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    Is Gluten Causing You Numbness or "Pins and Needles"?


    Dr. Vikki Petersen D.C, C.C.N


    • Journal of Gluten Sensitivity Winter 2014 Issue


    Image Caption: Image: CC--Roger H. Goun

    Celiac.com 12/06/2016 - Neurological problems are a very common effect of gluten intolerance. Whether you have celiac disease or gluten sensitivity, there is research showing that gluten can cause nervous system problems in affected individuals.


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    What kind of problems? When it comes to the nervous system, symptoms run the gamut from depression to schizophrenia, from migraines to brain fog, and from seizures to numbness and pain.

    I want to share more information with you about a particular type of nervous system ailment called peripheral neuropathy. The name basically means damage to the nerves of the extremities (arms and legs) that typically manifests in numbness and pins and needles-type pain that all of us have experienced at one time or another if we sat on our feet too long or fell asleep in a weird position and had a hand ‘go to sleep'. While these latter type incidents are normal, having such symptoms occur when no pressure is being put on the nerve is abnormal.

    Not only is it uncomfortable to have such sensations, but when truly numb, accidents from tripping or burning oneself can occur due to not having adequate sensation.

    I think it is interesting to note that the most common occurrence of peripheral neuropathy is seen in type I diabetes, an autoimmune disease. Celiac is also an autoimmune disease and according to the University of Chicago's Center for Peripheral Neuropathy, 10% of those diagnosed with celiac disease have a neurological problem, and peripheral neuropathy is quite common.

    Taking it a step further, we know that gluten creates a leaky gut and we know that a leaky gut is associated with autoimmune disease, through several wonderful studies brought to us by Dr. Alessio Fasano and his team. Therefore, seeing a connection between gluten and peripheral neuropathy is not unexpected based on research.

    Further, despite a dearth, or scarcity, of research on gluten sensitivity, doctors currently engaged in such research cite peripheral neuropathy as one of the most common symptoms associated with gluten sensitivity. In fact neurological symptoms are frequently associated with gluten sensitivity before any digestive symptoms ever develop. And in some cases, the nervous system disorders are present with no digestive disturbances. A lack of any digestive symptoms is perhaps one of many reasons why these individuals' gluten sensitivity is missed by their doctors.

    When it comes to comparing gluten sensitivity to celiac disease, according to Dr Fasano, 30% of the patients he diagnoses with gluten sensitivity suffer a neurological ailment, a much higher percentage than that associated with celiac disease.

    How Do You Know if You Have Peripheral Neuropathy?
    The symptoms of peripheral neuropathy are numbness, a feeling of hot/cold or a pins and needles feeling that tends to start at the ends of your body's long nerves, meaning your feet and hands, before moving upwards. The symptoms can be in legs and/or arms, right side and/or left.

    Certainly, considering that type 1 diabetes is the most common cause of peripheral neuropathy, with an estimated 50% suffering some type of nerve damage, that would be the first thing to rule out.

    What Should You Do?
    If you have these symptoms and your doctor has ruled out diabetes and any other obvious sources of the problem (including any drugs you may be taking that create neuropathy as side effects), you may fit into the category of "idiopathic neuropathy". This means that you have the problem but the reason is unknown. Or is it?

    Let's look at the result of a study where researchers worked with more than 200 individuals with neuropathy, 140 of whom fell within the ‘idiopathic' category. These smart doctors tested those 140 people for antibodies to gluten, specifically utilizing the anti-gliadin antibody test – AGA-IgA and AGA-IgG. This blood test is a general blood test that is not specific to celiac disease or gluten sensitivity, but shows that the body's immune system is reacting negatively to these proteins in gluten called gliadin.

    Of those tested, 34% were positive to one or both tests, compared to 12% of the general population. Interestingly, a full 9% of those tested in the ‘idiopathic' group actually had celiac disease, compared to 1% of the general population. And perhaps even more interesting, 80% of that same idiopathic group had the genes for celiac disease, either HLA-DQ2 or HLA-DQ8. 80%!! In the normal population that number is about 40%.

    Our takeaway message is that peripheral neuropathy has a rather high correlation to immune reaction to gluten – be it celiac disease or gluten sensitivity. Therefore anyone you know who suffers with such symptoms absolutely should be checked for gluten intolerance. Regaining one's strength and correcting nervous system abnormalities is well worth the change in diet when gluten is the cause. Such cases have been described in the literature where the only treatment that led to success was a gluten-free diet.

