After 8-24 months of elimination diets--a decrease in the mean value of the LIE infiltration in the mucosa was revealed in both treated groups.
×