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    Introducing Gluten During Infection Carries No Increased Risk of Celiac Disease


    Jefferson Adams

    Celiac.com 03/23/2010 - Introducing gluten to a baby's diet during a period of infection does not increase the risk of the child developing celiac disease later on, according to a study by Swedish researchers.


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    The team of researchers, led by Dr. Jonas F. Ludvigsson of Sweden's Karolinska Institute, used data from the population-based All Infants in Southeast Sweden study to search for independent associations of childhood infections with the risk of developing celiac disease.

    The team had parents chronicle their children's diet and infectious diseases in their first year of life, including breastfeeding start and stop dates, and dates the babies first ate gluten-containing foods.

    They enrolled a total of 9,408 children, and logged a total of 42,826 reports of infectious disease in the first year of life, including 4,003 episodes of gastroenteritis.

    Of 2,528 children who suffered infection at the time of gluten introduction, 18 developed celiac disease, while 26 of 6,880 children without infection developed celiac disease; for a total of 44 biopsy-proven cases of celiac disease after the children's first birthday  (p = 0.035). 167 children suffered from gastroenteritis during gluten introduction, but just one child developed celiac disease, compared to 43 of 9,241 with no gastroenteritis during gluten introduction (p = ns).

    Once adjusted for age at gluten introduction, age at breastfeeding termination, and age at infection, the results showed no significant connection between infection or gastroenteritis at the time of gluten introduction and the later development of celiac disease.

    The team pointed out that they lack data on specific infection types, which limits the scope of their conclusions, and that further study is warranted.

    "We cannot rule out the possibility that specific pathogens constitute risk factors for celiac disease, because risk estimates for infection at the time of gluten introduction were of borderline significance," they said, noting that the study design precluded identification of subclinical infections.

    The added that "because celiac disease is increasingly diagnosed in adulthood, screening...and a longer follow-up period would be required for complete elucidation of the possible relationship between infections and [the development of] celiac disease."

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  • Related Articles

    Jefferson Adams
    Celiac.com 09/28/2009 - According to the results of a new Swedish study,  patients with mild intestinal inflammation and gluten sensitivity face an elevated risk of death, even in the absence of symptoms severe enough to merit a clinical diagnosis of celiac disease.
    A number of studies have shown that people with gluten sensitivity and intestinal inflammation, but just how great is the risk? However, of those previous studies that show an increased risk of death associated with the disease, many were not population-based, lacked children and outpatients, while others were hampered by small numbers of participants.
    A team of Swedish researchers led by Jonas F. Ludvigsson, MD, PhD, of Sweden's Örebro University Hospital, recently set out to conduct a large-scale, population-based study regarding mortality risk levels for people with celiac disease, and also for those with "gluten intolerance."
    Ludvigsson and colleagues examined histopathology data from tissue biopsies collected from 46,121 Swedish patients nationwide between July 1969 and February 2008. Of those patients, 29,096 had celiac disease, while 13,306 showed inflammation of the small intestine and 3,719 showed latent celiac disease, elevated blood antibodies used as markers for celiac disease, but no sign of gut inflammation or damage.
    The researchers compared the patient data to records of the Swedish Total Population Register to calculate mortality rates for the three groups of patients. They found that among the patients there were 3,049 deaths among those with celiac disease, 2,967 deaths for those with inflammation, and 183 deaths for patients with latent celiac disease.
    The overall risk was not great, mortality risk was 75% higher for patients with mild intestinal inflammation at a median follow-up of 7.2 years (95% CI 1.64 to 1.79), and 35% higher for patients with latent celiac disease, or gluten sensitivity, at median follow-up of 6.7 years (95% CI 1.14 to 1.58).
    The study also revealed that people diagnosed with celiac disease faced a 30% greater risk of death at a median follow-up of 8.8 years (95% CI 1.33 to 1.45). That means that over the 8.8 years following the study, 30% more people with celiac disease died compared to the control group.
    These findings confirm previous studies that show higher mortality rates in celiac patients. Major causes of death for people with celiac disease are cardiovascular disease and cancer.
    Still, overall mortality risk associated with celiac disease and intestinal inflammation for gluten intolerance was small, with just 2.9 additional deaths per 1,000 person-years for people with celiac disease, and 10.8 and 1.7 additional deaths per 1,000 person-years for people with inflammation and latent celiac disease, respectively.
    Of the population-based study, Jonas F. Ludvigsson, MD, PhD, of Örebro University Hospital in Sweden, and colleagues writes,
    "we examined risk of death in celiac disease according to small-intestinal histopathology...Excess mortality was observed independent of histopathology, but absolute excess mortality risk was small, especially in children."
    In an accompanying editorial, Peter H. R. Green, MD, of Columbia University Medical Center, writes that the study's findings on patients with latent celiac disease, those patients who, in the United States, would be labeled as having "gluten sensitivity," were the most intriguing.
    Dr. Green writes that until recently, "gluten sensitivity has received little attention in the traditional medical literature, although there is increasing evidence for its presence in patients with various neurological disorders and psychiatric problems."
    Furthermore, researchers currently know little about the long-term consequences of mild gut inflammation. In such cases, patients typically show no sign of villous atrophy,  the flattening of the innermost membrane of the intestinal wall common to people with clinical celiac disease.
    Overall, the "risk of death among patients with celiac disease, inflammation, or latent celiac disease is modestly increased," the researchers concluded.
    The researchers speculate that the increase in mortality might result from chronic inflammation that damages patients' small intestines (the duodenum, specifically) or from malnutrition that saps their vitamins and energy.
    The researchers did not, however, rule out the possibility that mortality may be due to other existing conditions. They also cautioned that some patients with inflammation may have been misclassified as having latent celiac disease or partial villous atrophy, skewing mortality rates upward for the latent celiac disease group.
    Green concludes that the "study by Ludvigsson and colleagues reinforces the importance of celiac disease as a diagnosis that should be sought by physicians. It also suggests that more attention should be given to the lesser degrees of intestinal inflammation and gluten sensitivity."
    Source:
    JAMA. 2009;302(11):1171-1178.


