• 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

    77,337
    Total Members
    3,093
    Most Online
    Lovisa
    Newest Member
    Lovisa
    Joined
  • 0

    T-bet and pSTAT-1: New Genetic Markers for Celiac Disease?


    Jefferson Adams

    Celiac.com 01/18/2013 - Up-regulation of T-bet and phosphorylated signal transducers and activators of transcription (pSTAT)1 are key transcription factors for the development of T helper type 1 (Th1) cells, and have been found in the mucosa of patients with untreated celiac disease.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    CC--Mervi EskelaninA team of researchers recently set out to determine if T-bet and pSTAT-1 expression in PBMC from celiac disease patients might offer new genetic markers of disease activity.

    The research team included G. Frisullo, V. Nociti, R. Iorio, A.K. Patanella, D. Plantone, A. Bianco, A. Marti, G. Cammarota, P.A. Tonali, A.P. Batocchi. They are affiliated with the Department of Neurosciences at Catholic University in Rome, Italy.

    For their study, the team used transcription factor analysis to determine whether T-bet and pSTAT1 expressions are up-regulated in the peripheral blood of celiac disease patients, and if they correlate with disease activity.

    They used flow cytometry to analyse T-bet, pSTAT1 and pSTAT3 expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes from peripheral blood of 15 untreated and 15 treated celiac disease patients and 30 controls. They also conducted a longitudinal study of five celiac patients before and after treatment with a gluten-free diet.

    For their evaluation, the team used enzyme-linked immunosorbent assay (ELISA), interferon (FN)-gamma, interleukin (IL)-17 and IL-10 production by peripheral blood mononuclear cell (PBMC) cultures.

    They found that T-bet expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes and IFN-gamma production by PBMC was higher in untreated than in treated celiac disease patients and control subjects.

    They also found that pSTAT1 expression was higher in CD4(+)T cells, B cells and monocytes from untreated celiac disease patients than from treated patients and control subjects.

    Compared with treated celiac disease patients and control subjects, untreated patients showed increased pSTAT3 only in monocytes.

    They confirmed their results using data obtained from the longitudinal evaluation of transcription factors.

    From their results, they conclude that flow cytometric analysis of pSTAT1 and T-bet protein expression in peripheral blood mononuclear cells could be useful and sensible markers in the follow-up of celiac disease patients to evaluate disease activity and response to dietary treatment.

    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   21 Members, 1 Anonymous, 1,090 Guests (See full list)

  • Related Articles

    Scott Adams
    Gastroenterology Volume 129, Issue 3, Pages 786-796 (September 2005) Celiac.com 09/14/2005 - Researchers have long thought that the resistance of gliadin prolamines to digestive enzymes is a primary contributor to celiac disease—which leads to the intestinal permeability and inflammation in those who are at risk. Taking prolyl-endopeptidase enzymes (PEP) orally has been proposed and explored as a possible treatment for celiac disease (including extensive research done at Stanford Universitys Celiac Sprue Research Foundation – CSRF). In an effort to determine the feasibility of such a treatment, researchers in France conducted both in vitro (outside a living organism) and ex vivo—using biopsy specimens of active celiac disease patients—studies on the effects of PEP on gliadin peptides.
    For the in vitro studies the researchers used radio-reverse-phase high-performance liquid chromatography and mass spectrometry to analyze the degradation by PEP of 3H-labeled gliadin peptides 56-88 (33-mer). In the ex vivo studies the researchers added PEP and 3H-peptides together onto the mucosal side of duodenal biopsy specimens that were mounted in Using chambers, and the peptide transport and digestion were analyzed using radio-reverse-phase high-performance liquid chromatography.
    The results indicate that in both in vitro and ex vivo studies the gliadin peptides were only partly degraded by 20 mu/ml of PEP. This concentration of PEP decreased the quantity of intact gliadin peptides (31-49 and 56-88) that crossed the intestinal biopsy specimens, but did not prevent the intestinal passage of toxic or immunostimulatory metabolites—for this the researchers determined that PEP concentrations of at least 500 mu/ml for at least 3 hours was required to achieve full detoxification of gliadin peptides, and thus prevent intestinal transport of active fragments—unfortunately this finding virtually eliminates PEP as a possible treatment option for those with celiac disease.
    The researchers conclude optimistically, however: "After prolonged exposure to high concentrations of PEP, the amount of immunostimulatory gliadin peptides reaching the local immune system in celiac patients is decreased. These results provide a basis to establish whether such conditions are achievable in vivo (in living organisms)."

