• Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    77,334
    Total Members
    3,093
    Most Online
    AudreyAken
    Newest Member
    AudreyAken
    Joined
  • 0

    Splenic Volume Differs in Complicated vs. Non-complicated Celiac Disease


    Jefferson Adams


    • Splenic volume is the key difference between complicated and non-complicated celiac disease.


    Image Caption: Photo: CC--Susan

    Celiac.com 11/17/2016 - Studies in small groups of patients indicated that splenic volume may be decreased in patients with celiac disease, refractory celiac disease (RCD) type II and enteropathy-associated T-cell lymphoma (EATL).


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    A team of researchers recently set out to assess splenic volume in a large group of uncomplicated celiac disease, RCD II and EATL patients and in healthy controls. The research team included Tom van Gils, Petula Nijeboer, Jan Hein TM van Waesberghe, Veerle MH Coupé, Kiki Janssen, Jessy A Zegers, Shaikh A. Nurmohamed, Georg Kraal, Sabine CI Jiskoot, Gerd Bouma, Chris JJ Mulder. They are variously affiliated with the Celiac Center Amsterdam, Department of Gastroenterology and Hepatology, the Department of Radiology, the Department of Epidemiology and Biostatistics, the Department of Nephrology, the Department of Molecular Cell Biology and Immunology at VU University Medical Center, Amsterdam, The Netherlands, and with the Department of Radiology, St Jansdal, Harderwijk, The Netherlands.

    For their retrospective cohort they included 77 patients with uncomplicated celiac disease (of whom 39 in remission), 29 patients with RCD II, 24 patients with EATL, and 12 patients with both RCD II and EATL. The control group included 149 healthy living kidney donors. The team used computed tomography to determine splenic volume.

    The median splenic volume in the uncomplicated celiac disease group was significantly larger than in controls (202 cm3 (interquartile range (IQR): 154–275) versus 183 cm3 (IQR: 140–232), p = 0.02). After correction for body surface area, age and gender, the ratio of splenic volume in uncomplicated celiac disease versus controls was 1.28 (95% confidence interval: 1.20–1.36; p less than 0.001).

    On average, RCD II patients showed smaller splenic volume (118 cm3 (IQR 83–181)) than the median splenic volume in the control group (p less than 0.001).

    These results show wide variation in splenic volume among patients. In uncomplicated celiac disease, splenic volume is typically enlarged. Lower splenic volume in RCD II patients may be clinically relevant, given the the compromised immune conditions of these patients.

    Source:

    0


    User Feedback

    Recommended Comments

    There are no comments to display.



    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • Popular Contributors

  • Ads by Google:

  • Who's Online   12 Members, 1 Anonymous, 969 Guests (See full list)

  • Related Articles

    Jefferson Adams
    Celiac.com 05/24/2016 - People with type II refractory celiac disease (RCD), suffer from severe malabsorption syndrome and face a poor prognosis, as there is currently no effective treatment.
    Prompted by the regenerative and immune-influencing properties of mesenchymal stem cells (MSCs), a research team recently set out to assess the viability, safety, and efficacy of a series of infusions of autologous bone marrow-derived MSCs in a 51-year-old woman with type II RCD.
    The research team included R Ciccocioppo, A Gallia, MA Avanzini, E Betti, C Picone, A Vanoli, C Paganini, F Biagi, R Maccario, and GR Corazza. They are variously affiliated with the Department of Internal Medicine, Fondazione IRCCS Policlinico San Matteo and Università degli Studi di Pavia, the Department of Internal Medicine, Fondazione IRCCS Policlinico San Matteo and Università degli Studi di Pavia, the Cell Factory and Research Laboratory, Department of Pediatrics, Fondazione IRCCS Policlinico San Matteo and Università degli Studi di Pavia, the Clinic Cytometry Laboratory, Department of Hematology, Fondazione IRCCS Policlinico San Matteo and Università degli Studi di Pavia, Department of Molecular Medicine, Fondazione IRCCS Policlinico San Matteo and Università degli Studi di Pavia, all in Pavia, Italy.

