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  • Scott Adams
    Scott Adams
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    Primary Biliary Liver Cirrhosis Linked to Celiac Disease

    Aliment Pharmacol Ther. 2005; 21 (5): 515-518.

    Celiac.com 06/08/2005 – Australian researchers searched Medline and other references for cases of celiac disease and liver disease from 1966 to 2003. They found six studies that reported liver biochemistry in 591 celiac disease patients—out of which a full 248 had abnormal results—the most common of which being elevated transaminases. In 115 of 130 patients with elevated transaminases a gluten-free diet returned the levels to normal.

    The researchers found a much greater association of primary biliary cirrhosis and advanced liver disease in those with celiac disease than expected, and conclude that abnormal liver biochemistry is frequent in untreated celiac disease—and those with it should undergo tissue transglutaminase screening for celiac disease—which could lead to a proper diagnosis in many cases. In rare cases celiac-induced hepatitis may progress to end-stage liver disease.


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    I was diagnosed with celiac in 2000, and in 2004 had surgery and my liver enzymes elevated. An ultrasound revealed fatty liver, but the enzymes have remained elevated, were going down, and now going back up again. I am seeking further testing and evaluation for possible cirrhosis.

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    Have not been "officially" diagnosed with Celiac, but am pretty sure I have it since every time I eat anything with gluten, I suffer incredible after-effects. Been on a mostly gluten-free diet for about 3-4 years, but occasionally fall off wagon and have some pizza or a cupcake, then my innards get all inflamed & sore & swollen again.

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    Nov 26th will mark the one year anniversary of the passing of my younger sister of liver cancer. Because I have had GI issues and was (I think) erroneously diagnosed as having moderate severe colitis, I am concerned that perhaps she also had celiac, but instead was also misdiagnosed and had her GB removed. She complained after the removal that she wasn't feeling better. So now my concerns for my own self are higher as I am finding that there is more to worry and be concerned about then just watching my diet. Thank you for all the articles and info this site has.

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    I have primary biliary cirrhosis, diagnosed in 2009. Then I got pregnant and all my liver test results were all so high including my bile acids which made me so very itchy. After having my little girl, it took 4 months for the Usro medication to start working and for the itch to stop. I have been in urso for 3 years now and been fine. I am now pregnant again and the itch has come back which I knew it was. My urso dose has increased from 1g a day to 3g a day, maximum dose I can be on. I just received a phone call from my consultant to say all my liver tests results have gone down to normal levels except the bile acids which have gone up. The doctor did seem quite surprised about the other going down as they didn't do that before. I told her I was on a gluten free diet and had been for 2 months now. I am amazed at the blood results going into normal levels as they have never been normal. But bile acids have increased but I know from experience and from going to a London hospital i who specialize in liver problems in pregnancy, that bile acids are related to hormone levels and of course pregnancy has increased these massively. So in understanding that gluten could have possibly lowered my other liver function tests they could not touch the bile acids if they are hugely affected by hormones, as I see it, gluten would not have any affect on hormones levels. So I am quite amazed and do believe the gluten free diet is helping me. It is a long term thing now, but am happy and very interested to see what my liver results are like in a years time and very interested to read articles like this.

     

    Thanks,

    Liz

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    I have PBC, underwent a Liver transplant in Nov 2009, and I can't understand why my Doctors never once mentioned this to me? I had my Transplant at UCSF by Dr. Nancy Asher. This possibility was never discussed with me, and since then, my daughter who is now 30, has been diagnosed with an auto-immune disease, guess what that disease is called? celiac disease!!!!!

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  • About Me

    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

    Jefferson Adams
    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.


