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    Poles Finding More Celiac Disease, Less Symptoms


    Jefferson Adams

    Celiac.com 04/02/2009 - A recent study finds rates of celiac disease in Polish children are four times higher than estimated, and are only slightly lower than those of other northern European populations—at about 1 in 124 persons. Moreover, they found that symptoms in those diagnosed were typically absent, minimal or vague.


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    To date, the only epidemiological studies of celiac disease undertaken in Poland had been carried out within limited areas and involved mainly symptomatic patients or high-risk groups. Until now, celiac was thought to affect about 1 in 400 children in the country. A team of researchers based in Poland recently set out to determine actual rates of celiac disease among Polish children.

    The research team was made up of Anna B. Szaflarska-Poplawska, Monika Parzecka, Lucyna Muller, Waldemar Placek. The team enrolled 3235 local children aged 12 to 15 years from the city of Bydgoszcz, and conducted screens for antiendomysial antibodies IgA endomysium (EmA) and IgG EmA. Patients with positive  IgA EmA and/or IgG EmA results were offered a small-bowel biopsy.

    They found that 25 children showed positive IgA EmA and/or IgG EmA results (0.8%). 11 children elected to undergo biopsy. 7 showed histological features of celiac disease of either Marsh stage III-B or III-C, 4 children showed normal histology, while 14 children opted to skip the small-bowel biopsy.

    As is common with celiac disease, more girls than boys were affected (P<0.0001), while 2 of the 7 children with celiac disease showed no symptoms, and the other 5 presented only vague or mild symptoms.

    Original national estimates put the incidence of celiac disease among children in Poland at1 in 404, while the team’s serologic sampling shows that to be nearly four times higher at 1 in 124.

    The authors note that these updated figures are slightly lower than those of other countries, and that symptoms were generally absent, or vague and unclear symptoms course, despite the presence of advanced lesions in the small bowel. Overall, though, it seems that the rates found in Poland match rates in North America, which all hover at about 1% of the population.

    Of particular interest is the rise of asymptomatic, or vaguely symptomatic instances of the disease, in which damage is occurring, but no outward signs are present.

    Medical Science Monitor 2009.

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    Guest Sharon

    Posted

    Recently, I went back to the celiac.com "archives" and read this piece. Being of Polish descent, I found this intriguing, as my symptoms were there for decades but were insidious and subtle; they moved from system to system, yet never incapacitated me as I stayed of strong mind and will. As I grew older, it was easy for doctors to blame my issues on my weight, peri-menopause and menopause, then simply aging. Even the doctor who diagnosed me wanted to put me on an anti-depressant a few years before my diagnosis, only to discover I had one of the lowest Vitamin D levels she had ever seen. I am in my mid-fifties, and while I am one of those obese celiac disease folks and I still have weight to get off (it quickly stabilized on the gluten-free diet), I feel and look ten years younger! If I could only get my stubborn relatives of Italian (another big ethnic group with celiac disease) and Polish descent to listen and get tested, or at least go gluten-free to see if their symptoms and disorders (similar to what I suffered) lessen.

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    ----------
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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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    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). 
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    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.
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    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