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Found 20 results

  1. Celiac.com 12/05/2017 - It's not uncommon for people with celiac disease to have other medical conditions, including liver disease, glossitis, pancreatitis, Down syndrome, and autism. By the same token, people with one or more of these associated disorders can be at greater risk for having or developing celiac disease. Until recently, though researchers didn't have much good data on the numbers behind those risk levels. A new database study of more than 35 million people changes that. The study found that, for example, people with autism have celiac disease at rates that are 20 times higher than those without autism. You read that right. People with autism are 20 times more likely to have celiac disease than people from the general population. Reporting on his team's findings at the World Congress of Gastroenterology 2017, lead investigator Daniel Karb, MD, a second-year resident at University Hospitals Case Medical Center in Cleveland, says that doctors who treat autistic patients may want to keep an eye out for celiac-like symptoms. "If you have a patient who is autistic and they have all these unusual symptoms, you might want to screen them for celiac disease," said Karb. Researchers have long known that people with celiac disease can present with unusual symptoms that fall outside the classic celiac symptoms of malabsorption, steatorrhea, malnutrition, abdominal pain, and cramping after eating, "but this is putting numbers to it," said Dr Karb. For their study, Dr. Karb and his colleagues searched the Explorys database, which aggregates electronic health record data from 26 major integrated healthcare systems in the United States. Combing through the records of 35,854,260 people in the database from 2012 to 2017, they found 83,090 celiac disease diagnoses. The investigators uncovered significant connections between celiac disease and 13 other autoimmune disorders, such as type 1 diabetes, Crohn's disease, and ulcerative colitis. In fact, the team found that, except for a condition called primary biliary cholangitis, "[e]very autoimmune disease [they] looked at is associated with celiac disease," Dr. Karb reported. The study indicates that "there is a large undiagnosed burden of celiac disease," he explained. "And a lot of it is probably because of these atypical presentations." As research continues, look for more connections between celiac disease and other inflammatory conditions to be more fully detailed. For more on the World Congress of Gastroenterology 2017. Source: Medscape.com
  2. Celiac.com 09/15/2016 - Some doctors and clinicians have reported cases of severe sprue-like enteropathy associated with olmesartan, but, until now, no clear demonstration of an increased risk has been documented by epidemiological studies. Now, a French nationwide observational cohort study has shown a connection between severe intestinal malabsorption and the drug olmesartan, according to results presented by a team of researchers. Olmesartan is an angiotensin II receptor antagonist which has been used for the treatment of high blood pressure. Olmesartan is also sold commercially under the name Benicar. The research team included Mickael Basson, Myriam Mezzarobba, Alain Weill, Philippe Ricordeau, Hubert Allemand, Francois Alla, and Franck Carbonnel. They are variously affiliated with the French National Health Insurance Fund, Paris, France, and the Université Paris-Sud, Assistance Publique-Hôpitaux de Paris and Gastroenterology unit, Hôpitaux Universitaires Paris Sud, Le Kremlin Bicêtre, France. The team set out to assess, in a nationwide patient cohort, the risk of hospitalization for intestinal malabsorption associated with olmesartan compared with other angiotensin receptor blockers (ARB) and ACE inhibitors (ACEIs). From the French National Health Insurance claim database, they included all adult patients initiating ARB or ACEI between 1 January 2007 and 31 December 2012, with no prior hospitalization for intestinal malabsorption, no serology testing for celiac disease, and no prescription for a gluten-free diet product. Their main endpoint was incidence of hospitalization with a discharge diagnosis of intestinal malabsorption. The team included 4,546,680 patients, for a total of 9,010,303 person-years, and observed 218 events. Compared with ACEI, the adjusted rate ratio of hospitalization with a discharge diagnosis of intestinal malabsorption was 2.49 (95% CI 1.73 to 3.57, p Average length of hospital stay for intestinal malabsorption was longer in the olmesartan group than in the other groups (p=0.02). Compared with ACEI, the adjusted rate ratio of hospitalization for celiac disease was 4.39 (95% CI 2.77 to 6.96, p<0.0001). These results show that olmesartan is assoc qiated with higher rates of hospitalization for intestinal malabsorption and celiac disease. Source: Gut. doi:10.1136/gutjnl-2015-309690
  3. 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.