    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 07/23/2014 - Transaminasemia develops through various pathways in patients with celiac disease. Currently, there is not much information on risk factors specifically attributable to celiac disease.
    A team of researchers recently set out to determine what factors contribute to hypertransaminasemia in patients with celiac disease. The research team included B. Zanini B, R. Baschè A., Ferraresi, M.G. Pigozzi, C. Ricci, F. Lanzarotto, V. Villanacci, and A. Lanzini.
    They analyzed data collected from consecutive patients referred from January 1997 through December 2009 to the celiac disease clinic at the Spedali Civili of Brescia, Italy. They then used serologic and biopsy analysis to assess the factors influencing hypertransaminasemia in 683 patients with celiac disease (group A), and 304 patients with functional gastrointestinal syndromes (group . Both groups were about the same average age and range.
    The research team detected hypertransaminasemia in 138 patients in group A (20%). Factors associated with the condition included malabsorption (odds ratio [OR], 2.22; P = .004), diarrhea (OR, 1.72; P = .005), and increasing severity of mucosal lesion (Marsh-Oberhuber class; OR, 1.46; P = .001), but not body mass index (BMI) or the blood levels of tissue-transglutaminase antibodies (tTG).
    The team also detected hypertransaminasemia in 22 patients from group B (7%), which they found to be associated with the World Health Organization's BMI categories (OR, 7.9; P < .001). A total of 313 patients from group A had significantly higher levels of tTG at baseline (25.2 ± 16.9 U/L aspartate aminotransferase [AST]) than a similar bunch from group B (20.6 ± 9.9 U/L AST, P < .0001). These levels were related to BMI in group B (P = .0012), but not group A.
    Patients eating gluten-free diets saw levels of AST decrease from 25.2 ± 16.9 U/L to 19.9 ± 6.6 U/L (P < .0001). This decrease was independent of the changes of duodenal histology and tTG and correlated with BMI (P = .0007). Meanwhile, the prevalence of hypertransaminasemia in gluten-free patients decreased from 13% to 4%.
    These study results show that hypertransaminasemia is more common in people with celiac disease than in patients with functional gut syndromes. Also, hypertransaminasemia is related to the severity of the duodenal lesion and malabsorption, but unrelated to BMI.
    By contrast, the control group, with functional gut syndromes, showed a positive correlation between the levels of AST and BMI. This relationship was restored when patients with celiac disease began to follow gluten-free diets.
    Source:
    Clin Gastroenterol Hepatol. 2014 May;12(5):804-810.e2. doi: 10.1016/j.cgh.2013.10.033. Epub 2013 Nov 7.

    Jefferson Adams
    Celiac.com 03/16/2015 - Researchers don't really have too much data on celiac disease in patients with cryptogenic cirrhosis or idiopathic noncirrhotic intrahepatic portal hypertension (NCIPH).
    In India, a research team recently set out to look for celiac disease in patients with portal hypertension. The research team included Rakhi Maiwall, Ashish Goel, Anna B. Pulimood, Sudhir Babji, J. Sophia, Chaya Prasad, K. A. Balasubramanian, Banumathi Ramakrishna, Susy Kurian, G. and John Fletcher.
    For their study, the team enrolled 61 consecutive patients with portal hypertension having cryptogenic chronic liver disease, including 14 with NCIPH, along with 59 patients with hepatitis B- or C-related cirrhosis as control subjects.
    They looked at tissue transglutaminase (tTG) antibody and duodenal histology in study patients. They found six cases of celiac disease, including two NCIPH patients, while they found none in control subjects.
    Duodenal biopsies for a significant percentage of the remaining study subjects showed villous atrophy, crypt hyperplasia, and lamina propria inflammation, not accompanied by raised intraepithelial lymphocytes (IELs), far more commonly than in controls.
    Study subjects with portal hypertension having cryptogenic chronic liver disease showed an unexpectedly high rate of tTG antibody positivity (66%), as compared to 29% in controls (p-value < 0.001), which could indicate false-positive test result.
    This study showed that 10% of patients with unexplained portal hypertension (cryptogenic chronic liver disease) had associated celiac disease. In addition, an unexplained enteropathy was seen in a significant proportion of study patients, more so in patients with cryptogenic chronic liver disease. This finding warrants further investigation.
    Source:
    Indian Journal of Gastroenterology. November 2014, Volume 33, Issue 6, pp 517-523

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