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    Jefferson Adams
    Celiac.com 03/26/2007 - According to a recent Norwegian research report, the adverse immune response to gluten may be tied to a specific set of dendrite cells in the small intestine.
    A team led by Dr. Melinda Raki set out to compare the antigen-presenting cells in the small intestine of patients with celiac disease versus those from normal individuals.
    The study used multiple duodenal biopsy specimens from 14 patients with untreated celiac disease, 6 with treated celiac disease and 4 controls.
    Antigen presenting cells are so termed because they present gluten to the T-cells, which then contribute to the inflammation that damages the villi in the intestinal lining of those with celiac disease.
    Researcher found that in the normal duodenal mucosa, about 20% of the HLA-DQ2 molecules associated with celiac disease were Cd11c+ dendritic cells. These dendritic cells accrued in the celiac lesions of the untreated celiac subjects.
    When these CD11c+ cells were removed from the biopsy samples, they provoked an adverse gluten reaction in the T-cells.
    The study indicates that a greater knowledge of antigen-presenting cells will yield a more complete understanding of the dynamics of celiac disease, the means by which inflammation occurs, and the means by which it can be controlled or avoided altogether.
    Gastroenterology 2006;131:428-438.

    Jefferson Adams
    Patients Diagnosed in Childhood Might Evolve toward Latency on a Normal Diet
    Celiac.com 05/23/2007 - The results of a study recently published in the journal Gut indicate that some people who suffer from celiac disease might not need to remain on a gluten free diet for their entire lives, and that some celiac patients might be able to safely introduce gluten containing foods without suffering a relapse.
    Previous Studies Showing Positive Response to Wheat Introduction in Patients with Celiac Disease are Promising, But Incomplete
    Several studies have shown that some patients diagnosed with celiac disease in childhood were able to remain on a gluten-containing diet after gluten challenge without suffering a relapse. However, most of these studies included a small number of patients, or followed the patients for only a short period after gluten was reintroduced into their diets.
    These previous studies also limited their evaluation largely to assessment of celiac disease serology and histology of duodenal biopsies, and did not attempt to identify what factors might predict the development of tolerance to gluten.
    Determining Long-term Response to Gluten Consumption in Celiac Disease Patients
    A research team made up of doctors Tamara Matysiak-Budnik (1), Georgia Malamut (1,2), Natacha Patey-Mariaud de Serre (3), Etienne Grosdidier (2), Sylvie Seguier (3), Nicole Brousse (3), Sophie Caillat-Zucman (4), Nadine Cerf-bensussan (1), Jacques Schmitz (5) and Christophe Cellier (1,2), set out to determine whether children diagnosed with celiac disease must follow a gluten free diet for life.
    To determine the effects of reintroducing gluten into the diets of celiac patients, the research team set out to monitor the clinical and physical progress of adult celiac patients who had been diagnosed as children, who underwent a gluten challenge, and who were asymptomatic.
    The study focused on a specific group of patients, all but two of whom were diagnosed as children and followed until adulthood in the Department of Pediatric Gastroenterology in Necker Hospital and thereafter at the Georges Pompidou European Hospital in Paris; after which, they were entered into a local register of adult celiac patients and were recruited for the study based on two criteria: celiac disease diagnosed in childhood; and adherence to a normal diet.
    The patients in the study were from 18 to 65 years old, and had been diagnosed with celiac disease in childhood. The research team recorded data in the following categories: biological parameters of malabsorption; bone mineral density; clinical celiac status; gluten intake; HLA genotype; serological markers of celiac disease; as well as histological and immuno-histochemical parameters in duodenal biopsies.