    The team began by isolating, expanding, and characterizing mesenchymal stem cells using standard clinical protocols. For each patient, the team arranged to monitor malabsorption indexes, mucosal architecture, and percentage of aberrant intraepithelial lymphocytes at the time of enrollment, at each infusion, and after 6 months.
    The also arranged to assess mucosal expression of interleukin (IL)-15 and its receptor. Once the team determined that the expansion of MSCs was feasible, they provided the patient with four systemic infusions of 2 × 106 MSCs per kg body weight 4 months apart, with no adverse effects.
    Over the course of the treatment, the patient experienced gradual and durable improvement of her condition, including normalized stool frequency, body mass index, laboratory test results, and mucosal architecture. Most impressively, the expression of IL-15 and its receptor almost completely vanished.
    Based on this clinical case, treatment of RCD with serial MSC infusions seems to offer a path to recovery from this life-threatening condition, while blocking the IL-15 pathogenic pathway.
    This is the first successful treatment of refractory celiac disease. Stay tuned for further developments regarding the use of stem cell infusions to treat refractory celiac disease.
    Source:
    Mayo Clin Proc. 2016 Apr 14. pii: S0025-6196(16)30004-0. doi: 10.1016/j.mayocp.2016.03.001.

    Jefferson Adams
    Celiac.com 07/11/2016 - Collagenous sprue is a rare form of small bowel enteropathy characterized by a thickened basement membrane and is considered to be directly related to celiac disease.
    Doctors have numerous treatment strategies for celiac sprue, but there is currently no effective standardized therapy. One medical team recently described four cases of celiac sprue and proposes thioguanine (6-TG) treatment, based on their results.
    The research team included Tom van Gils, Tine van de Donk, Gerd Bouma, Foke van Delft, E Andra Neefjes-Borst, and Chris JJ Mulder. They are variously affiliated with the Department of Gastroenterology and Hepatology, VU University Medical Center, Amsterdam, The Netherlands, Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
    The team reviewed 4 cases of celiac sprue. They got their data from the prospective database of patients referred to their celiac centre. The team had an expert pathologist evaluate the small bowel biopsies.
    None of the patients had ever shown celiac-specific antibodies, and all were negative for HLA-DQ2 and HLA-DQ8 phenotype. Three patients were treated with a combination of 6-TG and budesonide, and 1 patient received 6-TG only. All patients improved remarkably.
    They found normalized thickening of the basement membrane in 2 patients, and complete histological improvement, including full recovery of villi, in 1 patient. In the third patient, the thickened basement membrane was only very focally recognized. The thickened membrane remained in the last patient, likely due to the short follow-up time.
    Celiac sprue should be separated from celiac disease. Based on the lack of typical HLA phenotyping and the absence of celiac-specific antibodies, there seems to be no relation with celiac disease in these four patients.
    A promising treatment option might be 6-TG with or without budesonide. Larger study groups are needed to develop an effective standardized treatment for celiac sprue.
    This is exciting for folks with celiac sprue, as they previously had no good treatment options at all.
    Source:
    BMJ Open Gastro 2016; 3:e000099. doi:10.1136/bmjgast-2016-000099

