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    Eosinophilic Esophagitis: Do You Know Anyone Who Suffers?


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


    • Journal of Gluten Sensitivity Spring 2014 Issue


    What is eosinophilic esophagitis (EoE)? Let's break it down:

    • The esophagus is the long tube that connects your mouth to your stomach. What goes through your esophagus? Food and drink.
    • Eosinophils are a type of white blood cell that increases in the case of allergy.


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    EoE is a condition where eosinophils have infiltrated the lining of the esophagus causing inflammation and discomfort. It affects both children and adults, more males than females, and can manifest in failure to thrive and feed in infants, as well as heartburn and difficulty swallowing solid food in older patients. EoE results in a stiffening of the esophagus with strictures, making it quite difficult and uncomfortable to swallow.

    It seems fairly clear that if white blood cells associated with food allergy increase in an area of the body that food passes through, the obvious conclusion to form is that the individual is eating something they are having a negative reaction to—right?

    Yet standard treatment for this condition, which is rising in incidence, is drugs (specifically proton pump inhibitors) and mechanical dilation of the restricted esophagus when these other medications fail to work. I do find it interesting that we are seeing more and more of this condition over the last 20 years, during which time the American diet has continued to worsen.

    Diagnosis is made from an endoscopy that evaluates swallowing and includes a biopsy of the esophagus that reveals a high eosinophil count.

    Causes of EoE include acid reflux, which affects the lining of the esophagus, often causing ulcers, while less common causes are viruses (herpes simplex) and fungal medications that become stuck in the esophagus, creating the inflammation seen with the condition.

    Due to the acid reflux component and the tendency in our country to treat with drugs first, proton pump inhibitors that lessen acid production and therefore lessen the symptoms of acid reflux, are recommended as the first order of treatment—even in children. The protocol is 4 to 8 weeks of the drug, after which time the symptoms are re-evaluated to see if they have improved or remain the same. If they remain, a diagnosis of EoE is made.

    I'm not saying that short-term use of proton pump inhibitors has no value. If someone has a bacterial infection of the stomach (H. pylori) that can result in ulcers, or an active ulcer, this drug is effective. It can also provide symptomatic relief for someone who is miserable with the symptoms of EoE. But it's not the root cause ‘answer' for the condition and it particularly upsets me when very young children come in who are already on the drug.

    Why?
    The problem with the protocol that uses proton pump inhibitors is two-fold:

    • It's typically not addressing the root cause, which is a food reaction.
    • It's likely making the real root cause worse. This is interesting. If the problem is actually a food reaction or allergy, a proton pump inhibitor that lessens acid production actually compromises the ability of the body to digest food. This compromised digestion makes it MORE likely that an allergy or food reaction will develop.

    Fortunately, a new study sheds light on how effective dietary treatment can be. On February 14, 2014, the journal Gastroenterology published an article entitled "Efficacy of Dietary Interventions in Inducing Histologic Remission in Patients with Eosinophilic Esophagitis: a Systematic Review and Meta-analysis.

    The researchers evaluated 581 references and data from 1317 patients, both children and adults who received different dietary treatments. The treatments included amino acid-based elemental formulas (basically a liquid diet that is completely allergen free), elimination diets based on allergy testing and 6-food elimination diets that include the removal of wheat, milk, soy, eggs, peanuts, tree nuts, fish, and shellfish.

    What the researchers looked for was the ability to reduce infiltration of the eosinophils in follow-up biopsies. This would mean that the body's immune system was no longer mounting an inflammatory response.

    Their findings were as follows:

    • Elemental diets (liquid and allergy-free) were effective in 91% of cases.
    • The Six food elimination diet was effective in 72% of the cases.
    • Foods removed based on the result of allergy tests were effective in 46% of the cases.

    Both adults and children seemed to respond equally.

    What can we learn from this study?
    Eliminating common allergens, including gluten, a known inflammatory agent, is a great place to start when trying to improve this condition. A full 91% and 72% improved when common allergic foods were removed. Those are some pretty impressive percentages.

    I have found an interesting trend in our country. If doctors have the option of giving a prescription or asking a patient to make a dietary change, they will opt for the prescription. It's certainly easier to swallow a pill rather than make a dietary and lifestyle change. I'll grant you that. But is it right?
    When you appreciate that the pill is a mere band-aid and a highly temporary one at that, what really is a doctor doing for someone in NOT insisting that they change their diet? The truth of the matter is that taking the ‘easy' way out is not only cowardly, it is irresponsible.

