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Found 16 results

  1. Celiac.com 10/24/2018 - Although some research has shown a connection between a gluten-free diet, altered macronutrient intake and metabolic syndrome, not much good data exists on the risk of nonalcoholic fatty liver disease in patients with celiac disease who follow a gluten-free diet. A team of researchers recently set out to assess the prevalence and relative risk of nonalcoholic fatty liver disease in celiac patients treated with a gluten-free diet. The research team included F. Tovoli; G. Negrini; R. Farì; E. Guidetti; C. Faggiano; L. Napoli; L. Bolondi; and A. Granito of the Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. For many patients with metabolic syndrome, nonalcoholic fatty liver disease is common. To try to get some better information, the researchers devised a case-control study, with prospective enrollment of celiac disease outpatients following a gluten-free diet and control subjects. For the study, the team matched patients by age, gender and metabolic risk factors, such as overweight, diabetes mellitus, total cholesterol, and triglycerides, using a 1:1 ratio. The team diagnosed nonalcoholic fatty liver disease according to the criteria set by the European Association for the Study of the Liver. In all, they compared 202 celiac disease patients and 202 control subjects. The raw rate of nonalcoholic fatty liver disease was 34.7% and 21.8% in the celiac disease and control group, respectively. Using binary logistic regression, the team demonstrated that those with celiac disease faced an increased risk for nonalcoholic fatty liver disease. Meanwhile, the relative risk for nonalcoholic fatty liver disease was substantially higher in non-overweight celiac disease patients. Nearly 35% of celiac disease patients on a gluten-free diet also had nonalcoholic fatty liver disease, that’s a risk three times greater than the general population. The team recommends that doctors tailor their celiac treatment approaches to better help celiac disease patients with nonalcoholic fatty liver disease to get proper nutritional intake, which will help to reduce the risk of long-term liver-related events. Source: Aliment Pharmacol Ther. 2018;48(5):538-546.
  2. Just a warning to avoid acetimenophen (Tylenol, APAP). This link is a story about a woman who took several OTC meds for a cold and her liver was destroyed by the acetimenophen in them. Did you know they also call acetimenophen APAP on some med labels? So she took several meds with it and her liver was ruined. http://wjla.com/news/nation-world/ohio-woman-treats-cold-symptoms-ends-up-with-a-liver-transplant A WebMD article on unrecognized ingredients in OTC drugs is linked below. The tricky thing is you have to check cold meds etc for APAP and acedtimenophen and make sure you aren't exceeding the liver destroying toxic limit each day with the combo of meds. https://www.webmd.com/pain-management/news/20110502/many-unaware-of-otc-pain-relievers-ingredients-risks#1 Not something most people are thinking about at the drug store I figure.