    Jefferson Adams
    Celiac.com 10/17/2016 - Refractory celiac disease is a severe condition with few good treatment options, and which often eventually results in death. A group of researchers recently set out to create a prognostic model to estimate survival of patients with refractory celiac disease.
    The research team included A. Rubio-Tapia, G. Malamut, W. H. M. Verbeek, R. L. J. van Wanrooij, D. A. Leffler, S. I. Niveloni, C. Arguelles-Grande, B. D. Lahr, A. R. Zinsmeister, J. A. Murray, C. P. Kelly, J. C. Bai, P. H. Green, S. Daum, C. J. J. Mulder, and C. Cellier. They are variously affiliated with the Mayo Clinic, Rochester, MN, USA, the Hopital Europeen Georges-Pompidou, Paris, France, the Hospital Dr. Carlos Nonorino Udaondo, Buenos Aires, Argentina, the Columbia University Medical Center, New York, NY, USA, Beth Israel Deaconess Medical Center, Boston, MA, USA, the Charite-University Medicine Berlin, Berlin, Germany, and the VU University Medical Centre, Amsterdam, The Netherlands.
    Before setting up their prognostic model, the team first assessed predictors of 5-year mortality using Cox proportional hazards regression on subjects from a multinational registry. The team used bootstrap resampling to internally validate the individual factors and overall model performance. To calculate a risk score for 5-year mortality, the team averaged all estimated regression coefficients gathered from 400 bootstrap models that they formulated from their multinational cohort of 232 patients diagnosed with refractory celiac disease across seven centers.
    Average patient age was 53 years and the group included 150 women out of the 232 patient total. A total of 51 subjects died during a 5-year follow-up, which put the cumulative 5-year all-cause mortality at 30%.
    The results from a multiple variable Cox proportional hazards model showed that the following variables were significantly associated with 5-year mortality: age at refractory celiac disease diagnosis (per 20 year increase, hazard ratio = 2.21; 95% confidence interval, CI: 1.38–3.55), abnormal intraepithelial lymphocytes (hazard ratio = 2.85; 95% CI: 1.22–6.62), and albumin (per 0.5 unit increase, hazard ratio = 0.72; 95% CI: 0.61–0.85). A simple weighted three-factor risk score was created to estimate 5-year survival.
    The team's prognostic model for predicting 5-year mortality among patients with refractory celiac disease may help clinicians to guide treatment and follow-up.
    Source:
    Alimentary Pharmacology & Therapeutics. DOI: 10.1111/apt.13755View/save citation

    Jefferson Adams
    Celiac.com 11/03/2016 - Refractory celiac disease type II (RCDII) often transforms into an enteropathy-associated T-cell lymphoma (EATL), a serious condition that requires intensive treatment. Current treatment strategies for RCDII include cladribine(2-CdA) and autologous stem cell transplantation (auSCT).
    A team of researchers recently set out to assess long-term survival in refractory celiac disease type II, and to define clear prognostic criteria for EATL development comparing two treatment strategies. They also wanted to evaluate histological response as prognostic factor. The research team included P Nijeboer, RLJ van Wanrooij, T van Gils, NJ Wierdsma, GJ Tack, BI Witte, HJ Bontkes, O Visser, CJJ Mulder, and G Bouma. They are variously affiliated with the Department of Gastroenterology, the Department of Nutrition and Dietetics, the Department of Epidemiology and Biostatistics, the Department of Pathology, and the Department of Haematology at VU University Medical Centre in Amsterdam, The Netherlands.
    For their study, they retrospectively analyzed 45 patients. All patients received 2-CdA, after which they were either closely monitored (monotherapy, n=30) or received a step-up approach, including auSCT (step-up therapy, n=15). Ten patients (22%) developed EATL, nine of whom had received monotherapy. Absence of histological remission after monotherapy was associated with EATL development (p=0.010). A total of 20 patients (44%) died, with an average survival of 84 months.
    Overall survival (OS) in the monotherapy group was far better in those with complete histological remission compared to those with without histological remission.
    The monotherapy patients, who achieved complete histological remission, showed comparable EATL occurrence and OS as compared to the step-up therapy group (p=0.80 and p=0.14 respectively).
    Histological response is an accurate parameter to evaluate the effect of 2-CdA therapy and this parameter should be leading in the decisions whether or not to perform a step-up treatment approach in RCDII.
    Source:
    United European Gastroenterology Journal, April 2016; DOI: 10.1177/2050640616646529

  • 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