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    No Higher Rotavirus Risk for Adult Celiac Disease Patients


    Jefferson Adams
    Image Caption: New study on Rotavirus and celiac disease

    Celiac.com 09/03/2010 - Many patients who show up at hospitals and clinics with non-specific gastrointestinal symptoms have rotavirus infection


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    A team of researchers recently studied a large cohort of adults with non-specific gastrointestinal complaints to see if people with celiac disease had any higher for rotavirus.

    The research team included Mohammad Rostami-Nejad, BS, Kamran Rostami, MD,PhD, Maryam Sanaei, MSc, Seyed R. Mohebbi, PhD, David Al-Dulaimi, MD, Ehsan Nazemalhosseini-Mojarad, MSc, Pekka Collin, MD, Chris J. Mulder, MD, PhD, Mohammad R. Zali, MD, FACG.

    They are associated variously with the Research Center of Gastroenterology and Liver Diseases at Shaheed Beheshti University in Tehran, Iran; the School of Medicine of the University of Birmingham, UK, the Department of Gastroenterology at Alexander Hospital in Redditch, UK; the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital in Finland, and with the Department of Gastroenterology at VU University Medical Center in Amsterdam, The Netherlands.

    The team conducted the study at the Research Center of Gastroentrology and Liver Disease at Taleghani Hospital in Tehran, Iran.

    For their study, they randomly selected 5176 individuals living in Tehran, Iran between September 2006 and September 2007. Using a questionnaire, they found 670 case of GI symptoms, each of whom was invited for additional study, including stool sampling and blood tests.

    The researchers screened stool samples for rotavirus using amplification of specific gene (VP6), light microscopy and formalin-ether concentration methods. They also tested subjects for celiac disease including anti-transglutaminase (tTG) antibodies and total immunoglobulin A (IgA).

    The research team found the VP6 gene in 150 (22.3%) individuals. 22 subjects showed positive results for anti-tissue transglutaminase (tTG-IgA) (95% CI 2.3-5.1), while three patients who were IgA deficient tested positive for the IgGtTG antibody.

    Eight of 25 patients (32%) showed amplification of VP6 gene, and positive blood screens for celiac disease, while 142 of 645 with negative celiac blood tests (22%) showed amplification of VP6 gene. They found no statistically important difference between the two groups (p=0.2).

    Unlike earlier studies in children, this adult study shows that rates of active rotavirus infection were about the same for adults who tested positive for tTG antibody as they were for adults who tested negative for tTG antibody. Based on this study, there is no higher rotavirus risk for adults with celiac disease.

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    Guest Sally Ongaro

    Posted

    Interesting article. The more we know about celiac disease and what to look out for in connection with it the better. Happy to read that there are no worries about having an increased possibility of rotavirus infections!

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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 01/25/20010 - Women with celiac disease face greater risks for adverse pregnancy outcomes. A team of researchers recently set out to examine the effects of treated and untreated maternal celiac disease on infant birthweight and preterm birth. Among their findings are that expectant mothers with celiac disease face a higher risk of underweight and early-term birth than those without celiac disease.
    The research team included A.S. Khashan, T.B. Henriksen, P.B. Mortensen, R. McNamee, F.P. McCarthy, M.G. Pedersen and L.C. Kenny. They are affiliated variously with the Anu Research Centre of the Department of Obstetrics and Gynecology at the University College Cork at Cork University Maternity Hospital in Ireland, the Perinatal Epidemiology Research Unit in the Department of Paediatrics at Aarhus University Hospital, the National Centre for Register-based Research at the University of Aarhus, Denmark, and the Biostatistics Group, University of Manchester, Manchester, UK.
    For their data, they used a population-based cohort study of all live births in Denmark between 1 January 1979 and 31 December 2004. During that period, 836,241 mothers gave birth to a total of 1,504,342 babies. Mothers with diagnosed celiac disease gave birth to 1105 of those babies, while 346 were born to women with undiagnosed celiac disease.
    The team considered mothers with diagnosed celiac disease to be following a gluten free diet, and those with undiagnosed celiac disease to be on a gluten-inclusive diet. The team measured outcomes based on birthweight, small for gestational age (SGA: birthweight <10th centile), very small for gestational age (VSGA: birthweight <5th centile) and preterm birth. They then compared the results for the treated and untreated celiac disease mothers with those of a celiac-free reference group.
    The research team found that mothers with untreated celiac disease gave birth to smaller babies [difference = –98 g (95% CI: –130, –67)], with a higher risk of SGA [OR = 1.31 (95% CI: 1.06, 1.63)], VSGA [OR = 1.54 (95% CI: 1.17, 2.03)] and early birth [OR = 1.33 (95% CI: 1.02, 1.72)] compared with women with no celiac disease.
    The good news is that mothers with treated celiac disease showed no increased risk of reduced mean birthweight, or of delivering SGA and VSGA infants or preterm birth compared with mothers with no celiac disease.
    From the results, the research team concluded that untreated maternal celiac disease increases the risk of low birthweight, SGA and VSGA, and preterm birth.
    Diagnosis and treatment of maternal celiac disease with a gluten-free diet seems to return the birthweight and preterm birth rate to one comparable to women without celiac disease.
    This study drives home the importance of expectant mothers with celiac disease maintaining a gluten-free diet to promote a healthy delivery.
    Source: Human Reproduction, doi:10.1093/humrep/dep409


