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Found 8 results

  1. Celiac.com 06/12/2017 - Previously, Transcranial Magnetic Stimulation in de novo celiac disease patients has signaled an imbalance in the excitability of cortical facilitatory and inhibitory circuits. Researchers have reported that, after about of 16 months on a gluten-free diet, patients experience a global increase of cortical excitability, which suggests some kind of compensation for disease progression, likely mediated by glutamate. To better assess these finding, a team of researchers recently conducted cross-sectional evaluation of the changes in cortical excitability to TMS after a much longer gluten-free diet. The research team included M. Pennisi, G. Lanza, M. Cantone, R. Ricceri, R. Ferri, C.C. D’Agate, G. Pennisi, V. Di Lazzaro, and R. Bella. They are variously affiliated with the Spinal Unit, Emergency Hospital "Cannizzaro", Catania, Italy, the Department of Neurology IC, I.R.C.C.S. "Oasi Maria SS.", Troina, Enna, Italy, the Department of Medical and Surgical Sciences and Advanced Technologies, Section of Neurosciences, University of Catania, Catania, Italy, the Gastroenterology and Endoscopy Unit, University of Catania, Catania, Italy, the Department "Specialità Medico-Chirurgiche,” University of Catania, Catania, Italy, and the Institute of Neurology, Campus Bio-Medico University, Rome, Italy. For their study, the team enrolled twenty patients who had followed an adequate gluten-free diet for about 8.35 years, on average. They then compared the results with twenty de novo patients, and twenty more healthy controls. The team measured Transcranial Magnetic Stimulation, recorded from the first dorsal interosseous muscle of the dominant hand, as follows: resting motor threshold, cortical silent period, motor evoked potentials, central motor conduction time, mean short-latency intracortical inhibition and intracortical facilitation. De novo patients showed a shorter cortical silent period, while responses for gluten-free diet participants were similar to controls. Regardless of diet, all celiac patients showed a significantly smaller amplitude of motor response than did control subjects, Again, without regard to diet, all celiac patients showed a statistically significant decrease of mean short-latency intracortical inhibition and enhancement of intracortical facilitation with respect to controls. The team also observed that gluten-free celiac patients showed more intracortical facilitation compared to non-gluten-free patients. Neurological examination and celiac disease-related antibodies were both negative. This study showed that a gluten-free diet helps to mitigate the electrocortical changes associated with celiac disease. Even so, in many patients, an intracortical synaptic dysfunction, mostly involving excitatory and inhibitory interneurons within the motor cortex, may persist. The calls for further investigation into the clinical significance of subtle neurophysiological changes in celiac disease. Source: PLoS One. 2017 May 10;12(5):e0177560. doi: 10.1371/journal.pone.0177560. eCollection 2017.
  2. Celiac.com 06/02/2009 - Celiac disease is an autoimmune disorder thatis triggered by gluten, and it is being diagnosed more often than inthe past. Previously considered quite rare, it is now estimated tooccur in 1 in 100-150 people in all societies (with the possibleexception of Japan). Physical activity counters some of the lastingsymptoms of celiac disease, but some of the symptoms actually mayinhibit physical activity. Older adults (+55) with celiac disease mayhave positive or negative attitudes toward physical activity. As itstands, we’re not sure whether celiac disease helps or hinders theirwill to exercise. There are many symptoms associated with celiac disease. They mayinclude neurological symptoms, physical symptoms and overall feelingsof fatigue or depression. This makes celiac disease difficult toidentify, but also forces individuals with celiac disease to find theirown individualized balanced lifestyles. Balanced lifestyles areespecially important for older adults with celiac disease because, asanyone diagnosed with a disease knows, they must maintain theirphysical wellbeing in order to heal. Older adults with celiac diseaseare also at risk of gaining weight after starting a gluten free dietbecause their bodies absorb nutrients so much more efficiently thanbefore, and because many gluten-free breads and desert substitutes maybe higher in calories than their gluten-containing counterparts. Because each person with celiac disease exhibits different symptoms,each older adult with celiac disease must find their own way of livingwith the disease. Their will to excercise depends on how celiac diseasehas affected their appetite, energy level, mental health, nervoussystem and overall body functions. Research about the attitudes of older adults with celiac disease toward physical activity will help to understand: The general attitudes of older adults with celiac disease toward physical activity; The symptoms of celiac disease that directly or indirectly affect older adults’ attitudes toward physical activity; How physicians, recreation centres, celiac associations and theCanadian Government can work with people with celiac disease tomaintain or increase their levels of physical activity, and; Provide literature on nutrient deficiency and physical activityto patients in need of information or reassurance about their attitudestoward physical activity. Celiac disease may negatively affect the attitudes of people withceliac disease toward physical exercise and activity in two differentways. First, celiac disease symptoms inhibit exercise. Chronic andacute pain, fatigue, bruising and other symptoms associated withnutrient deficiency and celiac disease recovery could easily affect themotivation that people with celiac disease have to exercise. Second,the exercise may exacerbate symptoms of celiac disease. Certain studies have shown that allergies can exacerbate or inducefood-dependent allergy symptoms (Sampson, 2003). If someone with celiacdisease were to experience symptoms as if they were having an allergicreaction to gluten when they conducted certain exercises, they wouldeither try to