  4. 07/29/2013 - Rates of celiac disease in Caucasian populations of European origin are pretty well documented, but little is known about its prevalence in non-Caucasians. Also, data shows that celiac disease is one likely cause of iron-deficiency anemia, but little is known about how celiac disease might contribute to iron deficiency in Caucasians, and especially non-Caucasians. A team of researchers recently looked at for links between celiac disease and iron deficiency in both caucasians and non-caucasians. The study team included Joseph A. Murray, Stela McLachlan, Paul C. Adams, John H. Eckfeldt, Chad P. Garner, Chris D. Vulpe, Victor R. Gordeuk, Tricia Brantner, Catherine Leiendecker–Foster, Anthony A. Killeen, Ronald T. Acton, Lisa F. Barcellos, Debbie A. Nickerson, Kenneth B. Beckman, Gordon D. McLaren, and Christine E. McLaren. To find individuals with iron deficiency and to determine celiac disease rates, the team assessed samples collected from participants in the Hemochromatosis and Iron Overload Screening study. They looked at blood samples from white men 25 years or older and women 50 years or older who participated in the Hemochromatosis and Iron Overload Screening study. Individuals with serum ferritin levels ≤12 μg/L were group as iron deficient, while those with serum ferritin levels >100 μg/L in men and >50 μg/L in women served as a control group. The team analyzed all samples for human recombinant tissue transglutaminase immunoglobulin A; positive results were confirmed by an assay for endomysial antibodies. The team assessed patients with positive results from both celiac disease tests as having untreated celiac disease. They excluded from analysis all subjects with a positive result from only one of the two tests. They analyzed HLA genotypes and frequencies of celiac disease between Caucasians and non-Caucasians with iron deficiency. In all, the team found 14 cases of celiac disease among the 567 study subjects (2.5%), and just 1 case of celiac disease among the 1136 control subjects (0.1%; Fisher exact test, P = 1.92 × 10−6). The case of celiac disease in the control group was in a Caucasian control subject. There were no cases of celiac disease found in non-Caucasian controls. All 14 of the cases of celiac disease found by the team were in the Caucasian group of 363 (4%). There were no cases of celiac disease in the non-Caucasian group of 204 cases (P = .003). Overall, individuals with iron deficiency were 28-times more likely to have celiac disease (95% confidence interval, 3.7–212.8) than were healthy control subjects. Also, and interestingly, 13 of 14 cases with celiac disease carried the DQ2.5 variant of the HLA genotype. This study shows that celiac disease is linked with iron deficiency in Caucasians. In fact, among Caucasians, celiac disease is rare among individuals without iron deficiency. It also shows that celiac disease is rare among non-Caucasians—even among individuals with common features of celiac disease, such as iron deficiency. The study team recommends that doctors conduct celiac screening on men and postmenopausal women with iron deficiency. Source: Clinical Gastroenterology and Hepatology. Volume 11, Issue 7 , Pages 808-814, July 2013
  5. Am J Gastroenterol. 2003;98:625-629 Celiac.com 04/29/2003 – The findings of a recent study published in the March edition of American Journal of Gastroenterology indicate that around 4% of those who suffer from migraine headaches may have celiac disease, and in such cases a gluten-free diet can reduce or eliminate migraine symptoms. According to one of the researchers, Maurizio Gabrielli, MD (Gemelli Hospital in Rome, Italy), if further studies confirm these findings it could alter the current range of migraine treatments to include serological screening for celiac disease and the gluten-free diet for those with positive test results. Maurizio Gabrielli, MD and colleagues studied 90 patients who were diagnosed with idiopathic migraine, and found that 4.4% had celiac disease compared to 0.4% of 23 controls. The four migraine patients found to have celiac disease were treated for six months with a gluten-free diet and their symptoms decreased or were eliminated. The patients also showed an improvement in their cerebral blood flow on a gluten-free diet that was confirmed by using single-photon emission computed tomography scans.