  3. Can gluten-exposure cause elevated liver enzymes during DH rash outbreak?
  4. I was diagnosed with celiac disease in 2008. I have had a positive result since going gluten-free, with excellent health and perfect annual blood work. However, I just had my annual physical and lab work and my doctor just called to tell me that several liver function tests are significantly elevated (more than doubling since last year, and all outside the normal range now). Of course I am anxious as I await now a liver ultrasound and appt with a gastroenterologist to discuss potential liver-related problems. Has anyone here experienced liver damage or liver disease as a result of having celiac disease. Or, could this indicate yet another autoimmune disease coming on? Please share and advise! Thanks! ALT was 23 last year, now 58 AST was 24 last year now 29 (not significant and still within normal range) GTT was 53 last year (and only 17 the prior year), now 166 (normal range is >60) ALP was 73 last year and now is 195 (normal range is >117)
  5. Celiac.com 09/01/2015 - Current medical guidelines recommend routine screening of liver function tests (LFTs) in patients diagnosed with celiac disease. However, there isn't much good data on rates of liver disorders in celiac disease outside of Europe. A team of researchers recently set out to accurately estimate rates of LFT abnormalities in celiac disease in the USA, and to assess the effect of a gluten-free diet on LFTs. The research team included Natalia E Castillo, Rohini R Vanga, Thimmaiah G Theethira, Alberto Rubio-Tapia, Joseph A Murray, Javier Villafuerte, Alan Bonder, Rupa Mukherjee, Joshua Hansen, Melinda Dennis, Ciaran P Kelly and Daniel A Leffler. To identify adult patients with biopsy-proven celiac disease, they used a prospectively maintained database, which they matched with healthy controls. They defined abnormal LFT levels for women and men based on the Third National Health and Nutrition Examination Survey (NHANES III) criteria. The team gathered data on demographics, coexisting liver diseases, and laboratory work-ups including aspartate transaminase (AST) and alanine transaminase (ALT) values at the time of diagnosis and on a gluten-free diet. They later compared data from this group with data from 7,789 individuals participating in the National Health and Nutrition Examination Survey, 2009–2010, and applied univariate logistic regression, Wilcox on signed-ranks, Student's t-test, χ2, and Fischer's exact test for statistical analysis. In 463 celiac disease patients with ALT or AST levels at the time of celiac disease diagnosis, 40.6% had elevated LFTs compared with 24.2% of treated celiac disease patients (P<0.001). Similarly, nearly forty percent of celiac disease patients on the NHANES database showed abnormal ALT values compared with less than twenty percent of non-celiac patients (P=0.03). Just over forty percent of individuals will show elevated LFTs at celiac disease diagnosis, but the vast majority, nearly eighty percent of those patients will show normal LFTs within a year and a half of adopting a gluten-free diet. The team suggests that doctors check all celiac patients for LFTs, and coexisting liver disorder be considered in patients whose LFTs have not improved within a year on a gluten-free diet. Source: The American Journal of Gastroenterology 110, 1216-1222 (August 2015). doi:10.1038/ajg.2015.192
  6. Celiac.com 06/29/2015 - Non-alcoholic fatty liver disease is a common cause of chronic liver disease. There's good data showing that celiac disease changes intestinal permeability, and that treatment with a gluten-free diet often causes weight gain, but so far there is scant documentation of non-alcoholic fatty liver disease in patients with celiac disease. A team of researchers recently set out to assess increased risk of non-alcoholic fatty liver disease following diagnosis of celiac disease. The research team include Norelle R. Reilly, Benjamin Lebwohl, Rolf Hultcrantz, Peter H.R. Green, and Jonas F. Ludvigsson. They are affiliated with the Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, and the Department of Pediatrics at Örebro University Hospital, Örebro University in Örebro, Sweden. The team assessed the for risk of non-alcoholic fatty liver disease diagnosed from 1997 to 2009 in 26,816 individuals with celiac disease to 130,051 matched reference individuals. The team excluded patients with any liver disease prior to celiac disease. They also excluded individuals with a lifetime diagnosis of alcohol-related disorder to minimize misclassification of non-alcoholic fatty liver disease. They used Cox regression estimated hazard ratios for non-alcoholic fatty liver disease. Their results showed that over 246,559 person-years of follow-up, 53 individuals with celiac disease had a diagnosis of non-alcoholic fatty liver disease (21/100,000 person-years). In comparison, in the reference group showed 85 individuals diagnosed with non-alcoholic fatty liver disease during 1,488,413 person-years (6/100,000 person-years). This corresponded to a hazard ratio of 2.8 in the celiac group (95% CI), with the highest risk estimates of 4.6 seen in children (95% CI). The risk increase in the first year after celiac disease diagnosis was 13.3 (95% CI), but remained significantly elevated at 2.5 even beyond 15 years after celiac diagnosis of celiac disease (95% CI). Individuals with celiac disease do have an increased risk of non-alcoholic fatty liver disease compared to the general population. Excess risks were highest in the first year after celiac disease diagnosis, but continued at least 15 years after celiac diagnosis. This much more comprehensive study provides much clearer and convincing data than any of the previous studies, and will likely serve as a baseline that clinicians have been lacking to this point. Source: Journal of Hepatology, June 2015Volume 62, Issue 6, Pages 1405–1411. DOI: http://dx.doi.org/10.1016/j.jhep.2015.01.013
  7. 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.