    So many diseases and symptoms can be prevented and reversed by discovering their true underlying root cause and for many of those ailments it is gluten that is the culprit.
    Don't continue suffering nor let you friends and family members suffer. Find out why the symptom is there rather than just masking it with a drug.
    If you need assistance, consider calling us for a free health analysis – call 408-733-0400. Our destination clinic treats patients from across the country and internationally. You don't need to live local to us to receive assistance. We are here to help!
    To your good health,

    References:

    • Hadjivassiliou M. et al. Neuropathy associated with gluten sensitivity. Journal of Neurology, Neurosurgery, and Psychiatry. 2006 Nov;77(11):1262-6.
    • Rigamonti A. et al. Celiac disease presenting with motor neuropathy: effect of gluten-free diet. Muscle & Nerve. 2007 May;35(5):675-7.
    • University of Chicago Center for Peripheral Neuropathy. Types of Peripheral Neuropathy - Inflammatory - Celiac Disease.
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    Guest Anne Gagne

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    I wonder if anyone has looked into the correlation between essential tremors (familial shake) and celiac disease?

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    I've always wondered why sometimes I can't be touched. My skin feels like pins and needles. Not all the time.

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  • Related Articles

    Jefferson Adams
    Celiac.com 10/27/2014 - There have been a few reports tying cortical myoclonus with ataxia to celiac disease. Such reports also suggest that the former is unresponsive to a gluten-free diet.
    A team of researchers recently set out to determine if there is any significant connection between the two conditions. The research team included Ptolemaios G. Sarrigiannis, Nigel Hoggard, Daniel Aeschlimann, David S. Sanders, Richard A. Grünewald, Zoe C. Unwin, and Marios Hadjivassiliou.
    They are variously associated with the Departments of Gastroenterology, Neurology, Neurophysiology and Neuroradiology at Royal Hallamshire Hospital, in Sheffield, UK, and with the College of Biomedical and Life Sciences at Cardiff University in Cardiff, UK.
    The team presented detailed electro-clinical characteristics of a new syndrome of progressive cortical hyperexcitability with ataxia and refractory celiac disease. Regular follow ups of over 600 patients with neurological manifestations due to gluten sensitivity revealed 9 patients with this syndrome.
    They found that all nine patients, six men and three women, experienced asymmetrical irregular myoclonus involving one or more limbs and sometimes face. This was often stimulus sensitive and became more widespread over time. Three patients had a history of Jacksonian march, and five had at least one secondarily generalized seizure. Electrophysiology showed evidence of cortical myoclonus. Three showed a phenotype of epilepsia partialis continua at onset.
    All patients showed clinical, imaging and/or pathological evidence of cerebellar involvement. All patients followed a strict gluten-free diet, and most successfully eliminated gluten-related antibodies. However, all patients still showed evidence of enteropathy, suggests that refractory celiac disease is to blame.
    During the study, two patients died from enteropathy-associated lymphoma and one from status epilepticus. Five patients were treated with mycophenolate and one in addition with rituximab and IV immunoglobulins. These patients showed improvement of ataxia and enteropathy, but continued to suffer the effects of myoclonus.
    These results indicate that myoclonus ataxia might be the most common neurological manifestation of refractory celiac disease.
    The clinical involvement, apart from ataxia, covers the whole clinical spectrum of cortical myoclonus.
    Source:
    Cerebellum & Ataxias 2014, 1:11. doi:10.1186/2053-8871-1-11

    Jefferson Adams
    Celiac.com 06/01/2015 - Earlier research on celiac disease and neuropathy has been hampered by the use of inpatient data, low study power, and lack of information on neuropathic characteristics.
    A team of researchers recently set out to accurately assess both relative and absolute risk of developing neuropathy in a nationwide population-based sample of patients with biopsy-verified celiac disease. The research team included Sujata P. Thawani, MD, MPH; Thomas H. Brannagan III, MD; Benjamin Lebwohl, MD, MS; Peter H. R. Green, MD; and Jonas F. Ludvigsson, MD, PhD.
    They are variously affiliated with the Peripheral Neuropathy Center at the Neurological Institute of Columbia University College of Physicians and Surgeons, the Celiac Disease Center in the Department of Medicine at Columbia University College of Physicians and Surgeons in New York, New York, with the Department of Medical Epidemiology and Biostatistics at the Karolinska Institutet in Stockholm, Sweden, and with the Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden.
    For their study, the team collected data on small-intestinal biopsies conducted at Sweden’s 28 pathology departments from 1969 to 2008. They compared the risk of neuropathy in a total of 28 ,232 celiac disease patients, all with villous atrophy, Marsh 3, against results from 139, 473 age- and sex-matched non-celiac control subjects.
    They used Cox proportional hazards regression to estimate hazard ratios (HRs), and 95% confidence intervals (CIs), for neuropathy as defined by relevant International Classification of Diseases codes in the Swedish National Patient Register; including both inpatient and outpatient data.
    They found that patients with biopsy-verified celiac disease faced a 2.5 times higher risk of developing neuropathy (95% CI, 2.1-3.0; P < .001). Celiac patients also had an increased risk of developing chronic inflammatory demyelinating neuropathy (2.8; 1.6-5.1; P = .001), autonomic neuropathy (4.2; 1.4-12.3; P = .009), and mononeuritis multiplex (7.6; 1.8-32.4; P = .006).
    However, the team found no association between celiac disease and acute inflammatory demyelinating polyneuropathy (0.8; 0.3-2.1; P = .68).
    The team found a significantly increased risk of neuropathy in patients with celiac disease, and they are recommending that doctors screen patients with neuropathy for celiac disease.
    Source:
    JAMA Neurol. Published online May 11, 2015. doi:10.1001/jamaneurol.2015.0475