  6. Celiac.com 05/14/2000 - Scientists from the University of Maryland have discovered that people with the autoimmune disorder celiac disease have higher levels of the protein zonulin in their bodies. This discovery may ultimately lead to more insight into the causes of other autoimmune diseases, including diabetes, multiple sclerosis and rheumatoid arthritis. In people with celiac disease who eat gluten, which is found in wheat, rye and barley, an autoimmune reaction is set off that creates antibodies that end up attacking their intestines. This causes symptoms like diarrhea and abdominal pain, and may lead to long-term damage and a large host of other problems. Researchers at the University of Maryland have finally found the cause of this curious reaction: a protein in the body called zonulin. Zonulin is a human protein that acts like a traffic conductor for the bodys tissues by opening spaces between cells, and allowing certain proteins to pass through, while keeping out toxins and bacteria. People with celiac disease have higher levels of zonulin, which apparently allows gluten to pass through the cells in their intestines, which triggers an autoimmune response in their bodies. Until now, researchers could never understand how a big protein like gluten could pass through the immune system. According to author Alessio Fasano, M.D., people with celiac have an increased level of zonulin, which opens the junctions between the cells. In essence, the gateways are stuck open, allowing gluten and other allergens to pass. Further: I believe that zonulin plays a critical role in the modulation of our immune system...(f)or some reason, the zonulin levels go out of whack, and that leads to autoimmune disease. Ultimately these finding may help doctors understand the causes of other, more severe autoimmune disorders.
  7. Celiac.com 11/01/2012 - Although most instances of gluten sensitivity manifest as a chronic, autoimmune disorder of the small intestine (celiac disease), around 10% of gluten sensitive patients suffer neurological symptoms. Usually these neurological symptoms accompany the more common intestinal issues, but some patients exhibit neurological symptoms exclusively. For this reason, it is thought that gluten-related symptoms in different parts of the body could be the result of autoimmune reactions to different members of the transglutaminase gene family. A recent lab study suggests that neurological gluten-related symptoms could be the result of an immune reaction to a particular neuronal enzyme known as TG6, and that this reaction occurs separate from other autoimmune reactions to gluten. Sera were collected from 6 groups: 20 newly diagnosed celiac disease patients (pre gluten-free diet) with no neurological symptoms, 34 gluten ataxia patients who tested positive for anti-gliadin antibodies, 17 peripheral idiopathic neuropathy patients, also positive for anti-gliadin antibodies, a control group of 18 genetic (non-gluten related) ataxia patients or individuals with clear family history of ataxia, a second control group of 14 patients with various immune-mediated but gluten-unrelated diseases and a third control group of 19 healthy individuals. Sera were tested through a series of protein analyses and enzyme-linked immunosorbent assays. In the celiac disease group, 18 of 20 patients tested positive for the TG2 autoantibody, with the remaining two testing postive for the TG3 or TG6 autoantibodies. 55% of celiac disease patients had multiple transglutaminase autoantibodies: 45% of all celiac disease patients had antibodies for both TG2 and TG3, 45% had antibodies for both TG2 and TG6, and 35% had antibodies for TG2, TG3 and TG6. Gluten ataxia patients were separated into two groups: those with intestinal symptoms (group GAE), and those without (group GAo). TG2 autoantibodies correlated well with intestinal symptoms: 12 of 15 in the GAE group tested positive for TG2 autoantibodies, while only 1 of 19 in the GAo group tested positive for them. TG3 autoantibody results were similar: group GAE results were comparable to the celiac disease group, while group GAo was no different from the control groups. In contrast, both gluten ataxia groups had similar results for TG6 autoantibodies. Overall prevalence of TG6 autoantibodies in the gluten ataxia group was 62%, compared to 45% in the celiac disease group. Inhibition studies showed that in group GAE (gluten ataxia with intestinal symptoms), autoantibodies reacted separately from one another, with TG2 and TG6 autoantibodies reacting independently of one another to their respective TG isozymes. This, along with the fact that some patients tested positive exclusively for TG6 would suggest that intestinal and neurological gluten-related symptoms are caused by separate immune reactions to different TG isozymes (TG2 and TG6, respectively). This is further supported by postmorten analysis of a gluten ataxia patient without intestinal symptoms, where TG6 deposits were found in the brain (TG6 could not be detected in a normal cerebellum). The findings of this study suggest that with more research, doctors may have another diagnostic tool in the form of TG6 autoantibody tests. This would help determine which patients with gluten sensitivity might be most at risk for developing neurological symptoms. Source: http://www.ncbi.nlm.nih.gov/pubmed/18825674