    Jefferson Adams
    Celiac.com 10/12/2012 - What is the relationship between breastfeeding, the age of gluten introduction and rates of celiac disease?
    A number of studies have shown that increased breastfeeding may provide some protection against celiac disease. However, one study found no change in the overall prevalence of celiac disease in breastfed infants compared to controls, suggesting that breastfeeding may only delay the presentation of the disease but, does not prevent it. Other studies show no significant difference in the prevalence of celiac disease between breastfed and non-breastfed patients.
    Data from the Swedish celiac disease epidemic suggest a 3% prevalence of celiac disease in the children born during the epidemic. An analysis by Ivarsson et al. of children born during the epidemic, found that children under 2 years of age had a lower risk of celiac disease if they were still being breastfed when dietary gluten was introduced (odds ratio 0.59, 95, with a confidence interval 0.42–0.83). Children who continued breastfeeding after gluten was introduced to their diet showed a further decrease in the risk for celiac disease (OR 0.36, 95% CI 0.26–0.51).
    A meta-analysis that included the Ivarsson data, showed celiac disease risk was significantly lower in infants who were breastfed at the time of gluten introduction (pooled OR 0.48, 95% CI 0.40–0.59), compared to infants who were not breastfed at the time of first gluten exposure.
    A later study, by Akobeng and others, estimated that breastfeeding all babies in the UK at the time of gluten introduction, would prevent 2500 cases of celiac disease every year.
    The best data currently available on celiac disease and the age of gluten introduction comes from a prospective study by Norris et al. The study followed 1560 children in Denver between 1994 and 2004. This study showed that children exposed to gluten in the first 3 months of life had a fivefold increased risk of having celiac disease than children exposed to gluten between 4 and 6 months of age, while children exposed to gluten at 7 months old or later had an almost twofold increased risk compared with those exposed at 4 to 6 months (hazard ratio 1.87, 95% CI 0.97–3.60).
    When the analysis was limited to biopsy-diagnosed celiac disease, the hazard ratio was 23.97 (95% CI 4.55–115.9) for children exposed to gluten during the first 3 months of life compared to the 4–6 months exposure group, and 3.98 (95% CI 1.18–13.46) in the group exposed at 7 months or later
    What remains unclear, is whether breastfeeding and the age of introduction of gliadin prevent celiac disease or merely delay its onset.
    To clarify the relationship between breastfeeding, the age at which gluten is introduced into the diet, and celiac disease, the EU has funded a prospective study, called PREVENTCD, FP6, in 10 European centers. The PREVENTCD study recruited pregnant women with a family history of celiac disease, and determined HLA4 of the newborn at birth.
    By the end of December 2010, researchers had recruited a total of 1345 children at birth and enrolled 986 with positive HLA DQ status.
    Researchers instructed mothers to breastfeed for 6 months, if possible. Beginning at the age of 4 months, the researchers placed the infants into randomized study groups, and fed them 100 mg of gliadin or a non-gliadin placebo every day.
    The full data won't be available until all children reach the age of 3 years of age, but the researchers hope that the study will offer definitive answers on the relationship between breastfeeding and the age of gluten introduction and rates of celiac disease.
    Until new information become available, the ESPGHAN Committee on Nutrition recommendations remain in effect. This recommendations state that gluten should be introduced to infants no earlier than 4 months of age, and no later than 7 months, and that the introduction should be gluten be made while the infant is still being breastfed.
    This information was compiled by researcher R. Shamir of the Institute for Pediatric Gastroenterology, Nutrition and Liver Diseases, at the Schneider Children's Medical Center of Israel, Petah Tikva, affiliated with Sackler Faculty of Medicine, Tel Aviv University in Ramat Aviv, Israel.
    Source:
    Isr Med Assoc J. 2012 Jan;14(1):50-2.