    Jefferson Adams
    Celiac.com 12/28/2015 - Immune-mediated cerebellar ataxias include gluten ataxia, paraneoplastic cerebellar degeneration, GAD antibody associated cerebellar ataxia, and Hashimoto's encephalopathy.
    Despite the identification of an increasing number of immune-mediated cerebellar ataxias, there is no proposed standardized therapy.
    Recently, a research team set out to develop guidelines for treatment of immune-mediated cerebellar ataxias.
    The research team included H. Mitoma, M. Hadjivassiliou, and J. Honnorat. They are variously associated with the Department of Medical Education at Tokyo Medical University in Tokyo, Japan; the Academic Department of Neurosciences at Royal Hallamshire Hospital, Sheffield, UK; the University Lyon 1; INSERM, UMR-S1028, CNRS, UMR-5292, Lyon Neuroscience Research Center, Neuro-Oncology and Neuro-Inflammation Team, 7; and the National Reference Centre for Paraneoplastic Neurological Diseases, Hospices Civils de Lyon, Hôpital neurologique in Bron, France.
    For their study, the team evaluated the efficacies of immunotherapies in reported cases using a common scale of daily activity.
    Their resulting analysis focuses on the importance of removing autoimmune triggers (e.g., gluten or cancer), evaluating immunotherapy (e.g., corticosteroids, intravenous immunoglobulin, immunosuppressants), and adjusting according to each sub-type.
    Source:
    Cerebellum Ataxias. 2015 Nov 10;2:14. doi: 10.1186/s40673-015-0034-y. eCollection 2015.

    Jefferson Adams
    Celiac.com 08/10/2017 - Gluten ataxia is defined as sporadic ataxia with positive antigliadin antibodies without an alternative cause. Gluten ataxia patients often receive MRS at baseline and again after a period on a gluten-free diet.
    A research team recently set out to evaluate the effect of gluten free diet on magnetic resonance spectroscopy (MRS) of the cerebellum in patients with gluten ataxia.
    The research team included M Hadjivassiliou, RA Grünewald, DS Sanders, P Shanmugarajah, N Hoggard. They are with the Academic Departments of Neurosciences (M.H., R.A.G., P.S.), Gastroenterology (D.S.S.), and Neuroradiology (N.H.), Sheffield Teaching Hospitals NHS Trust, UK.
    The team included 117 consecutive patients with gluten ataxia in their report. Sixty-three followed a strict a gluten-free diet with elimination of antigliadin antibodies, 35 ate a gluten-free diet, but still tested positive for antigliadin antibodies, while 19 patients were not following a gluten-free diet.
    The N-acetylaspartate (NAA)/creatine (Cr) area ratio from the cerebellar vermis increased in 62 out of 63 (98%) patients on strict a gluten-free diet, in 9 of 35 (26%) patients on a gluten-free diet, but positive antibodies, and in only 1 of 19 (5%) patients not on a gluten-free diet. The NAA/Cr ratio decreased in all 14 ataxia control patients (cerebellar variant of multisystem atrophy), while the researchers saw no differences in the MRS results between patients with celiac disease and those without.
    Better NAA/Cr ratios seen on follow-up scans supports previous findings that gluten ataxia patients see clinical improvement a gluten-free diet
    Such improvements can occur regardless of existing enteropathy, so patients with positive serology and negative duodenal biopsy should still maintain a strict a gluten-free diet.
    Source:
    Neurology. 2017 Jul 19. pii: 10.1212/WNL.0000000000004237.doi: 10.1212/WNL.0000000000004237.

  • Recent Articles

    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:
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    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).
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    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

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257. &nbsp;doi: 10.1136/gutjnl-2015-310148.