  8. Celiac.com 07/08/2009 - Kids whose moms have autoimmune diseases such as type 1 diabetes, rheumatoid arthritis and celiac disease face a risk of autism that is up to three times higher than that of the general population, according to a new study. Although earlier studies have documented a connection between autism and a maternal history of type 1 diabetes and rheumatoid arthritis, this is the first study to document a link between autism and celiac disease, according to the study's authors. A team of researchers led by Dr. William W. Eaton, chairman of the Department of Mental Health at the Bloomberg School of Public Health at Johns Hopkins University recently set out to review data related to autoimmune deficiency and autism. Eaton's team collected data on 3,325 Danish children diagnosed with autism spectrum disorder, including 1,089 diagnosed with infantile autism. All of the children were born between 1993 and 2004, and their data was part of the Danish National Psychiatric Registry. Data on family members with autoimmune diseases came from the Danish National Hospital Register. The data showed that children whose mothers had autoimmune disease faced a higher risk of developing autism spectrum disorder than children of mothers who did not have these conditions. Moreover, children with a family history of type 1 diabetes faced an increased risk of infantile autism. Overall, the increased risk of autism in people with autoimmune diseases is not huge, Eaton said. "The increased risk for type 1 diabetes is a little less than two times, for rheumatoid arthritis it's about 1.5 times and for celiac disease it's more than three times," Eaton said. "That's enough to impress an epidemiologist, but not enough to make anybody in the general population start changing their behavior." Eaton added that this finding "reinforces the suggestion that autoimmune processes are connected somehow with the cause of autism and autism spectrum disorder, and...may point a flashlight to areas of the genome that connect to autism." The finding itself has no clinical significance, says Eaton, but could guide future efforts by researchers to determine the cause or causes of autism. One reason autoimmune diseases might have a role in autism lies in genetic history, Eaton said. Children who were underweight or premature at birth face a higher risk for autism, and both of these obstetric problems are associated with celiac disease, he added. There may be a significant overlap "in the genetics of some of the autoimmune diseases and autism," he said. "Autism is strongly inherited, but we don't have the faintest idea where...this finding is on the pathway of finding the cause of autism." Various environmental triggers may also affect the fetus, he said. Lead researcher, Dr. Hjordis O. Atladottir, from the Institute of Public Health at the University of Aarhus in Denmark calls the findings important because they support the theory that autism is somehow tied to problems with the immune system. PEDIATRICS
  9. Celiac.com 02/09/2009 - An extensive recent survey of the Swedish cancer registry reveals that people with celiac disease face a 5-fold increased risk of developing non-Hodgkin lymphoma, but that the risk has decreased by more than 50% over the last 40 years. Researchers at the National Cancer Institute (NCI) in Bethesda, Maryland, and Sweden's Karolinska Institute recently undertook a review of more than 60,000 lymphoma cases diagnosed in Sweden between 1965 and 2004. They matched those cases to individual lymphoma-free controls with similar characteristics. Dr. Ying Gao of the NCI and colleagues found 37,869 cases of non-Hodgkin's lymphoma, 8,323 cases of Hodgkin's lymphoma, 13,842 cases of chronic lymphocytic leukemia. The researchers also enrolled 236,408 matched controls and 613,961 first-degree relatives. The team used hospital discharge information to identify people with a history of celiac disease. The data revealed that people with a hospital discharge diagnosis of celiac disease faced a 5.35-fold increased risk of developing non-Hodgkin's lymphoma. The data also showed that risk of Hodgkin's lymphoma was mildly elevated, and thst celiac patients showed no elevated risk of developing chronic lymphocytic leukemia. The data showed that from 1975-1984, patients with celiac disease faced a 13.2-fold greater risk of non-Hodgkin's lymphoma; from 1985-1994, that level fell to a 7.90-fold increased risk, and from 1995-2004 that risk fell again to 3.84-fold increased risk. Siblings of those affected with celiac disease also faced a 2.03-fold greater risk of non-Hodgkin's lymphoma. At present, doctors do not clearly understand the causal link between the two. Earlier studies have indicated that the inflammation common to celiac disease leads drives lymphoma development. According to the research team, the study carries two basic messages: The first is that earlier detection of celiac disease is helping to lower the risk of developing lymphoma over time, so today, fewer people are detected in the late stages, when the risk of lymphoma is much greater. The second message is that people with a family history of celiac disease have a greater chance of developing lymphoma. This family connection was shown to be separate from the personal celiac disease history of the individual. Together, these revelations suggest that shared mechanisms might contribute to both celiac disease and lymphoma. The full report appears in the medical journal Gastroenterology, January 2009.