    Results Show 20% Long-term Latency in Celiac Patients who Eat Normal Diet
    Of those studied, 61 patients had returned to a normal diet, and were asymptomatic. 48 showed various degrees of villous atrophy (silent celiac disease), and 13 had no detectable atrophy (latent celiac disease) on duodenal biopsies. Compared to those with silent celiac disease, patients with latent celiac disease showed markedly less osteopenia/osteoporosis [1/9 (11%) versus 23/33 (70%), p<0.001)], and lower TcR- + intraepithelial T cell counts (38±20 vs. 55±15, p<0.01).
    Patients with latent celiac disease had a lower mean age at the time of their first gluten free diet compared to patients with silent celiac disease (14.4±5 vs 40.1±47 months, p<0.05).
    Compared to the seven control patients on a long-term gluten free diet, the latent patients did not differ significantly, except for a higher frequency of celiac disease-specific serum antibodies. However, a follow-up found that two of the patients with latent celiac disease had suffered a clinical and histological relapse.
    Results showed that of those patients who remained asymptomatic after the reintroduction of gluten, 20% showed long-term latency.
    The study concludes that some patients with celiac disease may not need to remain on a life-long gluten free diet, and that some may indeed be able to safely reintroduce gluten into their diets with no adverse effects. However, the latency patients may experience may be transient, and therefore a regular follow-up is necessary. Also, patients with silent celiac disease should remain on a gluten free diet.
    Participating hospitals:
    (1) INSERM, U793, Faculté de Médecine René Descartes, IFR94, Paris, France.
    (2) AP-HP, H&OCIRC;pital Européen Georges Pompidou, Department of Hepato-Gastroenterology,
    Paris, France.
    (3) AP-HP, H&OCIRC;pital Necker-Enfants Malades, Department of Pathology, Paris, France.
    (4) INSERM, Equipe Avenir, Faculté de Médecine René Descartes, Paris, France.
    (5) AP-HP, H&OCIRC;pital Necker-Enfants Malades, Department of Pediatric Gastroenterology, Paris, France.
    Gut 2006;13(10).
    Comments on this Study by Ron Hoggan
    This is dressed up like a new finding, but it isn't. There are a number of studies that show similar findings. Part of that problem lies in the interpretation of the biopsies, and part of the problem arises out of failing to recognize the variable nature of the disease. It has long been known to wax and wane for reasons beyond our ken. Samuel Gee (1888) and Gibbons (1889) both reported the cyclic nature of their patients symptoms. They cited a study to support the idea of a two year rule saying that relapse would usually occur within two years, yet Kuitunen P, Savilahti E, Verkasalo M., in Late mucosal relapse in a boy with coeliac disease and cows milk allergy. Acta Paediatr Scand. 1986 Mar;75(2):340-2. reported one patient who at 4.3 years on a normal diet showed normal villous architecture. It was not until a follow-up biopsy at more than 8 years of eating a gluten-containing diet that he showed villous atrophy. These findings, along with all the other studies that have shown long delays in some patients before relapsing, argue strongly for Michael N. Marsh's position that we should concentrate on treating any immune system that is sensitized to gluten with a gluten-free diet. His rectal challenge is an excellent tool for identifying such sensitized immune systems. Dr. Fines fecal antibody test probably fits into the same category. The underlying assumption is that the biopsy will identify all cases of intestinal lesion regardless of the possibility of patchy lesions that are well documented in the literature. They deal with increased IEL counts as if they were a feature of latent celiac disease when that is not the case. There are several other points on which this study falters. They admit that the latency can be transient. Unfortunately, they have not exchanged emails with people where they have returned to eating gluten and have developed an abdominal cancer. I exchanged emails with such a young man who blamed himself for having killed himself with his carelessness about his diet. How awful that was for him! Yet these authors seem to think it is quite acceptable for patients to indulge during their latency periods and only consider a diet if there is a relapse of intestinal lesion.
     

