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Found 29 results

  1. Celiac.com 12/15/2010 - A small study in Swedish children has found no association between early childhood psychological stress and later development of celiac disease. Previous studies have shown links between psychological stress and a number immunological diseases, such as inflammatory bowel disease. A team of researchers sought to look more closely at the connection between psychological stress in families and biopsy-proven celiac disease in children. The team included Karl Mårild, Anneli Sepa Frostell, and Jonas F. Ludvigsson. Their measure of psychological stress included factors such as serious life events, parenting stress, and parental worries. Using a questionnaire data from the ABIS study (All Babies In southeast Sweden), the team collected data on 11,000 children at one-year, and on 8,800 at two-years old. They confirmed celiac disease though observing of villous atrophy in small intestinal biopsy, and confirmed the diagnosis through patient chart data. Their data showed that no association between future celiac disease and a serious life event in the family in the child's first 1 or 2.5 years after childbirth (Odds Ratio (OR) = 0.45; 95% Confidence Interval (CI) = 0.01–2.65; P = 0.72; and OR = 1.21; 95% CI = 0.43–3.05; P = 0.64, respectively). They also found no association between celiac disease and parenting stress at age 1 year and at 2.5 years (OR = 0.40; 95% CI = 0.01–2.38; P = 0.73 and OR = 0.74; 95% CI = 0.01–4.56; P = 1.00, respectively). No children exposed to parental worries at 2.5 years were diagnosed with celiac disease before end of follow-up, compared to 25 diagnosed out of 8082 children not exposed to parental worry (OR = 0.00; 95% CI = 0.00–2.34; P = 0.64). Nor was there any associations between the combined measures of stress and celiac disease. This particular study found no association between celiac disease in Swedish children and psychological stress early in life. However, a wider and more statistically robust study is needed to entirely rule out any possible associations between early psychological stresses in children and later development of celiac disease. Source: BMC Gastroenterology. 2010;10(106)
  2. Eur Psychiatry. 2004 Aug;19(5):311-4. Celiac.com 09/12/2004 - Israeli researchers conducted a study designed to determine whether or not an association exists between celiac disease and schizophrenia. Past studies have indicated that such a connection may exist. The researchers screened 50 consecutive patients over 18 years old who were diagnosed with schizophrenia and their matched controls for celiac-specific anti-endomysial IgA antibodies. All patients also completed a detailed questionnaire. There were no significant differences between the groups in gender, Body Mass Index (BMI) or country of birth, and the mean age of the study group was significantly higher than the controls. All tests for anti-endomysial antibodies in both groups were negative, and the researchers concluded that "In contrast to previous reports, we found no evidence for celiac disease in patients with chronic schizophrenia as manifested by the presence of serum IgA anti-endomysial antibodies. It is unlikely that there is an association between gluten sensitivity and schizophrenia" Celiac.com Comments on this Study: This was a relatively small study that did not include other celiac disease screening methods, such as IgG (antigliadin antibody), tTG (tissue Transglutaminase), or intestinal biopsies. A recent study has shown that only 77% of those with total and 33% of those with partial villous atrophy actually have positive blood tests for celiac disease, so many cases of celiac disease may be missed by using only blood tests to screen for it. Further, about 4% of celiacs are anti-endomysial IgA deficient, so anyone in this subclass would have been missed in the study. Given such a small number of people in the study--50--if even one celiac were missed it would greatly affect the outcome of the study. Both groups should have been given much more comprehensive celiac disease screening to ensure that no cases of celiac disease were missed. In the article by Dr. Hadjivassiliou titled Gluten Sensitivity as a Neurological Illness he says: The introduction of more celiac disease specific serological markers such as anti-endomysium and more recently transglutaminase antibodies may have helped in diagnosing celiac disease but their sensitivity as markers of other manifestations of gluten sensitivity (where the bowel is not affected) is low. This certainly reflects our experience with patients with gluten sensitivity who present with neurological dysfunction. Endomysium and transglutaminase antibodies are only positive in the majority but not in all patients who have an enteropathy. Patients with an enteropathy represent only a third of patients with neurological manifestations and gluten sensitivity. Antigliadin antibodies unlike endomysium and transglutaminase antibodies are not autoantibodies. They are antibodies against the protein responsible for gluten sensitivity. Only one third of the patients with neurological disorders associated with gluten sensitivity have villous atrophy on duodenal biopsy. Even some with biochemical markers of malabsorption such as low serum vitamin B12, low red cell folate, or vitamin D concentrations had normal conventional duodenal histology. These cases may illustrate the patchy nature of bowel involvement in coeliac disease and the inaccurate interpretation of duodenal biopsies by inexperienced histopathologists. Preliminary data based on staining of the subpopulation of T cells in the small bowel epithelium suggests that these patients have potential celiac disease. There are, however, patients where the immunological disorder is primarily directed at the nervous system with little or no damage to the gut. Our practice is to offer a gluten-free diet to these patients unless the HLA genotype is not consistent with susceptibility to gluten intolerance (that is, other than HLA DQ2, DQ8, or DQ1). All patients are followed up and any clinical response is documented.
