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    Jefferson Adams
    Celiac.com 02/02/2012 - A team of researchers recently conducted a prospective controlled study on a gluten-free diet and autoimmune thyroiditis in patients with celiac disease.
    The research team included S. Metso, H. Hyytiä-Ilmonen, K. Kaukinen, H. Huhtala, P. Jaatinen, J. Salmi, J. Taurio, and P. Collin. They are affiliated with the Department of Internal Medicine at Tampere University Hospital in Tampere, Finland.
    Prior to the study, there had been contradictory data regarding the ways in which early diagnosis and a gluten-free diet might slow the progression of associated autoimmune diseases in celiac disease.
    The research team investigated the course of autoimmune thyroid diseases in newly diagnosed celiac disease patients, both before and after gluten-free dietary treatment.
    For their study, the team examined twenty-seven adults with newly diagnosed celiac disease, both at the time of diagnosis and after one year on gluten-free diet.
    They also recorded and examined previously diagnosed and subclinical autoimmune thyroid diseases. The team used ultrasound to measure thyroid gland volume and echo-genicity. They also measured autoantibodies against celiac disease and thyroiditis, and conducted thyroid function tests.
    As a control group, they enrolled twenty-seven non-celiac subjects, all of whom followed a normal, gluten-containing diet.
    The data showed that, upon diagnosis, ten of 27 celiac disease patients had either manifest (n = 7) or subclinical (n = 3) thyroid diseases. Only three of 27 control subjects (10/27 vs. 3/27, p = 0.055) had thyroid disease.
    After treatment with a gluten-free diet, thyroid volume continued to decrease significantly in the patients with celiac disease compared with the control subjects, indicating the progression of thyroid gland atrophy regardless of the gluten-free diet.
    Overall, celiac patients faced a higher risk of thyroid autoimmune disorders than non-celiac control subjects. Moreover, a gluten-free diet did not seem to stop or reverse the progression of autoimmune disease after one year.
    Source:

    Scand J Gastroenterol. 2012 Jan;47(1):43-8. Epub 2011 Nov 30.

    Jefferson Adams
    Celiac.com 05/07/2012 - People with celiac disease face a higher risk of developing primary hyperparathyroidism (PHPT) in the early years after their celiac disease is diagnosed, according to a new report from Sweden. The report appears in the The Journal of Clinical Endocrinology & Metabolism.
    A team of researchers recently set out to examine the risk of primary hyperparathyroidism (PHPT) in people with celiac disease. The researchers included Dr. Jonas F. Ludvigsson, Olle Kämpe, Benjamin Lebwohl, Peter H. R. Green, Shonni J. Silverberg and Anders Ekbom. They are affiliated with the Department of Pediatrics (J.F.L.) at Örebro University Hospital in Örebro, Sweden, the Clinical Epidemiology Unit (J.F.L., A.E.) of the Department of Medicine at Karolinska Institutet in Stockholm, Sweden; the Department of Medical Sciences (O.K.) at Uppsala University and University Hospital in Uppsala, Sweden; and Celiac Disease Center (B.L., P.H.R.G.), and Division of Endocrinology, Department of Medicine (S.J.S.) at Columbia University College of Physicians and Surgeons in New York city, USA.
    At least one other study has suggested an association between celiac disease and primary hyperparathyroidism.
    For their study, Dr. Jonas F. Ludvigsson from Orebro University Hospital and colleagues examined the risk of PHPT among 17,121 patients with biopsy-verified celiac disease. They found that patients with celiac disease faced a 1.91-fold increased risk of PHPT compared to 85,166 matched controls.
    Ignoring the first year, due to a risk of ascertainment bias, the team found that the risk level for PHPT increased 3.29-fold through 60 months, and disappeared after that period.
    The decrease in risk level over time may be due to the beneficial effect of the gluten-free diet, the team noted. For every per 100,000 person-years at risk, the absolute risk level from one to five years of follow-up was 61 cases in patient, compared with just 22 cases in controls. The overall risk level was even greater, by 2.53 times, when the outcome was restricted to PHPT with an adenoma diagnosis in the National Cancer Registry.
    A review of the data show that the increased risk of PHPT persisted after restricting the analysis to 1987 or later, which post-date changes in ICD coding. The risk for PHPT was slightly higher for women diagnosed with celiac disease after menopause than for women diagnosed earlier in life.
    Their study does not "provide any insight into the nature of the association between celiac disease and PHPT," the authors admit. They are unsure whether the association  is causal or whether celiac disease and PHPT might be tied another unidentified condition.
    Because most patients with untreated celiac disease have vitamin D and calcium deficiencies, the team expected to find a "constellation of celiac disease and elevated parathyroid hormone levels," but that they did not expect to see a connection between celiac disease with hypercalcemia and PHPT.
    The team calls for future studies to focus on thoroughly investigating the connection, so that researchers can understand all possible aspects of the link between these two conditions.
    Source:
    J Clin Endocrinol Metab 2012

