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
Function Tests - http://www.aafp.org/afp/990415ap/2223.html
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:
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
Free full text:
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.