    Jefferson Adams
    Celiac.com 01/14/2013 - Sweden has seen a sharp rise in cases of celiac disease in children under two years of age. A research team recently studied the possible connection between early infections and celiac disease, along with their possible role in the explosion of celiac cases in Swedish children.
    The research team included Anna Myléus, Olle Hernell, Leif Gothefors, Marie-Louise Hammarström, Lars-Åke Persson, Hans Stenlund and Anneli Ivarsson.
    They are affiliated with the Epidemiology and Global Health, Department of Public Health and Clinical Medicine at Umeå University, Pediatrics unit of the Department of Clinical Sciences at Umeå University, the Immunology unit of the Department of Clinical Microbiology at Umeå University in Umeå, Sweden, and with the International Maternal and Child Health, Department of Women's and Children's Health in Uppsala University in Uppsala, Sweden.
    The team used a questionnaire to carry out a population-based incident case-referent study. The questionnaire went out to 475 cases and 950 referents, and included questions on family characteristics, infant feeding, and the child's general health.
    All cases of celiac disease cases were diagnosed before two years of age, and fulfilled the diagnostic criteria of the European Society for Pediatric Gastroenterology, Hepatology and Nutrition.
    The team randomly selected referents, matched by criteria, from the national population register.
    The final analysis included 373 (79%) cases of confirmed celiac disease and 581 (61%) referents, for a total of 954 children.
    For each case of celiac disease, the team matched complete information on main variables of interest with one or two referents.
    The results showed that children who suffered three or more parental-reported infectious episodes, regardless of type of infection, during the first six months of life faced a significantly higher risk for later celiac disease..
    This risk remained after the team adjusted for infant feeding and socioeconomic status (odds ratio [OR] 1.5; 95% confidence interval [CI], 1.1-2.0; P=0.014).
    Infants who had several infectious episodes, and whose parents introduced dietary gluten in large amounts, compared to small or medium amounts, after breastfeeding was discontinued faced an even greater risk (OR 5.6; 95% CI, 3.1-10; P<0.001).
    This study suggests that children who suffer repeated infections before age two face an increased risk for developing celiac disease later on. The risk was even greater in children who suffered repeated infections and whose parents introduced gluten in large quantities after weening.
    The team concludes that early infections probably made a minor contribution to the rise in celiac disease cases in Swedish children relative to the amounts of gluten introduced into the children's diets after weening.
    Source:
    BMC Pediatrics 2012, 12:194 doi:10.1186/1471-2431-12-194

    Jefferson Adams
    Celiac.com 09/23/2013 - Patients with non-celiac gluten sensitivity (NCGS) do not have celiac disease, but see an improvement in symptoms when they adopt gluten-free diets.
    A team of researchers recently investigated the specific effects of gluten after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates (fermentable, oligo-, di-, monosaccharides, and polyols [FODMAPs]) in patients with suspected NCGS.
    The research team included Jessica R. Biesiekierski, Simone L. Peters, Evan D. Newnham, Ourania Rosella, Jane G. Muir, and Peter R. Gibson.
    The team performed a double-blind cross-over trial of 37 subjects (aged 24−61 y, 6 men) with NCGS and irritable bowel syndrome (based on Rome III criteria), but not celiac disease.
    They assigned study participants randomly to groups given a 2-week diet of reduced FODMAPs, and were then placed on high-gluten (16 g gluten/d), low-gluten (2 g gluten/d and 14 g whey protein/d), or control (16 g whey protein/d) diets for 1 week, followed by a washout period of at least 2 weeks.
    The researchers then evaluated serum and fecal markers of intestinal inflammation/injury and immune activation, and indices of fatigue.
    The team then crossed twenty-two participants over to groups receiving gluten (16 g/d), whey (16 g/d), or control (no additional protein) diets for 3 days, using visual analogue scales to evaluate symptoms.
    They found that gastrointestinal symptoms consistently and significantly improved for all patients during reduced FODMAP intake, but significantly worsened to a similar degree when their diets included gluten or whey protein.
    The team saw gluten-specific effects in just 8% of study subjects. They saw no diet-specific changes in any biomarker. During the 3-day re-challenge, participants’ symptoms increased by similar levels among groups. Gluten-specific gastrointestinal effects were not reproduced. An order effect was observed.
    A placebo-controlled, cross-over re-challenge study showed no evidence of specific or dose-dependent effects of gluten in patients with NCGS placed diets low in FODMAPs.
    Source:
    Gastroenterology, Volume 145, Issue 2, Pages 320-328.e3, August 2013. More info on the FODMAP diet from Stanford Univerisity.

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