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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.

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    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.

    Scott Adams
    Author: Hagander B; Berg NO; Brandt L; Nord en A; Sj olund K; Stenstam M.
    Source: Lancet, 1977 Aug 6, 2:8032, 270-2.
    In an attempt to determine the frequency of liver injury in adult coeliac disease (A.C.D.) the case records of 74 consecutive patients were examined. In 13 cases histological sections of the liver were available and in 5 of these there were signs of reactive hepatitis. Histological signs of distinct hepatic injury with cirrhosis and/or chronic active hepatitis were found in 7 other patients. In 5 of these serum-IgA was normal, whereas 16 out of 20 control patients with liver cirrhosis not associated with A.C.D. had raised serum-IgA. Serum-aspartate-aminotransferase and serum-alanine-aminotransferase were determined in 53 patients; 29 had raised concentrations. In 19 patients serum-aminotransferases were repeatedly determined before and during the dietary regimen and there was a significant reduction in enzyme concentrations during treatment. The median concentration of serum-alkaline-phosphatase was also reduced during treatment but not significantly. The histological evidence of liver injury in 16% and the abnormal liver-function tests in 39% of the patients indicate that hepatic injury is common in A.C.D. Since liver-function tests or liver biopsy specimens were available for only about two-thirds of the patients, liver damage in A.C.D. may be more common than indicated by these results. The effect of a gluten-free diet on aminotransferase concentrations indicates that the liver injury may be reversible and suggests that in some A.C.D. patients, progressive liver damage may be prevented by suitable treatment. Since A.C.D. is not always recognized, the diagnosis should be considered in patients with liver disease of unknown aetiology.

    Roy Jamron
    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.

    Jefferson Adams
    Celiac.com 11/25/2010 - Portal hypertension is high blood pressure within the portal vein and its tributaries. Non-cirrhotic intrahepatic portal hypertension (NCIPH) is portal hypertension that occurs within the liver, that is not triggered by cirrhosis. NCIPH is generally regarded to have a benign prognosis.
    A research team examined whether gut-derived prothrombotic factors may contribute to the pathogenesis and prognosis of non-cirrhotic intrahepatic portal hypertension (NCIPH). Their results led them to conclude that gut-derived prothrombotic factors may in fact contribute to the pathogenesis and prognosis of NCIPH.
    The team included C. E. Eapen, Peter Nightingale, Stefan G. Hubscher, Peter J. Lane, Timothy Plant, Dimitris Velissaris, and Elwyn Elias.
    For their study, the team followed a cohort at a tertiary referral center. They analyzed prognostic indicators in 34 NCIPH patients. The team also looked for associated gut disorders.
    Survival rates for transplant-free NCIPH patients from ï¬rst presentation with NCIPH at 1, 5, and 10 years was 94% (SE: 4.2%), 84% (6.6%), and 69% (9.8%), respectively.
    Importantly, 18 patients (53%) showed decompensated liver disease.
    Three patients (9%) showed ulcerative colitis while ï¬ve of 31 patients (16%) tested had celiac disease. Kaplan–Meier analysis showed that the presence of celiac disease was a predictor of shorter transplant-free survival for these patients (p = 0.018).
    Multivariable Cox regression analysis showed that people who were older when ï¬rst presenting with NCIPH, those with hepatic encephalopathy, and those with portal vein thrombosis had lower rates of transplant-free survival
    More than one-third (36%) of NCIPH patients showed elevated levels of initial serum IgA anticardiolipin antibody (CLPA), compared with just 6% with Budd–Chiari syndrome (p = 0.032, Fisher’s exact test) and no patients with celiac disease
    without concomitant liver disease (p = 0.007).
    Under the team's prognostic factors, 53% of NCIPH patients ultimately progress to liver failure, and their data suggest that intestinal disease plays a role in the pathogenesis of intrahepatic portal vein occlusion leading to NCIPH.
    Source:

    Dig Dis Sci. DOI 10.1007/s10620-010-1278-2

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    This  thread has been so helpful. My tests came back negative, but i experience a lot of these symptoms when  i eat wheat  and grains.  I get this severe pain underneath my left and right ribs that radiates all down my sides. It feels almost like a burning / tight sensation and almost like the inside of my stomach is itchy! Super bloated to the point of looking pregnant, chronic d, brain fog, irritability, super loud stomach gurgling, gas.  Ive just started the diet  so I'm  still quit
    I wrote you in thread asking what you found out ? My little guy is saying the same thing. 
    What did you find out about your daughter ? My son is 6 and has used the exact same sentence!! He feels like there is a bubble in his throat. He has been complaining on and off for the last year and recently it seems he complains more Ans Wants me to make a doctor appt. he had reflux bad as a baby until about 2.5 and allergies to fomula Ans my milk but since then I thought that all went away. 
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