    Destiny Stone
    Celiac.com 08/18/2010 - The importance of an accurate celiac disease diagnosis is becoming increasinglymore evident to health practitioners and the general public worldwide. While the outcomes of undiagnosed celiac disease are still unclear,current  studies are attempting to find an answer.
    Between 1995 and 2001, serum samples were obtained from 16,886 Olmsted County, Minnesota citizens 50 years of age or older with unknown celiac status.
    Out of 16,847 adults studied, 129 cases were discovered to have undiagnosed celiac disease. 127 undiagnosed celiacs and 254 unmatched controls were then submitted for a systematic evaluation in search of over 100 possibly coexisting ailments.
    The scientists found that while celiac disease has been associated with an elevated risk for cancer, this study found no significant risk increase for cancer in undiagnosed celiacs compared to the control group.
    Researchers also found that those patients with undiagnosed celiac disease displayed an increased rate of osteoporosis and hypothyroidism. Furthermore, undiagnosed celiacs were also found to typically have a lower body mass index, and lower levels of ferritin and cholesterol, and to be less prone to arthritis and have a reduced rate of glucose intolerance. The correlation between lower arthritis and glucose intolerance in undiagnosed celiacs is speculated to be a result of a lower body mass index. 
    In conclusion, researchers were not able to determine a connection between undiagnosed celiac in older adults and comorbidity. In fact, except for impaired bone health, most undiagnosed celiacs in this study displayed little comorbidity and they did not have increased mortality rates when compared to the control group.
    Researchers of this study therefore concluded that there may be advantages and disadvantages to being an older undiagnosed celiac.
    Source:

    Gastroentrology doi:10.1053/j.gastro.2010.05.041

    Gryphon Myers
    Celiac.com 07/22/2013 - Celiac disease is known to be caused by a combination of genetic and environmental factors. The genetic markers are fairly well established by now, but the environmental factors that are associated with celiac disease are still pretty foggy. A recent study suggests that antibiotic use might be one such factor.
    In a population-based case-control study analyzing Swedish population data, antibiotic use was compared against diagnosis of celiac disease. 2,933 people with celiac disease diagnoses were linked to the Swedish Prescribed Drug Register, in order to provide a history of antibiotic use. 2,118 people with inflammation (early celiac disease) and 620 people with normal mucosa but positive celiac disease blood test results were also compared. The control group consisted of 28,262 individuals matched for age and sex from the general population.
    The results of the study significantly suggest that antibiotic use is associated with celiac disease, at an odds ratio of 1.4 (1.27-1.53 confidence interval). Early celiac disease was also connected, with an odds ratio of 1.90 (1.72-2.10 confidence ratio), as well as positive celiac disease blood tests, at 1.58 odds ratio (1.30-1.92 confidence interval). Even when antibiotic use in the last year was ruled out, the results were very similar at 1.30 odds ratio (1.08-1.56 confidence interval). When ruling out patients with additional diseases, which could potentially be factors, the results were also very similar at 1.30 odds ratio (1.16-1.46 confidence interval).
    What does all that mean? A 1.4 odds ratio basically means that people who had a history of antibiotic use were 1.4 times as likely as those who had not taken antibiotics to develop celiac disease. The fact that inflammation associated with early celiac disease was also highly connected suggests that antibiotics' role in disrupting the biology of the GI tract could in some way cause celiac disease. There is still some question of causality, but it would seem that antibiotics could very likely be a culprit in the development of celiac disease, and should be avoided when possible.
    Source:
    http://www.biomedcentral.com/1471-230X/13/109/abstract

    Jefferson Adams
    Celiac.com 01/06/2014 - A team of researchers recently set out to clarify the role of the immune system and intestinal epithelium in the origins of celiac disease.
    The research team included S. Ben-Horin, S. Polak-Charcon,I. Barshack, O. Picard, E. Fudim, M. Yavzori, C. Avivi, C. Mardoukh, A. Shimoni, Y Chowers, Y. and Maor, of the Department of Gastroenterology in Chaim Sheba Medical Center at Tel-Aviv University, Tel Hashomer in Tel-Aviv, Israel.
    For five years, the team followed a patient with childhood celiac disease who had undergone an allogeneic bone marrow transplant (BMT) for chronic myelogenous leukemia, and subsequently resumed consuming a gluten-containing diet.
    Using standard serology testing, along with CFSE-based proliferation assays of peripheral blood CD4+ cells and of intestinal LPL towards gliadin-TTG antigens, the team assessed immunological memory to gliadin epitopes in both the control patient and in 5 newly diagnosed celiac patients.
    They used combined immuno-histochemistry and fluorescent in-situ hybridiazation (FISH) to determine the origin of the intestinal lymphocytes.
    They found that the patient remained healthy for more than 5 years of follow-up after receiving BMT from a HLA-matched woman, and ceasing the gluten-free diet. The continued to show negative periodic antibodies tests and unremarkable serial duodenal biopsies.
    In vitro tests showed lack of a memory response of the patient's peripheral blood and lamina propria CD4+ T-cells towards TTG, gliadin or TTG-treated gliadin, whereas memory responses were common in the newly diagnosed celiac patients.
    Immuno-FISH of post-BMT duodenal mucosa showed that all the epithelial cells had the chromosomal phenotype of XY. In contrast, CD45+ lymphocytic lineage cells were all donor-derived XX cells, presumably originating in the transplanted bone marrow and re-populating the intestinal wall.
    The resolution of celiac disease after allogeneic BMT does occur, and is associated with absent gliadin-specific memory response, and with a dichotomous lymphocyte-epithelial chimeric intestine. These findings suggest that the origins of celiac disease are deeply connected to the immune system, rather than the epithelial area.
    Source:
     J Clin Immunol. 2013 Nov;33(8):1395-402. doi: 10.1007/s10875-013-9943-9. Epub 2013 Oct 20.

  • 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