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    Roy S. Jamron holds a B.S. in Physics from the University of Michigan and an M.S. in Engineering Applied Science from the University of California at Davis, and independently investigates the latest research on celiac disease and related disorders.

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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.

    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 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 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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    I was misdiagnosed IBS over 20 plus years. I was diagnosed IBS by symptoms only. My cousin is a gold standard celiac. My story is complicated my medical records now state I am NCGS. Overtime my convoluted story it has come to light I am a DH celiac.  I have always had gi issues My whole life ! Numerous skin rash issues dermatitis etc, and plenty of odd symptoms that I realize now we're celiac. I had your symptoms and many more ataxia etc. No IBS was found on my scopes. It might not be
    Doritos does make a few gluten-free versions.     
    Just wanted to chime in. During my 2 plus years of healing I had joint pain and muscle pain with some of the nightshade mainly peppers and tomato. I stopped them. I can now eat them again. My theory is when my gut gets cc my holey gut dumps some of my food in my blood stream and my already ticked off immune system let's me know what is allowed. Apparently for a time nightshades  of potato, tomatos, and peppers were an issue. I was able to gradually introduce potatoes first and then tomatos, then
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