  10. American Journal of Psychiatry 163:521-528, March 2006 Celiac.com 03/14/2006 – Danish researchers have found yet another link between celiac disease and schizophrenia. In a large epidemiologic study the researchers looked at 7,704 Danish people who were diagnosed with schizophrenia between 1981 and 1998, including their parents, and matched them to comparison control subjects. The data linkage required that the autoimmune disease be diagnosed before the diagnosis of schizophrenia. The researchers found that patients with a history of an autoimmune disease had a 45% increased risk for schizophrenia, and nine autoimmune disorders were indicators of a higher prevalence for schizophrenia when compared to the controls. The researchers conclude: “Schizophrenia is associated with a larger range of autoimmune diseases than heretofore suspected. Future research on co-morbidity has the potential to advance understanding of pathogenesis of both psychiatric and autoimmune disorders.”
  11. Celiac.com 03/21/2011 - Two recent population-based studies, both performed in Sweden by Dr. Jonas Ludvigsson, have concluded that people who have had biopsies that reveal villous atrophy are at increased risk of both ischemic heart disease and asthma. But at least regarding heart disease, the bulk of the risk may simply be attributable to inflammation. The team of researchers looked at biopsy data collected from all twenty-eight of Sweden’s pathology departments between 2006 and 2008. The data included biopsies performed as far back as 1969, and represented 44,446 individuals: 28,190 with celiac disease, as ascertained by small intestine morphology; 12,598 with duodenal/jejuna inflammation lacking villous atrophy; and 3,658 with latent celiac disease, defined as those with positive celiac serology but normal mucosa. 219,392 healthy controls who had never had biopsies were included as controls. They concluded that celiac disease and inflammation of the small intestine were both modestly associated with ischemic heart disease, whereas latent celiac disease was not. Although these findings agree in kind, if not in degree, with reports previously published by others, this study had a number of flaws. First of all, the researchers lack data on individual adherence to a gluten free diet. The authors note that “low dietary adherence is associated with persistent inflammation and therefore might explain the increased risk of ischemic heart disease observed in patients with celiac disease.” They also lack data on blood pressure, smoking status, body mass index, lipid levels, exercise routines, and other established risk factors for ischemic heart disease. Because they found the highest risk in the first year following biopsy, they cede that this risk could be attributable to enhanced inflammation, enhanced stress surrounding a diagnosis with celiac disease, or even an increase in reporting rather than incidence due to more vigilant medical care immediately following the diagnosis with celiac disease. They even note that gastrointestinal and cardiac symptoms are easily confused, further confounding their analysis. The second study compared the same 28,190 Swedes with villous atrophy to 140,000 controls. It reported that people with celiac disease were 60% more likely to develop asthma than those without it, and conversely, that people with asthma are more likely to develop celiac disease. “A potential mechanism could be that asthma and celiac disease share some immunological feature,” said Dr. Ludvigsson. “If you have it, you are at increased risk of both diseases.” He also noted that vitamin D deficiency can play a causative role in both diseases, and should be assessed on both celiac patients and asthmatics. Sources: Circulation 2011; 123: 483-490 Journal of Allergy and Clinical Immunology February 11, 2011 / doi:10.1016/j.jaci.2010.12.1076
  12. Eur J Gastroenterol Hepatol 2000;12:1195-1199. Celiac.com 01/20/2001 - Italian researchers have identified several key factors that contribute to bone loss in adults with celiac disease, including the following: Gender Malnutrition Disease Severity Physical Activity They also conclude that, contrary to current belief, age at diagnosis, sunlight exposure and smoking do not seem to be significant factors in bone mineral density. In their study, Dr. Gino Roberto Corazza (University of Pavia) and associates evaluated 39 adults with untreated celiac disease, including 18 who had symptoms and 21 who did not. The researchers used dual-energy X-ray absorptiometry to measure lumbar spine and femoral neck bone mineral density, and assessed the patients physical activity, cigarette smoking, nutritional status and exposure to sunlight. The results of the study indicate that femoral and lumbar bone mineral density was lower in patients with symptoms than patients without, and women tended to have lower mineral bone density than men. This finding, in combination with other factors were associated with reduced bone mineral density in the femoral neck, lumbar spine or both. Further, the key factors seem to be the severity of the patients symptoms and their nutritional status, both of which had significant effects on both lumbar and femoral bone mineral density. The patients levels of physical activity affected only femoral bone mineral density, and the gender of the patient affected mainly the lumbar density. This is one of the first studies of its kind, and Dr. Corazzas group stresses the need for follow-up studies to determine whether additional therapeutic measures such as moderate and on-going physical activity and a more rapid implementation of a gluten-free diet might be useful in increasing the bone mass gain in people with celiac disease.