    Jefferson Adams
    Celiac.com 01/05/2017 - Patients who have both pancreatic disease and celiac disease can experience adverse endocrine and exocrine changes. When this happens, severe clinical changes with marked nutritional alteration may result. For some patients, a gluten-free diet can help improve endocrine and exocrine pancreatic function.
    Also, numerous studies show that people with celiac disease have higher rates of type 1 diabetes mellitus. In part, this relationship was possibly due to shared human leukocyte antigen alleles, DR3, and by linkage disequilibrium, DQ2. Besides this hypothesized common "immune-mediated" etiopathogenesis, some celiacs with pancreatic disease likely have developed secondary diabetic changes from severe exocrine pancreatic failure, driven in part by celiac-induced protein malnutrition.
    Some researchers estimate that more than one in five celiac patients have defective pancreatic function, possibly due to impaired release of peptides, because of mucosal endocrine cell loss.
    Researcher Hugh J. Freeman recently set out to evaluate the prevalence of type 1 diabetes in celiac disease. He is a gastroenterologist affiliated with the Department of Medicine, University of British Columbia, Vancouver, BC, Canada.
    Prospective studies using an initial screening IgA tissue transglutaminase antibody assay (tTG) were done at the university center, while a total of 125 male and 108 female children and adolescents with type 1 diabetes mellitus were evaluated from an established pediatric diabetes clinic. Of these, 15 male and 11 female patients had elevated tTG titers, of whom 19 were also positive for endomysial antibodies. Among these cases, 1 was already known to have celiac disease. Small intestinal biopsies were done in the other 18 children positive for both antibodies.
    In all, histopathological changes consistent with celiac disease were detected, ranging from increased numbers of intraepithelial lymphocytes to severe crypt hyperplastic villous atrophy (i.e., so-called Marsh 3 lesion). Studies also suggested that serial tTG titers in insulin-dependent diabetic children might play a useful clinical role in monitoring compliance to a gluten-free diet, possibly of value since close monitoring of compliance of children to a gluten-free diet may be exceedingly difficult.
    In this study, over 40% of diabetic children were asymptomatic, and yet, prospective serological screening facilitated selection for small intestinal biopsy evaluation. Overall, 7.7% of this entire pediatric patient population had biopsy features common in celiac disease. A subsequent European study found 8.6% of diabetic children and adolescents to have tTG positivity; many had no symptoms, or only non-specific or mild gastrointestinal symptoms.
    Prior studies have shown increased serum amylase levels in about 25% of patients, indicating possible low-grade pancreatic inflammation. Later studies examined exocrine pancreatic function in celiac disease by measuring fecal elastase-1 concentrations along with magnetic resonance imaging (MRI) showed pancreatic insufficiency in 4 of 90 celiacs, or 4.4% (1 mild, 3 severe), while MRI was normal in all 4 of these celiac patients.
    In contrast, a study from India shows exocrine pancreatic insufficiency in 10 of 36 young adults under 30 years of age, based on fecal elastase determinations. Of these, over 80% showed reversal of elevated fecal elastase values on a gluten-free diet.
    Most had moderate to severely abnormal small bowel biopsies (i.e., Marsh 2-3C) and only 1 had recurrent bouts of acute pancreatitis. Structural changes based on imaging studies were rarely encountered.
    Although his own study, like a number of others, has documented the relationship between pancreatic exocrine function and celiac disease, Dr. Freeman calls for further longer-term study to determine if these observations can be verified by other centers.
    Source:
    Ann Gastroenterol. 2016 Jul-Sep; 29(3): 241–242. Published online 2016 May 20. doi: 10.20524/aog.2016.0048 PMCID: PMC4923808

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    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