    After the drug stops working, then what? Realize that throughout the period of time that the patient was on the drug, they were continuing to eat whatever was actually creating the problem and therefore their esophagus became more and more inflamed. While the human body's ability to heal is quite miraculous, once sufficient hardening and strictures have occurred in the esophagus, a full return to normalcy might not be possible. It is important that we intervene with the correct therapy quickly.

    Another facet to the ‘drug over food' decision on the part of most doctors is that they themselves don't change their own diets. I have often spoken with doctors who are themselves unhealthy yet they refuse to change their diets and are therefore convinced that they won't get their patients to make lifestyle changes either. Thus, they don't tend to recommend it because they are already convinced it won't occur.

    Is it fair to the patient to take the easy way out while they continue to worsen? I don't think so.
    Personally, I can tell you that here at HealthNOW Medical Center we have seen many cases of EoE and each one of them was associated with a food reaction, often gluten and dairy. And, because we practice what we preach, we have no trouble with our patients following our dietary and lifestyle change recommendations.

    If you know any youngster, adolescent or adult suffering with this condition, show them (or their parent) this article. A simple dietary change could be all that is needed to improve this serious condition.

    If your health is not at the level you desire, consider contacting us for a free health analysis—call 408-733-0400. Our destination clinic treats patients from across the country and internationally so you do not need to live local to us to receive care. We are here to help!

    Reference:

    • Gastroenterology. 2014 Feb 14. pii: S0016-5085(14)00217-0. doi: 10.1053/j.gastro.2014.02.006. [Epub ahead of print]
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    Guest Linda Ostrow

    Posted

    NOPE. I've eliminated gluten as a result of a celiac disease diagnosis and my acid reflux is getting worse. I also have Barrett´s Esophagus which I didn't find mentioned in this article. I always thought my BE was a result of gluten but now I'm not at all sure.

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    Guest Ruth M Kratzer

    Posted

    Very interesting article. I have been having some acid reflux lately.

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    Diana Gitig Ph.D.
    Celiac.com 12/16/2011 - To date, symptoms of gastroesophageal reflux disease (GERD) - heartburn and acid regurgitation - have been among the only GI symptoms absent from the list of common manifestations of celiac disease. They are usually definitive indicators of gastric acid reflux. But a report from Julio César Bai's group in Buenos Aires notes that at the time of diagnosis, patients with celiac disease were more likely to complain of GERD symptoms than healthy controls. Moreover, maintaining a gluten free diet alleviated these symptoms. Their results are reported in Clinical Gastroenterology and Hepatology.GERD is a chronic condition usually resulting from the reflux of acidic stomach contents up into the esophagus. It is commonly treated with proton pump inhibitors, but some cases are refractory to this treatment. There has been conflicting data as to whether GERD symptoms are more common in people with celiac, and whether a gluten free diet might help. Dr. Bai's group designed a two pronged study to answer these questions: They undertook a cross sectional analysis of 133 people upon their diagnosis with celiac over the course of 2005, and a longitudinal assessment of 53 of them as they maintained a gluten free diet over the next four years.
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    Nachman F, Vázquez H, González A, Andrenacci P, Compagni L, Reyes H, Sugai E, Moreno ML, Smecuol E, Hwang HJ, Sánchez IP, Mauriño E, Bai JC. Gastroesophageal reflux symptoms in patients with celiac disease and the effects of a gluten-free diet. Clin Gastroenterol Hepatol. 2011 Mar;9(3):214-9. Epub 2010 Jun 30.
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    Leffler DA, Kelly CP. Celiac disease and gastroesophageal reflux disease: yet another presentation for a clinical chameleon. Clin Gastroenterol Hepatol. 2011 Mar;9(3):192-3. Epub 2010 Dec 8.

    Jefferson Adams
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    J Clin Gastroenterol. 2012 Jan;46(1):e6-e11.

    Jefferson Adams
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    Source:
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    Jefferson Adams
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    Canadian Journal of Gastroenterology and Hepatology. Volume 2016 (2016), Article ID 1980686, 9 pages

    Jefferson Adams
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    Archives of Disease in Childhood Published Online First: 12 April 2017. doi: 10.1136/archdischild-2016-311944

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    Dr. Ron Hoggan, Ed.D.
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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