  13. Celiac.com 09/29/2006 - A new study identified a peptide which causes an immune reaction in a majority of active celiac disease patients but no such reaction in any celiac disease patients on a gluten-free diet. Antibodies to this celiac peptide also recognize and bind to the rotavirus protein VP-7 and cause increased intestinal permeability. Antibodies to VP-7 produced in rabbits also increase intestinal permeability. The celiac peptide also binds to Toll-like receptor 4 and activates monocytes (white blood cells active in innate immunity.) IgA and IgG antibodies to rotavirus protein VP-7 are present in a majority of celiac disease patients and to a much lesser percent of the general population. This suggests VP-7 may be involved in the pathogenesis of celiac disease through a molecular mimicry mechanism. Below is the abstract of the study: PLoS Medicine Volume 3, Issue 9, SEPTEMBER 2006 In Celiac Disease, a Subset of Autoantibodies against Transglutaminase Binds Toll-Like Receptor 4 and Induces Activation of Monocytes Methods and Findings: "In our attempt to clarify the pathogenesis of celiac disease, we screened a random peptide library with pooled sera of patients affected by active disease after a pre-screening with the sera of the same patients on a gluten-free diet. We identified a peptide recognized by serum immunoglobulins of patients with active disease, but not by those of patients on a gluten-free diet. This peptide shares homology with the rotavirus major neutralizing protein VP-7 and with the self-antigens tissue transglutaminase, human heat shock protein 60, desmoglein 1, and Toll-like receptor 4. We show that antibodies against the peptide affinity-purified from the sera of patients with active disease recognize the viral product and self-antigens in ELISA and Western blot. These antibodies were able to induce increased epithelial cell permeability evaluated by transepithelial flux of [3H] mannitol in the T84 human intestinal epithelial cell line. Finally, the purified antibodies induced monocyte activation upon binding Toll-like receptor 4, evaluated both by surface expression of activation markers and by production of pro-inflammatory cytokines." Conclusions: "Our findings show that in active celiac disease, a subset of anti-transglutaminase IgA antibodies recognize the viral protein VP-7, suggesting a possible involvement of rotavirus infection in the pathogenesis of the disease, through a mechanism of molecular mimicry. Moreover, such antibodies recognize self-antigens and are functionally active, able to increase intestinal permeability and induce monocyte activation. We therefore provide evidence for the involvement of innate immunity in the pathogenesis of celiac disease through a previously unknown mechanism of engagement of Toll-like receptor 4."
  14. Arch Neurol 2005;62:1574-1578. Celiac.com 11/29/2005 – According to Dr. Thomas H. Brannagan and colleagues at Weill Medical College of Cornell University, New York, some cases of small-fiber neuropathies are caused by untreated celiac disease and may be treatable with a gluten-free diet. The researchers report on eight patients who had neuropathy with asymmetric numbness or paresthesias in various parts of their body that began at different ages--ranging from childhood to 59 years. Out of the 8 patients in the study 5 were diagnosed with celiac disease after their neuropathy began. All patients were treated with a gluten-free diet and their neuropathy symptoms were re-evaluated--four reported improvement, one had no improvement, and 2 reported worsening of symptoms. The researchers conclude: “Patients with celiac disease may have a neuropathy involving small fibers, demonstrated by results of skin biopsy. The pattern of symptoms, with frequent facial involvement and a non–length-dependent pattern on skin biopsy findings, suggests a sensory ganglionopathy or an immune-mediated neuropathy. Improvement of symptoms in some patients after initiating a gluten-free diet warrants further study.”