  8. 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.
  9. Celiac.com 12/06/2007 - About one person or so in every hundred has celiac disease, which means they suffer from a variety of associated symptoms along with intestinal damage and associated conditions. Research shows a connection between celiac disease and a variety of hepatic disorders. People with celiac disease have a higher instance of certain disorders of the liver. One of the most commonly presented liver problems among celiac patients is isolated hypertransaminasemia with non-specific histologic changes. Following a gluten-free diet usually returns the liver enzymes and histologic function to their normal state. People with celiac disease can also have unrelated liver conditions, such as primary biliary cirrhosis, autoimmune hepatitis, or primary sclerosing cholangitis. Most people don’t know much, if anything about celiac disease. Even most people with celiac disease or gluten intolerance face a long learning curve to get up to speed on all of the related issues that concern them. Many people with celiac disease understand that it is a condition in which an auto-immune mediated reaction to the presence of gluten from wheat, rye or barley cause damage to the lining of the intestine, which, if left untreated exposes them to greater risks of certain types of cancer, along with diabetes, and many other conditions. Even though it is well known among physicians that celiac disease is associated with a variety of other conditions, until recently, those associated with malabsorption were the best documented. Most doctors and researchers believed that these associated conditions were the direct result of, or closely associated with the malabsorption and a compromised nutrient uptake facing untreated celiac patients. Recently, however, evidence has begun to emerge that shows celiac disease to be a multi-system disorder that might affect a wide array of organs, including the bones, the heart, the skin, the liver, and the nervous system. Evidence is emerging that shows that beyond damaging the liver outright, celiac disease might also compound the impact of chronic liver diseases when the two occur together. To better understand the relationship between celiac disease and various liver disorders, researchers Alberto Rubio-Tapia and Joseph A. Murray conducted a review aimed at exploring the spectrum and pathogenesis of liver maladies associated with celiac disease, and to better describe the connection between celiac disease and those liver maladies to better establish a baseline for diagnosis and therapy to help those with chronic liver ailments and to better diagnose and treat celiac disease. Study Method In June 2007, the researchers searched PubMed for English-language journals that included full-length articles with the following keywords: celiac disease, sprue, liver disorders, liver involvement, liver tests, hepatitis, cholangitis, and cirrhosis. The researchers looked at 259 cases of patients with chronic hepatitis C, and found that they were three times more likely than a control group of normal volunteers to have celiac disease. The rate was 1.2% versus .4% for the control group. A second study showed a prevalence of celiac in 534 patients with chronic hepatitis to be 1.3%. Lastly, people with celiac disease show a high rate of non-response to hepatitis B vaccine. Non-response rates were 54% in children with celiac disease and 68% in adult celiacs. Hemochromatosis Celiac’s connection to hemochromatosis is twofold. Case histories show that iron overload and diagnosis of hereditary hemochromatosis often follows successful celiac treatment. Also, British patients with celiac disease showed a greater occurrence of mutation in the gene (HFE) controlling hemochromatosis, which might indicate that enhanced iron production is an adaptation to the reduced nutrient absorption associated with celiac. However, a study of Italian celiac patients showed no such increase in mutations. Researchers suspect that any relationship might be coincidental, as both conditions affect large numbers of Caucasians. Nonalcoholic Fatty Liver Disease About 10% to 25% of the general population will develop nonalcoholic fatty liver disease. Nearly 1 in 3 Americans diagnosed with celiac disease is overweight or obese. Two different studies have shown the number of biopsy-confirmed celiac disease in about 3.5%, or over three times that of the normal population. Liver Transplant Of 185 patients who underwent transplant, 4.3%, over 4 times the normal population, were positive for celiac disease. In nearly all cases, the cause of the end-stage liver disease requiring transplantation was autoimmune. Gluten Withdrawal In patients with nonalcoholic fatty liver disease, a gluten-free diet coincided with a normalization of liver blood test abnormalities, but the exact effects of a gluten-free diet on liver abnormalities in non-alcoholic fatty liver disease and other liver disorders needs to be clarified through further study. Conclusions A gluten-free diet is an effective medical therapy for most patients with celiac disease and liver disorders. The effect of a gluten-free diet on the progression of liver diseases associated with celiac disease is less clear. Clearly more studies need to be conducted to further elucidate the relationship between celiac disease and various disorders of the liver. HEPATOLOGY 2007; 46:1650-1658.