  3. Celiac.com 06/12/2009 - In a medical first, researchers at UCLA have made a connection between intestinal inflammation and systemic chromosome damage in mice, a discovery that may pave the way for early identification and treatment of human inflammatory disorders, some of which raise the risk for various kinds of cancer, according a study published in Cancer Research. Scientists discovered that local intestinal inflammation caused DNA damage to lymphocytes of the peripheral blood circulating throughout the body. So, contrary to conventional medical wisdom, chromosome damage is not limited to the immediate intestine, but involves body tissues far away from the actual inflammation. Their results showed single- and double-strand DNA breaks in the blood, and chromosome damage in peripheral blood indicating systemic genetic damage. Inflammatory diseases have been linked to some lymphomas and abdominal, liver and colorectal cancers, said Robert Schiestl, lead author, and professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist. Finding inflammation early – before any symptoms surface - and treating the associated causes quickly may prevent the damage that eventually triggers these cancers, he said. Before the study, researchers had no knowledge that "intestinal inflammation causes damage that can be found throughout the body,” said Schiestl, adding that this "may help explain how inflammation leads to these cancers.” Intestinal inflammation can be caused by such maladies as Crohn’s disease, inflammatory bowel disease, ulcerative colitis and Celiac disease. Nearly 1.5 million Americans, and 2.2 million Europeans currently suffer from inflammatory bowel diseases and global incidence is on the rise, Schiestl said. The discovery opens up the possibility of using chromosome damage in the peripheral circulating blood as a biomarker to spot intestinal inflammation before any symptoms surface. Researchers were able to detect chromosome damage in the blood of specially bred mice before the onset of colitis, said Aya Westbrook, a graduate student of the UCLA Molecular Toxicology Interdepartmental Program and the paper's first author. Westbrook added that disease severity correlated directly with higher levels of chromosome damage in the blood. Chromosome damage, according to study author Dr. Jonathan Braun, professor and chairman of the Department of Pathology and Laboratory Medicine at UCLA, may be the “earliest detectable indicator” of intestinal inflammatory disease. Currently, the only way to diagnose patients with inflammatory bowel disease is through full endoscopic exam, which is both invasive and costly. In theory, Braun said, a biomarker blood test might replace the invasive endoscopic exam and allow physicians to identify early inflammatory disease before it develops fully. Spotting disease and being able to ward it off early is one of the Holy Grails of all medicine. This breakthrough could “change the natural history of these diseases,” Braun said. For the first time, doctors might have a tool that can actually help spot inflammation, the earliest precursor to multiple kinds of cancer, at its earliest stages, long before any actual disease develops. This could lead to the prevention of tens of thousands of cancers. UCLA researchers have launched a clinical trial to confirm their findings in humans, Schiestl said. They’re focusing on patients with Crohn’s disease and ulcerative colitis. They're hoping the discovery will permit them to test new strategies for treating smoldering disease, which we’ve never been able to identify before,” Schiestl said, adding that they might be able to assess new drugs for treating early inflammatory disease. The research may also show why some patients with inflammatory disease develop cancers, while others endure chronic inflammation for decades, yet remain cancer-free. Researchers suspect that some unknown molecular mechanisms might work to protect some patients and not others. Finding such mechanisms might lead to tests for predicting which patients with intestinal inflammatory diseases are predisposed to cancer. Cancer Research: June 1 2009, Volume 69, Issue 11
  4. Mayo Clin Proc 2004;79:476-482. Celiac.com 05/25/2004 - The results of a study conducted by Dr. G. Richard Locke III and colleagues at the Mayo Clinic College of Medicine in Rochester, Minnesota do not show an association between irritable bowel syndrome (IBS) and celiac disease. The case-control study was based on the respondents of a bowel disease questionnaire that was sent to random Olmsted County residents who were 20 to 50 years old. The researchers evaluated 150 subjects, 72 of whom reported having symptoms of IBS and dyspepsia, and 78 controls with no gastrointestinal symptoms. In the group with symptoms they found that 50 had IBS, 24 had dyspepsia and 15 had both conditions. Serological screening of both groups for celiac disease showed no significant difference between them—two controls, two IBS subjects and two people with dyspepsia tested positive for celiac disease. The researchers conclude that celiac disease alone cannot explain the presence or IBS or dyspepsia in the subjects. The results of this study are interesting, but probably not large enough to be statistically significant. The total number of people with celiac disease in each group was astounding: 2 out of 50 with IBS (4%) 2 out of 24 with dyspepsia (6%) 2 of the 78 controls (2.6%) These findings do not necessarily contradict previous IBS/celiac disease studies that looked at hospital outpatients who are more likely to have more severe and prolonged symptoms than a group that selects itself from the general public by responding to a questionnaire. Additionally most of the earlier studies that concluded that there was a connection between celiac disease and IBS were conducted before more recent epidemiological studies that have shown just how high the incidence of celiac disease in the general population is--now estimated between 0.8% and 1.3%--this study suggests 2 -3%. These recent epidemiological studies have also shown that a large percentage of celiacs have little or no symptoms, perhaps due to the length of time or the severity of the disease. A 1 in 20 diagnosis of celiac disease in patients with IBS/dyspepsia is consistent with other studies, and is still high and suggests that testing for celiac disease should be done routinely on these patients. No studies have ever suggested that all or even most IBS patients have celiac disease, just that the incidence is higher than that of the normal population. I propose that if this study had been done on exactly the same people several years from now, the 2 people in the control group who were found to have celiac disease may well develop symptoms that would put them in either the IBS or dyspepsia group, which would create a statistically significant result that would contradict this studys result. Last, perhaps the results of this study really support a more broad conclusion: Everyone ought to be screened for celiac disease, not just those with symptoms.
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