  15. Nat Genet. 2005 Nov 13 Celiac.com 11/29/2005 - The following is an abstract of a study by Dutch researchers which demonstrates a new level of understanding with regard to the role that specific genes play in the cause of celiac disease. These findings may eventually lead to a treatment that lies beyond the gluten-free diet: Celiac disease is probably the best-understood immune-related disorder. The disease presents in the small intestine and results from the interplay between multiple genes and gluten, the triggering environmental factor. Although HLA class II genes explain 40% of the heritable risk, non-HLA genes accounting for most of the familial clustering have not yet been identified. Here we report significant and replicable association (P = 2.1 x 10(-6)) to a common variant located in intron 28 of the gene myosin IXB (MYO9B), which encodes an unconventional myosin molecule that has a role in actin remodeling of epithelial enterocytes. Individuals homozygous with respect to the at-risk allele have a 2.3-times higher risk of celiac disease (P = 1.55 x 10(-5)). This result is suggestive of a primary impairment of the intestinal barrier in the etiology of celiac disease, which may explain why immunogenic gluten peptides are able to pass through the epithelial barrier.
  16. JAMA. 2005;293:2343-2351, 2410-2412 Celiac.com 05/31/2005 – Researchers in the United States have found that introducing gluten too early or too late in an infants diet may play a key role in whether or not they eventually develop celiac disease autoimmunity. From 1994 to 2004 the researchers followed 1,560 high-risk children (those with either HLA-DR3 or DR4 alleles, or with a first-degree relative with type 1 diabetes) who were periodically screened for celiac disease autoimmunity. Positive results were defined by two positive tissue transglutaminase (tTG) blood serum tests, or one positive tTG and a positive small bowel biopsy. The researchers conducted a prospective observational study in which the parents of the children in the study responded to a questionnaire regarding the timing of gluten introduction into their childrens diets. To avoid a bias on the answers the researchers purposely did not include children who already had celiac disease. During the mean duration period of the study (4.8 years), 51 children developed celiac disease autoimmunity. Their findings indicate that children who were first introduced to gluten when they were less than 3 months of age had a five-fold increased risk of developing celiac disease autoimmunity when compared to children who were first introduced to gluten at 4-6 months old. Additionally, those who were first introduced at 7 months or older had a marginally increased risk of getting celiac disease autoimmunity when compared with the same group. Based on these findings the researchers recommend that parents should introduce cereals into their childrens diets at 4-6 months of age—even though this conflicts with recent recommendations by the American Academy of Pediatrics, who recommend breast-feeding only until 6 months of age. The researchers stress that much larger international prospective studies need be done in this area to answer the many questions that this study raises.
  17. J Tropical Pediatrics 2004, 50:37-40 Celiac.com 03/30/2004 – Researchers in India have discovered that serum prolactin levels in those with celiac disease are elevated in direct proportion to the severity of the disease. Dr. Gaurav Kapur and colleagues from the Lady Hardinge Medical College, New Delhi screened serum prolactin levels in 41 children who were diagnosed with celiac disease, 21 of which were on a gluten-free diet for more than a year. The results were compared to 41 healthy controls. The researchers found that serum prolactin levels were highly elevated in those with active celiac disease (average of 48.3 ng/mL), and present at lower levels in those on a gluten-free diet (average of 18.3 ng/mL). The healthy controls had an average level of 9.3 ng/mL. The longer the disease was left untreated along with the increase in severity of villous atrophy, the higher the levels of serum prolactin that were detected. The researchers conclude that serum prolactin levels can be used to determine the severity of celiac disease in patients, and this option is more economically viable than the use of other options.