    Jefferson Adams
    Celiac.com 07/21/2014 - The presence of HLA haplotype DR3–DQ2 or DR4–DQ8 is associated with an increased risk of celiac disease. In addition, nearly all children with celiac disease have serum antibodies against tissue transglutaminase (tTG).
    A research team recently set out to determine the risk of celiac disease autoimmunity and celiac disease, by age and by halpotype, in children. The research team included Edwin Liu, M.D., Hye-Seung Lee, Ph.D., Carin A. Aronsson, M.Sc., William A. Hagopian, M.D., Ph.D., Sibylle Koletzko, M.D., Ph.D., Marian J. Rewers, M.D., M.P.H., George S. Eisenbarth, M.D., Ph.D., Polly J. Bingley, M.D., Ezio Bonifacio, Ph.D., Ville Simell, M.Sc., and Daniel Agardh, M.D., Ph.D. for the TEDDY Study Group.
    The team studied 6403 children with HLA haplotype DR3–DQ2 or DR4–DQ8 prospectively from birth in the United States, Finland, Germany, and Sweden. The study’s primary end point was the development of celiac disease autoimmunity, which the team defined as the presence of tTG antibodies on two consecutive tests at least 3 months apart. The secondary end point was the development of celiac disease itself, which they defined as either a diagnosis on biopsy or persistently high levels of tTG antibodies.
    The average follow-up was 5 years, with an overall range of 46 to 77 months. A total of 786 children (12%) developed celiac disease autoimmunity. A total of 350 children underwent biopsy, and 291 of those were diagnosed with celiac disease. Another 21 children did not undergo biopsy, but showed persistently high levels of tTG antibodies.
    For children with a single DR3–DQ2 haplotype, rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 11% and 3%, respectively. For those with two copies (DR3–DQ2 homozygosity) rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 26% and 11%, respectively.
    The adjusted hazard ratios for celiac disease autoimmunity were 2.09 (95% confidence interval [CI], 1.70 to 2.56) among children with one gene, and 5.70 (95% CI, 4.66 to 6.97) among children with both genes, as compared with children who had the lowest-risk genotypes (DR4–DQ8 heterozygotes or homozygotes).
    Living in Sweden was also independently associated with an increased risk of celiac disease autoimmunity (hazard ratio, 1.90; 95% CI, 1.61 to 2.25). Children with the HLA haplotype DR3–DQ2, especially homozygotes, were found to be at high risk for celiac disease autoimmunity and celiac disease early in childhood.
    People in Sweden face a higher risk for celiac disease autoimmunity and celiac disease than residents of other countries. These finding highlight the importance of studying environmental factors associated with celiac disease.
    Source:
    N Engl J Med 2014; 371:42-49July 3, 2014. DOI: 10.1056/NEJMoa1313977

  • 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