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    In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I founded The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

  • Related Articles

    Scott Adams
    Author: Bardella MT; Fraquelli M; Quatrini M; Molteni N; Bianchi P; Conte D
    Address: Cattedra di Gastroenterologia, Universit a degli Studi di Milano, IRCCS Ospedale Maggiore, Italy.
    Source: Hepatology, 1995 Sep, 22:3, 833-6
    The prevalence of hypertransaminasemia and the effect of gluten-free diet (GFD) were evaluated in 158 consecutive adult celiac patients, 127 women and 31 men, aged 18 to 68 years (mean, 32). At diagnosis, 67 patients (42%) had raised aspartate and/or alanine transaminase levels (AST and ALT; mean, 47 IU/L, range, 30 to 190; and 61 IU/L, range, 25 to 470, respectively), whereas 91 patients had normal liver function tests (LFT). Patients with and without hypertransaminasemia were comparable for epidemiological data, body mass index (18.5 vs. 19.6), and severity of intestinal histological involvement. All patients were given a strict GFD and were followed for 1 to 10 years (median, 4). At 1 year, a highly significant improvement in intestinal histology was observed in both groups.

    Roy Jamron
    Celiac.com 05/31/2006 - I previously discussed how liver abnormalities are highly prevalent in celiac disease. Why damage to the liver occurs is unknown, and gluten toxicity and increased intestinal permeability have been proposed as factors. The following free full text article appearing in the current issue of Gastroenterology may shed light on why liver damage occurs in celiacs.
    Toll-like receptors (TLRs) reside on the surface of many cells which participate in the immune system. TLRs sense molecules present in pathogens but not the host, and when the immune system senses these molecules, chemicals are released which set off inflammatory and anti-pathogen responses. One class of molecules recognized by TLRs and common to most pathogenic bacteria is lipopolysaccharides (LPS).
    Gluten increases intestinal permeability in celiacs. The disruption of the intestinal barrier permits endotoxins, such as LPS, from gut bacteria to reach the portal vein of the liver triggering a TLR response from immune cells in the liver. Proinflammatory mediators are released cascading into the release of more chemicals leading to inflammation and liver damage. This may be the cause of liver damage in celiacs. Gluten itself could also trigger a liver immune response. Kupffer cells in the liver are capable of antigen presentation to T cells, along with liver dendritic cells, and could initiate a T cell response to gluten within the liver.
    The following article is somewhat technical, but discusses the role of various liver cells involved in the immune process and how intestinal permeability and TLRs contribute to liver injury. The article is a good read and provides valuable information about the liver I have not seen elsewhere.
    Gastroenterology Volume 130, Issue 6, Pages 1886-1900 (May 2006)
    Toll-Like Receptor Signaling in the Liver
    Robert F. Schwabe, Ekihiro Seki, David A. Brenner
    Free Full Text:
    http://www.gastrojournal.org/article/PIIS0016508506000655/fulltext

    Jefferson Adams
    Celiac.com 07/03/2009 - A new study provides demonstrates that small intestinal bacterial overgrowth and increased intestinal permeability are both associated with non-alcoholic fatty liver disease (NAFLD).
    Previous studies have suggested that bacteria from the intestine might play a role in NAFLD, which is the hepatic component of the Metabolic Syndrome. NAFLD can worsen to nonalcoholic steatohepatitis, and some experts have wondered if this progression might be promoted by liver exposure to gut bacteria.
    A team of researchers, led by Antonio Grieco of Rome, set out to answer this question by investigating gut permeability in patients with NAFLD and comparing the results to patients with untreated celiac disease and known susceptibility to this condition, and with healthy volunteers.
    The research team included Luca Miele, Venanzio Valenza, Giuseppe La Torre, Massimo Montalto, Giovanni Cammarota, Riccardo Ricci, Roberta Masciana, Alessandra Forgione, Maria Gabrieli, Germano Perotti, Fabio Vecchio, Gian Ludovico Rapaccini, Giovanni Gasbarrini, Christopher Day, and Antonio Grieco.
    They studied 35 patients with biopsy-confirmed NAFLD, 27 with celiac disease and 24 healthy volunteers. For each participant, the research team checked levels of small intestinal bacterial overgrowth using a glucose breath test. They evaluated intestinal permeability by examining urinary excretion of Cr-EDTA. They then assessed the integrity of tight junctions within the gut via duodenal biopsy.
    "The main findings of this study are that both intestinal permeability and the prevalence of small intestinal bacterial overgrowth are increased in patients with NAFLD and correlate with the severity of steatosis," the authors report. "Disruption of tight junction integrity may explain the increased permeability in these patients."
    The authors hypothesize that small intestinal bacterial overgrowth and/or the associated increase in gut permeability may cause steatosis. This hypothesis is supported by studies on mice, and by reports that probiotics can improve steatosis resulting from a high fat diet.
    One important note was that the study showed no connection between either small intestinal bacterial overgrowth or intestinal permeability and steatohepatitis or fibrosis, which suggests gut bacteria do not play a role in the transformation of NAFLD to more serious liver disease.
    "In conclusion," the authors write, "we have demonstrated that NAFLD is associated with increased intestinal permeability and small intestinal bacterial overgrowth and that these factors are associated with the severity of hepatic steatosis."
    More study is needed to nail down the exact causal relationship, which, once understood, could help scientists develop new therapies for NAFLD that incorporate the microbiome of the gut.''
    According to colleagues Elisabetta Bugianesi and Ester Vanni of the University of Turin, "The study...raises the possibility that gut microbiota and intestine permeability are important mediators of diet-induced metabolic disturbances in NAFLD."
    Bugianesi and Vanni add that lifestyle-focused therapy would likely present the best treatment for NAFLD, but suggest that influencing gut flora by antibiotics, prebiotics, and probiotics might help offset the effects of unbalanced diets on metabolic conditions.

    Article: "Increased Intestinal Permeability and Tight Junction Alterations in Non-Alcoholic Fatty Liver Disease (NAFLD)."
    Editorial: "The Gut-Liver Axis in Nonalcoholic Fatty Liver Disease (NAFLD): Another Pathway to Insulin Resistance?" Bugianesi, Elisabetta; Vanni, Ester. Hepatology; June 2009.

    Hepatology. 2009 Jun;49(6):1877-87.
     

    Jefferson Adams
    Celiac.com 09/09/2013 - Many people with celiac disease show slightly elevated liver enzymes, though these enzyme levels usually return to normal after gluten-free diet.
    A team of researchers recently set out to investigate the cause and prevalence of altered liver function tests in celiac patients, basally and after 1 year of gluten-free diet.
    The research team included Giovanni Casella, Elisabetta Antonelli, Camillo Di Bella, Vincenzo Villanacci, Lucia Fanini, Vittorio Baldini, and Gabrio Bassotti.
    They are affiliated with the Medical Department, and the Clinical Pathology Department of Desio Hospital in Monza and Brianza, Italy, the Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology Section at the University of Perugia in Perugia, Italy, and with the Department of Laboratory Diagnostics, Pathology Section, Brescia, Italy.
    The team gathered data from 245 untreated celiac disease patients, 196 women and 49 men, ranging in age from 15 to 80 years. They then analyzed the data, and assessed the results of liver function tests performed before and after diet, as well as associated liver pathologies.
    They found that 43 (17.5%) of the 245 patients, showed elevated levels of one or both aminotransferases;
    In 41 patients (95%) the elevation was mild, meaning that it was less than five times the upper reference limit. The remaining two patients (5%) showed marked elevation, meaning levels more than ten times the upper reference limit.
    After patients eliminated gluten for one year, aminotransferase levels normalized in all but four patients, who had HCV infection or primary biliary cirrhosis.
    Celiac patients who show hypertransaminaseaemia at diagnosis, and who do not show normalization of liver enzymes after 12 months of gluten-free diet, likely suffer from coexisting liver disease.
    In such cases, the research team recommends further assessment to assess the possible coexisting liver disease.
    Spotting and treating coexisting liver disease in celiac patients is important for improving liver function and preventing possible complications.
    Source:
    Liver International. 2013;33(7):1128-1131.

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    It’s so awful isn’t it. Do you ever get dizziness and a numb face? Mines just awful atm and I constantly think oh it must be something more serious   It’s so awful isn’t it. Do you ever get dizziness and a numb face? Mines just awful atm and Iconstantly think oh it must besomething more serious  
    Vomiting, passing out, abdominal pain that occurs as soon as my stomach empties into the small intestine (I consume mushy, well-cooked foods then), hives, allergic reactions are way more severe, indigestion, anxiety, irrtability, fatigue, achy body, tingling, become lactose intolerant, constipation, diarrhea.  Yep, many things.  Symptoms can change too.  Celiac disease is like a chameleon.  Symptoms for me can last for about six months.  Most severe the first week and gradually getting better.  
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