  10. Celiac.com 04/12/2010 - A team of researchers recently set out to look at connections between psoriasis, the liver, and the gastrointestinal tract. The team was made up of Paolo Gisondi, Micol Del Giglio, Alessandra Cozzi & Giampiero Girolomoni. They are associated with the Section of Dermatology and Venereology of the Department of Medicine, at the University of Verona, Italy. Psoriasis is a common chronic inflammatory, immune-mediated skin disease that is often tied to other disorders, including psoriatic arthropathy, chronic inflammatory bowel diseases, and cardio-metabolic disorders. Additionally, about 50% of all patients patients with psoriasis suffer from non-alcoholic fatty liver disease, from 0.2–4.3% suffer from celiac disease, and about one half of one percent suffer from Crohn's disease. These associated conditions may have some common genetic traits, as well as common inflammatory pathways, and their presence offers important implications in the global approach to treating psoriasis. In particular, common systemic antipsoriatic drugs might have a negative affect on associated cardio-metabolic conditions and nonalcoholic fatty liver disease, and may have important interactions with drugs commonly used to treat psoriasis. Moreover, the team emphasizes the importance of encouraging psoriasis patients to drastically improve their modifiable cardiovascular and liver risk factors, especially obesity, alcohol and smoking intake, because improvements could have positive impact on both the psoriasis and the patient's general well-being. Source: Dermatologic Therapy, Volume 23 Issue 2, Pages 155 - 159 - DOI: 10.1111/j.1529-8019.2010.01310.x
  11. 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.
  12. 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.
  13. Celiac.com 03/06/2009 - A report in the February 3rd issue of Digestive and Liver Disease highlights the present understanding of transglutaminase function in gastrointestinal and liver diseases and therapeutic strategies that target transglutaminase activities. A team of American and Italian researchers recently set out to review the current body of literature regarding transglutaminase function in gastrointestinal and liver diseases and therapeutic strategies that target transglutaminase activities. The research team was made up of doctors L. Elli, C.M. Bergamini, C.M. Bardella, and D. Schuppan. They are associated with one or more of the following: Center for Prevention and Diagnosis of Celiac Disease, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, in Milan, Italy; the Department of Biochemistry, University of Ferrara, Via Luigi Borsari, Ferrara, Italy; the Department of Medical Sciences, University of Milan, Italy; and the Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, USA. Their report in the February issue of Digestive and Liver Disease highlights the present understanding of transglutaminase function in gastrointestinal and liver diseases and therapeutic strategies that target transglutaminase activities. Transglutaminases are a group of eight presently recognized calcium-dependent enzymes that act as catalysts to cross-link or deamidate proteins. They play a role in key biological functions such as the healing of wounds, the repair of damaged tissue, fibro-genesis, apoptosis, inflammation and management of the cell cycle. Thus, they play a role in numerous key patho-mechanisms of autoimmune, inflammatory and degenerative diseases, a number of which involve the gastrointestinal system. Transglutaminase 2 is of central importance, as it is crucial to the pathogenesis of celiac disease, and influences inflammation and fibro-genesis in inflammatory bowel and chronic liver disease. The recent review has implications for celiac disease, collagen, Crohn's disease, extra-cellular matrix, gliadin, inflammatory bowel disease; NFkB, and ulcerative colitis. Dig Liver Dis. 2009 Feb 3.
  14. 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.
  15. 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
  16. 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.
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