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    Full Gut Recovery Rare in Adult Celiac Disease Despite Gluten-free Diet


    Jefferson Adams

    Celiac.com 06/18/2009 - According to the results of a recent study, complete recovery of intestinal mucosa occurs very rarely in patients with celiac disease, despite adherence to a gluten-free diet.


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    Generally, when people with celiac disease go on a gluten-free diet, they can expect to enjoy some healing of small intestinal mucosa. However, new data casts doubt over how much of this benefit is experienced in adult celiac patients.

    In order to analyze the factors that influence histological outcome of a gluten-free diet in a large cohort of adult celiac patients, a team of researchers reviewed data on 465 consecutive celiac patients studied before and during the gluten-free diet.

    The team was made up of A. Lanzini, F. Lanzarotto, V. Villanacci, A. Mora, S. Bertolazzi, D. Turini, G. Carella, A. Malagoli, G. Ferrante, B.M. Cesana, and C. Ricci. The researchers made duodenal biopsies of subjects at diagnosis, and classified results. They found 11 cases of Marsh I, 25 cases of Marsh II, and 429 cases of Marsh III.

    After an average of 16 months on a gluten-free diet, 38 patients (8%) showed histological ‘normalization’, 300 patients (65%) showed  ‘remission’ with persistent intraepithelial lymphocytosis, 121 patients (26%) remained unchanged, while 6 patients (1%) showed ‘deterioration’.* Celiac disease-related blood tests were negative in 83% of patients with Marsh III lesion during the gluten-free diet.

    Researchers independently associated male gender and adherence to a gluten-free diet with histological ‘normalization’ and ‘remission’. There seemed to be no association between persistence of intraepithelial lymphocytosis and human lymphocyte antigen gene dose, or with Helicobacter pylori infection.

    From these results, the research team concluded that complete normalization of duodenal lesions is exceptionally rare in cases of adult celiac disease despite adherence to a gluten-free diet,  disappearance of symptoms, and  negative blood tests for celiac disease.

    Aliment Pharmacol Ther 29, 1299–1308

    *Author's note: Could such deterioration be due to undetected exposure to gluten over time?

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    Guest Gerta Farber

    Posted

    Certainly a valid report on this research, BUT it is highly unfair and even dangerous. We know that many FIRST recognized effects of gluten can be in other bodily areas, such as brain diseases! This report may cause assumptions by many that a gluten-free diet will not correct ANY symptoms caused by gluten! A very harmful omission and should be rectified by Jefferson Adams in some way!

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    Guest Ann in Pittsburgh

    Posted

    I wonder if some of the remaining damage is due to ongoing ingestion of other food items that can cause a similar but lesser reaction: eggs, dairy, soy, yeast, and others.

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    Guest John B. Symes, DVM (aka Dogtorj)

    Posted

    As much as we don't want to hear this kind of thing, I certainly believe it. Gluten is only one of the foods that damage intestinal villi, with casein (dairy), soy, corn and fluoride being other major contributors. And those with celiac disease are more likely to have problems with sensitivity to the others, thanks in part to Zonulin - that barrier-opening hormone released by the intestinal tract once enough villous damage is sustained.

     

    I'd like to see a study done on the rapidly rising number of people who are going GFCFSFCF. Then we would get a much better idea of just how much harm a trace amount of gluten is causing.

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    Guest Ignacio Abel

    Posted

    We just have to ask if gluten free is enough. Maybe it's not.

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    Guest Sandra Barwick

    Posted

    Don't shoot the messenger. This is a good report of interesting research. It says specifically that symptoms disappear. If symptoms have gone the body is healing somewhere.

    What it seems to show is that the gut is very slow to heal. They tested after 16 months and I think many of us know it can take several years - and that the hardest bit of the diet is the early bit, where you keep forgetting or don't realize it's in baking powder or chips or whatever.

    I wonder if they plan to test again in five years.

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    Guest Gloria Brown

    Posted

    Without description of what the patients consumed, this study is questionable. What did this group of people eat to qualify as truly gluten-free? Packaged foods overwhelmingly contain trace amounts of gluten, even those with gluten-free labeling. Therein could be the reason a "Gluten-free" diet for most Celiacs remains ineffective. Had this study been with a group of people who consumed only fresh foods and nothing packaged (including spices, teas, medications, meats, etc.) the findings could be useful.

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    Guest Stephanie

    Posted

    Interesting that the overwhelming majority of newly diagnosed celiacs in this study were at stage III damage - just goes to show how utterly the medical system is failing at diagnosing celiac disease before the patients are half-dead. Really a pity.

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    Guest katie

    Posted

    I have one word that explains why people don't heal: CROSS-CONTAMINATION! This is a HUGE issue still being ignored. As more people go gluten free, and instead of changing eating habits they just replace all those gluten carb foods with gluten-free---this will continue to be a problem. Until all the companies and food manufacturers are aware of the seriousness of Cross-Contamination from growing to shipping to storing to grinding----lack of healing will continue. The original 'healing' diet for Celiac was NO grains whatsoever. This is what lack of funding for study of a disease not cured by a pill does for us--------leaves people still sick and in the dark! Very sad.

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    Guest Brian

    Posted

    Data are data. Over-extrapolation by doctors of what they know to fill in their lack of knowledge about celiac patients like us, has caused many of us harm and decades of issues.

     

    The study looked at nothing by villi damage. While I have seen no supporting data, I suspect that the autoimmune diseases are the result of an overreaction to gluten in the gut or after leaking into the blood. So while villi damage likely means high levels of vitamins and minerals for me the rest of my life to avoid the clear expression of deficiencies I had before, I am OK with this. It works. It is like surviving a heart attack and managing afterward. It is not repairing itself to any great extent.

     

    The fact that my hypertension, arthritis, cluster headaches, fuzziness, anxiety, and depression all flare up with abdominal distress to trace amounts of gluten I finally track down in my food diary, says to me that avoiding gluten is paramount regardless if the villi are ever restored.

     

    Would have been nice if a normal gut was a possible outcome, but if it isn't it isn't.

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    Guest Leslie E Stevens

    Posted

    The canary in the cave: my daughter has "dh" (dermatitis herpetiformis) and we were shocked to discover that most foods/vitamins/supplements labeled "Gluten Free" ARE NOT.

    She develops excema within 20 minutes of eating contaminated food. It is almost IMPOSSIBLE to eat out without getting contaminated with gluten, even at restaurants with gluten-free menus. We have learned to only buy food/supplements that are labled "CGF" = Certified Gluten Free.

    The best that we can do is eat in our gluten free home, then we are all happy (the downside of contamination is also the dark psychological aspects that visits us... for those who don't

    have dh look for dilated pupils, and/or rapid heart beat/ depression/irritability, return of sleep apnea, dark eye circles....

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    Roy Jamron
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    Jefferson Adams
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     Am J Gastroenterol. 9 February 2010; doi: 10.1038/ajg.2010.10

    Jefferson Adams
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    Jefferson Adams
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    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.
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    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.
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    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