  18. Dig Dis Sci 2000;45:403-406. (Celiac.com 04/10/2000) Italian researcher Dr. Tarcisio Not, of Clinica Pediatrica, I.R.C.C.S., Trieste, and colleagues, have concluded that a relatively high percentage of patients with autoimmune thyroiditis also have celiac disease. They studied 172 patients who had autoimmune thyroid disorders, and two control groups. Their control groups were comprised of 498 patients with other diseases, and 4,000 healthy patients. The method used by the researchers was a blood test that looks for IgA-class endomysium antibodies using immunofluorescence. Their results, which were published in the February issue of Digestive Diseases and Sciences, show that the prevalence of celiac disease is 3.4% in patients with autoimmune thyroiditis, compared with 0.6% and 0.25% among the two control groups. They also found a connection between untreated celiac disease, gluten consumption, and autoimmune disorders. The researchers believe that undiagnosed celiac disease can cause other disorders by switching on some as yet unknown immunological mechanism. Untreated celiac patients produce organ-specific autoantibodies. Further, By following these subjects longitudinally, it has been seen that not only do the anti-gliadin antibodies and anti-endomysium antibodies disappear after 3 to 6 months of a gluten-free diet, but so do the organ-specific autoantibodies. In conclusion the Italian researchers suggest that patients with autoimmune thyroiditis could benefit from a screening for celiac disease, which could eliminate the symptoms and limit the risk of developing other autoimmune disorders.
  19. Dig Dis Sci 2000;45:403-406. (Celiac.com 04/10/2000) Italian researcher Dr. Tarcisio Not, of Clinica Pediatrica, I.R.C.C.S., Trieste, and colleagues, have concluded that a relatively high percentage of patients with autoimmune thyroiditis also have celiac disease. They studied 172 patients who had autoimmune thyroid disorders, and two control groups. Their control groups were comprised of 498 patients with other diseases, and 4,000 healthy patients. The method used by the researchers was a blood test that looks for IgA-class endomysium antibodies using immunofluorescence. Their results, which were published in the February issue of Digestive Diseases and Sciences, show that the prevalence of celiac disease is 3.4% in patients with autoimmune thyroiditis, compared with 0.6% and 0.25% among the two control groups. They also found a connection between untreated celiac disease, gluten consumption, and autoimmune disorders. The researchers believe that undiagnosed celiac disease can cause other disorders by switching on some as yet unknown immunological mechanism. Untreated celiac patients produce organ-specific autoantibodies. Further, By following these subjects longitudinally, it has been seen that not only do the anti-gliadin antibodies and anti-endomysium antibodies disappear after 3 to 6 months of a gluten-free diet, but so do the organ-specific autoantibodies. In conclusion the Italian researchers suggest that patients with autoimmune thyroiditis could benefit from a screening for celiac disease, which could eliminate the symptoms and limit the risk of developing other autoimmune disorders.
  20. Am J Gastroenterol 1999;94:2435-2440. (Celiac.com 04/10/2000) A study by Danish researchers that was published in the September issue of the American Journal of Gastroenterology concludes that treating women who have celiac disease before they become pregnant improves their birth outcomes. According to Dr. Bente Norgard and colleagues of the University of Aarhus, Denmark, Our study emphasizes the importance of encouraging fertile women to maintain a gluten-free diet once they have been diagnosed, because the time of establishing the diagnosis and subsequent treatment is the major predictor for a favorable birth outcome. The Danish team examined the outcomes of 211 newborns from 127 women with celiac disease, and compared them to 1,260 births to women without celiac disease, from data collected between 1977 and 1992 by the Danish Medical Birth Registry. Their results showed that birth outcomes were worse in women with untreated celiac disease than in women who had been hospitalized for celiac disease, and that the risk of low birth weight and intrauterine growth retardation were increased 2.6 and 3.4 fold respectively when compared to the infants born to women with celiac disease and no prior hospitalization for the disease. These same risks were not increased in women with celiac disease who had prior hospitalization for it. According to Dr. Norgard, Our results emphasize the importance of clinical awareness of this chronic disease. Their conclusion is that untreated celiac disease is a major risk factor for poor birth outcomes, and that the treatment of celiac disease in women is important in the prevention of fetal growth retardation.
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