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Celiac.com 11/10/2015 - Doctors might not need a biopsy to accurately diagnose celiac disease in asymptomatic children who have elevated anti-tTG, according to the latest study. In that study, researchers in Italy evaluated a new biopsy-sparing protocol for diagnosing celiac disease in symptomatic children with high anti-transglutaminase (anti-tTG). Their data showed that this approach might also work in asymptomatic children with elevated antibody levels. In 2012, the European Society of Pediatric Gastroenterology, Hematology, and Nutrition (ESPGHAN) published guidelines that said biopsies could be omitted in children and adolescents with signs and symptoms of celiac disease if they met certain guidelines. Dr. Francesco Valitutti of Rome's Sapienza University led a team that set out to assess the accuracy of serological tests to diagnose celiac disease in asymptomatic patients in 286 children and adolescents who had been diagnosed with celiac disease. Among 196 patients with anti-tTG antibodies at least 10 times ULN and EMA positive, 156 had symptoms and 40 were asymptomatic. More than 90% of the symptomatic children (142/156, 91%) showed severe lesion degree on biopsy, and an even higher percentage of asymptomatic patients (37/40, 92.5%) had severe lesions. There was no significant difference in histological damage between the "high-titer" symptomatic and asymptomatic children, according to the September 15th online report in The American Journal of Gastroenterology. Among the EMA positive children with lower titers of anti-tTG antibodies, 70% of symptomatic children and 81% of asymptomatic children showed severe lesions. The researchers add that asymptomatic patients should follow a gluten-free diet "as strictly as symptomatic ones, in order to prevent other autoimmune diseases and enteropathy-associated T-cell lymphoma." Otherwise, the new guidelines apply to patients with: TTG > 10 times ULN; an EMA of at least 1:80; a positive repeat serology to exclude laboratory error; HLA-DQ2 and/or -8 positivity; and a serological response to a gluten-free diet. If the research team can confirm these results in larger, multi-center prospective studies, their 'biopsy-sparing' protocol might be made available "to both symptomatic and asymptomatic patients with anti-tTG antibody titer (at least) 10 times the upper limit of normal (ULN) and anti-endomysial antibodies (EMA) and HLA-DQ2/DQ8 positive," Dr. Valitutti told reporters. Source: Am J Gastroenterol 2015
Celiac.com 05/27/2011 - Refractory Celiac Disease (RCD) is exactly what it sounds like: persistent malabsorption symptoms and intestinal villous atrophy even after following a gluten free diet. It is divided into two subtypes. RCDI has normal intraepithelial lymphocytes (IELs) while RCDII has abnormal IELs. RCDII is by far the more severe - there is no effective treatment, and it is often fatal within five years. Recent studies in Amsterdam and Paris have reported that RCDII can account for 28-75% of RCD patients. A group of researchers led by Ciaran Kelly at the Celiac Center at Beth Israel Deaconess Medical Center in Boston, the only specialized celiac center in New England, set out to determine if the same was true in the United States. They found a much lower incidence, 17%, of RCD patients with RCDII. An editorial by Malamut and Cellier accompanying Kelly's report in the American Journal of Gastroenterology suggests a number of factors that could account for the difference. Primary among them is the different methodology used to diagnose RCDII. In the US study only one method, immunohistochemistry, was used to ascertain whether the IELs were normal or not; in Europe they used three independent experimental techniques to confirm this data. The American researchers note that if they had in fact underdiagnosed RCDII they should have seen more severe cases of RCDI, and they did not. Malamut and Cellier point out that the Boston study may also have overdiagnosed RCDI by examining biopsy samples done only six months after institution of a gluten free diet, when villous atrophy may not have completely healed. An inflated number of RCDI cases would generate an erroneously low percentage of RCDII cases. But the Americans note that only four of the thirty-four cases of RCD they examined were from patients who had been on a gluten free diet for less than a year. Alternatively, the relative dearth of RCDII cases in the US as compared to Europe could be attributed to the different genetic backgrounds of the populations involved - the "melting pot" present in the US rather than the older stocks that may be in Europe. It has been reported that RCDII correlates with HLA-DQ2 homozygosity, and in fact, the HLA-DQ8 allele was found to be more common in celiac patients in New York than in those in Paris. It is also possible that an environmental factor, such as the amount or type of gluten consumed before diagnosis, could account for the discrepancy, but this remains to be investigated. Therapeutic options for the aggressive RCDII are still severely limited; research into it should certainly continue, on both continents. Sources: Roshan et al. The Incidence and Clinical Spectrum of Refractory Celiac Disease in a North American Referral Center. The American Journal of Gastroenterology 2011; 106: 923-928. Malamut and Cellier. Is Refractory Celiac Disease More Severe in Old Europe? The American Journal of Gastroenterology 2011; 106: 929-932.
Celiac.com 03/07/2011 - Although the HLA-DQ locus is clearly the strongest genetic factor influencing the development of celiac disease, it is certainly possible that other genes play supporting roles. Identifying these genes could help shed light on why certain genetically susceptible individuals develop celiac while others can happily (and healthily) eat gluten. NALP1 and NALP3 are genes that encode proteins involved in assembling the inflammasome, which is exactly what it sounds like – a complex of proteins that promotes inflammation. Gain-of function mutations – those that render the protein perpetually active, rather than responsive to activating signals – in NALP3 are known to cause autoinflammatory diseases, and NALP1 polymorphisms have been associated with the autoimmune diseases vitiligo, type I diabetes, and Crohn’s disease. NALP1 is found at high levels in T cells and Langerhans cells, but is also expressed in glandular epithelial structures including the stomach and gut. So a team of researchers in Trieste, Italy led by Dr. Sergio Crovella decided to check if polymorphisms in these genes might be associated with celiac disease as well. Their work is reported in the January 18, 2011 issue of The American Journal of Gastroenterology. They sequenced the DNA of 504 unrelated Italian children and adolescents with celiac disease and 256 healthy controls. They were looking for two particular polymorphisms in each gene, as these were already known to be associated with immune disorders. They did find differences in the frequency of the different individual alleles between celiac patients and controls, but these differences did not reach the levels of statistical significance. The combination of both NALP1 variants together, however, was significantly more common in study participants with celiac. NALP1 and NALP3 assemble the inflammasome by inciting the expression of the proinflammatory cytokine interleukin-1Î² , which in turn promotes autoreactive T cell function. The authors suggest that perhaps people with altered levels of responsiveness to interleukin-1Î² might be predisposed to autoimmunity. More work is needed to elucidate the role these NALP proteins might play in the intestinal damage that occurs in celiac disease. Source: Am J Gastroenterol advance online publication, 18 January 2011; doi: 10.1038/ajg.2010.474
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.