    Jefferson Adams
    Celiac.com 10/31/2014 - The relationship between the risk of celiac disease and both the age at which gluten is introduced to a child’s diet and a child’s early dietary pattern is unclear.
    A team of researchers set out to examine how the introduction of dietary gluten and HLA status impact the risk of celiac disease in children.
    The research team included Elena Lionetti, M.D., Stefania Castellaneta, M.D., Ruggiero Francavilla, M.D., Ph.D., Alfredo Pulvirenti, Ph.D., Elio Tonutti, M.D., Sergio Amarri, M.D., Maria Barbato, M.D., Cristiana Barbera, M.D., Graziano Barera, M.D., Antonella Bellantoni, M.D., Emanuela Castellano, M.D., Graziella Guariso, M.D., Maria Giovanna Limongelli, M.D., Salvatore Pellegrino, M.D., Carlo Polloni, M.D., Claudio Ughi, M.D., Giovanna Zuin, M.D., Alessio Fasano, M.D., and Carlo Catassi, M.D., M.P.H.
    They are variously affiliated with the Departments of Pediatrics (E.L.) and Clinical and Molecular Biomedicine (A.P.), University of Catania, the Department of Pediatrics, San Paolo Hospital (S.C.), and the Department of Developmental Biomedicine, University of Bari (R.F.), Bari, the Department of Immunopathology and Allergology, Udine Hospital, Udine (E.T.), the Department of Pediatrics, Azienda Ospedaliera IRCCS Santa Maria Nuova Hospital, Reggio Emilia (S.A.), the Department of Pediatrics, Sapienza University of Rome, Rome (M.B.), the Department of Pediatrics, University of Turin, Turin (C.B.), the Department of Pediatrics, San Raffaele Hospital (G.B.), and the Department of Pediatrics, Vittore Buzzi Children’s Hospital, Milan (G.Z.), the Department of Pediatrics, Bianchi Melacrino Morelli Hospital, Reggio Calabria (A.B.), Pediatric Gastroenterology Unit, Giannina Gaslini Institute, Genoa (E.C.), the Department of Pediatrics, University of Padua, Padua (G.G.), the Department of Pediatrics, Federico II University of Naples, Naples (M.G.L.), Pediatric Gastroenterology and Cystic Fibrosis Unit, University Hospital Gaetano Martino, Messina (S.P.), the Department of Pediatrics, Rovereto Hospital, Rovereto (Trento) (C.P.), the Department of Pediatrics, University of Pisa, Pisa (C.U.), and the Department of Pediatrics, Marche Polytechnic University, Ancona (C.C.) — all in Italy; and the Division of Pediatric Gastroenterology and Nutrition and Center for Celiac Research, MassGeneral Hospital for Children (A.F.), and the Celiac Program, Harvard Medical School (A.F., C.C.) — both in Boston.
    For their study, the team randomly divided 832 newborns who had first-degree relatives with celiac disease into groups that received their first dietary gluten at 6 months (group A) or 12 months (group .
    The team determined HLA genotype at 15 months of age, and conducted serologic screening for celiac disease at 15, 24, and 36 months, and again at 5, 8, and 10 years.
    Patients with positive serologic findings received intestinal biopsies. The primary focus was on rates of celiac disease autoimmunity and of overt celiac disease among the children at 5 years of age.
    A total of 707 children completed the 36 month trial. Of those, 553 had a standard-risk or high-risk HLA genotype and completed the study.
    At 2 years of age, substantially higher percentages of children in group A than in group B had celiac disease autoimmunity (16% vs. 7%, P=0.002) and overt celiac disease (12% vs. 5%, P=0.01). At 5 years of age, there were no longer significant differences between the groups in terms of autoimmunity (21% in group A and 20% in group B, P=0.59) or overt disease (16% and 16%, P=0.78 by the log-rank test). At 10 years, the risk of celiac disease autoimmunity was far higher among children with high-risk HLA than among those with standard-risk HLA (38% vs. 19%, P=0.001), as was the risk of overt celiac disease (26% vs. 16%, P=0.05).
    Other variables, including breast-feeding, were not associated with the development of celiac disease.
    So, the short take away here is that, according to this study, neither delayed introduction of gluten nor breast-feeding had any effect on celiac disease rates among at-risk infants. However, children who experienced later introduction of gluten showed a delay in the onset of disease.
    Lastly, the important predictor of disease was having a high-risk HLA genotype.
    Source:
    N Engl J Med 2014; 371:1295-1303October 2, 2014. DOI: 10.1056/NEJMoa1400697

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics