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  • Jefferson Adams
    Jefferson Adams

    Celiac Disease Five Times More Common in People with Severe Autoimmune Liver Disease

    Celiac.com 09/16/2008 - A team of researchers recently set out to examine the connection between celiac disease and primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis.

    The research team was made up of Alberto Rubio-Tapia, Ahmad S. Abdulkarim, Patricia K. Krause, S. Breanndan Moore, Joseph A. Murray, and Russell H. Wiesner.

    The team measured the rates of occurrence for tissue transglutaminase antibodies (tTGAs) and endomysial antibodies (EMAs) in end-stage autoimmune liver disease (ESALD). They then correlated autoantibodies and the human leucocyte antigen (HLA) haplotype. Finally, they assessed the effect of liver transplantation on antibody kinetics.

    The team tested tTGA levels on blood samples from 488 prior to transplant. 310 of these had ESALD, and 178 had non-autoimmune disease. The team tested positive samples for EMAs, and retested at 6-12 and =24 months after transplant. They then correlated their results with the HLA type of the recipient.

    The results showed that 3% of ESALD patients showed evidence of celiac disease compared to 0.6% of those with non-autoimmune disease.  This represents a five-fold greater risk for those with ESALD. The prevalence of tTGAs was 14.2 for ESALD patients compared to 5.4% for those with non-autoimmune disease (P = 0.0001). The prevalence of EMAs was 4.3 for ESALD patients compared to 0.78% for those with non-autoimmune disease (P = 0.01)—significantly higher for those with HLA-DQ2 or HLA-DQ8 haplotypes.

    After transplant, tTGAs and EMAs normalized in 94% and 100%, respectively, without gluten elimination. Also, three out of five patients with classical symptoms of celiac disease improved. The research team found two cases of intestinal lymphoma in two cases that showed no clinical signs of celiac disease.

    Patients with ESALD, particularly those with HLA-DQ2 or HLA-DQ8 gene haplotypes, showed greater occurrances of celiac disease-associated antibodies. Following liver transplants, both tTGA and EMA levels decreased without gluten withdrawal.

    The team also concluded that symptoms of celiac disease might be improved through immune suppression, but those improvements may not prevent the disease from progressing to intestinal lymphoma.

    The study doesn’t tell what effect, if any, early detection and treatment of celiac disease might have on rates of ESALD. It would be helpful to know if celiac disease contributes to liver disease, if liver disease contributes to celiac disease, or if some third connection links the two. Until then, we’ll just have to keep a tight eye on developments concerning celiac disease and liver disease.

    Liver Int. 2008; 28(4): 467-476.



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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Scott Adams
    Gastroenterology 2002;122:881-888.
    Celiac.com 05/02/2002 - In the April issue of Gastroenterology Dr. Pekka Collin of the University of Tampere, Finland, and colleagues describe four patients with severe liver disease who were also found to have celiac disease. One of the patients had congenital liver fibrosis, one had massive hepatic steatosis, and two had progressive hepatitis without apparent origin. Three of the four were considered for liver transplantation. In each case a gluten-free diet reversed heptic dysfunction.
    The reasearchers then studied the prevalence of celiac disease in 185 adults who had already undergone liver transplantation. Eight of them (4.3%) tested positive for celiac disease, and it had already been detected in six of the eight prior to transplantation. Only one the the diagnosed patients followed a strict gluten-free diet. Of these eight patients, three had primary biliary cirrhosis, one had autoimmune hepatitis, one had primary sclerosing cholangitis, and one had congenital liver fibrosis. Additionally, one of the patients had autoimmune hepatitis and one had secondary sclerosing cholangitis.
    The researchers also noted that not all of patients with both liver and celiac disease showed symptoms of celiac disease, which suggests that the liver disease may not be caused by malabsorption. Dr. Collin suggests that it could be a "gluten-dependent immunologically induced extraintestinal manifestation of celiac disease."
    The researchers conclude that some cases of serious liver disease may result from unrecognized celiac disease, and patients with severe liver disease should also be evaluated for celiac disease. Further, dietary treatment in patients with both celiac and liver diseases may prevent progression to hepatic failure, even in cases in which liver transplantation is considered.

    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 07/13/2011 - Some people who follow a gluten-free diet due to celiac disease may develop unusually elevated levels of liver enzymes, according to researchers from Finland. The results are reported online in the American Journal of Gastroenterology.
    Contrary to some earlier studies, the results show that only a small minority of these celiac disease patients showed elevated transaminase levels.
    Dr. Markku Maki from University of Tampere points out that doctors don't routinely test transaminase levels in newly diagnosed celiac disease patients.
    With this in mind, the research team examined the prevalence and gluten dependency of hypertransaminasemia in 313 untreated and 339 treated adult celiac disease patients and in 237 nonceliac control subjects.
    They checked transaminase levels in 130 celiac disease patients at diagnosis and after one year on a gluten-free diet. They also conducted a before and after gluten challenge in 25 treated celiac patients who showed clinical remission.
    Their cross-sectional study showed elevated aspartate transaminase (AST) levels in a similar proportion of untreated celiac patients (11%), treated celiac patients (8%), and healthy controls (9%). Earlier studies showed that up to half of celiac disease patients may have elevated serum liver enzyme levels at diagnosis.
    The celiac patients showed significantly higher rates of hypertransaminasemia when their celiac symptoms were severe or moderate than when their symptoms were mild or nonexistent (23% vs 9%; P=0.03).
    The team suggests that routine investigation of liver enzymes in celiac disease patients would likely provide the same yield as in the general population--"at least in populations with high clinical prevalence of celiac disease," they say.
    They further suggest that clinicians reevaluate strategies for routine investigation of liver enzymes in celiac disease patients.
    After one year, results of the gluten-free diet trial showed that serum AST levels dropped significantly, even to normal levels, in conjunction with the disappearance of clinical symptoms.
    In the gluten-challenge study, gluten antibodies reappeared in the blood samples of nine of the 25 celiac patients who had previously been in clinical remission. 18 of the 25 developed gastrointestinal symptoms. AST and 11 patients showed elevated levels of alanine transaminase (ALT).
    When the patients resumed their gluten-free diets, their symptoms resolved, serum endomysial antibodies became undetectable, and serum transaminase levels returned to normal levels.
    Dr. Maki says that "gluten may induce liver disease in celiac disease patients. Even if the liver manifestation is infrequent and mostly mild."
    This is a potentially important discovery, because as Dr. Maki points out, when people with celiac disease regularly consume wheat, rye, and barley gluten, "the environmental insult in celiac disease, seem to trigger an autoimmune loop in genetically susceptible persons where formed autoantibodies target the autoantigen, transglutaminase 2, also in the liver."
    Dr. Maki adds that the biological implications of this can be studied further. In the meantime, he stops short of recommending routine screening with liver function tests when celiac patients are first diagnosed, saying that there is simply no evidence to support that practice.
    However, he does say that if a case finding for celiac includes elevated liver enzymes, patients should be checked for normalization of liver values once on a gluten-free diet.
    Source:

     Am J Gastroenterol 2011.

    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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