push through, stop, or change their exercise program orschedule. They could exercise only in the morning, before breakfast andafter a long period of not eating, or they could choose activities withless physical impact, such as walking/hiking, or biking. Symptoms of celiac disease may also encourage exercise. If an olderadult with celiac disease finds out that they have low bone density,they may choose to increase their weight bearing activity to encouragebone growth. There is a long list of symptoms that are associated with celiacdisease. Some of the symptoms of celiac disease that are documented inliterature about include: No obvious physical symptoms (just fatigue, overall not feeling well) Gastrointestinal symptoms Fatigue Weight loss Pallor (unhealthy pale appearance) Flatulence Borborygmi (stomach rumbling) Nausea Vomiting Anorexia Voracious appetite Iron deficiency anemia Failure to thrive Lymphocytic gastritis Vitamin B12 deficiency Vitamin D deficiency Hypocalcaemia/ hypomagnesaemia Vitamin K deficiency Coetaneous bleeding Epitasis (nose bleeding) Hematuria (red urine) Gastrointestinal hemorrhage Celiac Disease affects the nutrient absorption level of the smallintestine, and people diagnosed with celiac disease should therefore betested for vitamin deficiencies. Side effects of nutrient deficiencyvary from person to person, but the level of nutrient deficiency mayaffect the amount that someone with celiac disease will exercise. Forexample, a person's calcium absorption rate may affect their bonedensity, and a person's iron absorption rate may affect their energylevels. In general, weight-bearing exercise is associated with strongerbone density. Anemia (lack of iron), though, decreases a person’senergy levels. Depending on the person, the two opposing influences offatigue and bone density loss may sway the person’s attitude towardexercise in different ways. This is the subject of a human geography honours project at theUniversity of Victoria. If you have any comments on the subject, pleasecontact me by using the comment form below this article. Related Articles: Sampson, H.A. (2003). Food Allergy. Journal of Allergy Clinical Immunology. 111:2, S540-S547. Sategna-Guidetti, C. et al. (2000). The effects of 1-year glutenwithdrawal on bone mass, bone metabolism and nutritional status innewly diagnosed adult coeliac disease patients. Alimentary Pharmacology& Therapeutics. 14, 35-43. Palosuo, K. (2003). Transglutaminase-mediated cross-linking of apeptic fraction of w-5 gliadin enhances lgE reactivity inwheat-dependent, exercise-induced anaphylaxis. Journal of Allergy andClinical Immunocology: 111:6, 1386-1392.
  3. Celiac.com 02/24/2014 - What kind of impact does gluten have in on the microbial gut activity of healthy people without celiac disease? A team of researchers set out to answer that question by studying the metabolism of gluten in healthy individuals, and the effects of gluten on their intestinal microbial activity. The research team included A. Caminero, E. Nistal, L. Arias, S. Vivas, I. Comino, A. Real, C. Sousa, J.M. de Morales, M.A. Ferrero, L.B. Rodríguez-Aparicio, and J. Casqueiro, all with the Área de Microbiología at the Universidad de León in León, Spain. The team analyzed fecal samples from eleven healthy subjects under four different diet regimens: a normal gluten diet, a strict gluten-free diet (GFD), a GFD with a supplemental intake of 9 g gluten/day and a GFD with a supplemental intake of 30 g gluten/day. In each case, they measured gluten content, fecal tryptic activity (FTA), short-chain fatty acids (SCFAs) and fecal glutenasic activity (FGA). Fecal gluten contents, FTA, SCFAs and FGA varied sharply, according to levels of dietary gluten intake. When patients received high gluten doses, over 30 grams per day, they showed sharply higher SCFA concentrations of around 70.5 mmoles per kg of feces, compared with concentrations of around 33.8 mmoles per kg feces during the gluten-free phase of the experiment. However, the FTA showed significant differences between the GFD (34 units) and the normal gluten-containing diet (60 units), and also between the GFD and the GFD + 30 g of gluten/day (67 units). In every case, when patients regularly consumed gluten, gluten was detected in the feces. This demonstrates that at least a portion of the ingested gluten is eliminated in the large intestine, thus offering a substrate for intestinal microbial proteases. The results also showed that fecal glutenasic activity increased proportionally with dietary gluten, showing an enzymatic activity of 993 units in DSG, 2,063 units in DSG + 9 g and 6,090 units in DSG + 30 g. Gluten consumption definitely influences the activity of intestinal microbes, and also increases gluten proteolytic activity in the feces of healthy, non-celiac individuals. Undoubtedly, more research needs to be done to determine what, exactly these findings mean for the study of celiac disease. Source: Eur J Nutr. 2012 Apr;51(3):293-9. doi: 10.1007/s00394-011-0214-3.
  4. Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H Natural killer cell activity in coeliac disease: effect of in vitro treatment on effector lymphocytes and/or target lymphoblastoid, myeloid and epithelial cell lines with gliadin Folia Microbiol, 1995 (Praha) 40; 6: 615-620. In this study researchers tested the levels of natural killer cell activation in normal people and compared the results with treated celiacs, and found no significant difference. However, after exposing the celiacs blood to gliadin for thirty minutes the researchers found a reduced activation of natural killer cells, which is the bodys first line of defense against malignancy. These results provide further support to the theory that gluten is a carcinogen to celiacs.
  5. Celiac.com 10/28/2009 - Celiac disease is a T cell-mediated autoimmune disease, and a number of clinicians have described up-regulation of T-bet and phosphorylated signal transducers and activators of transcription (pSTAT)1, both of which are key transcription factors for the development of T helper type 1 (Th1) cells, in the mucosa of patients with untreated celiac disease. A team of researchers recently used transcription factor analysis to examine whether celiac patients up-regulate T-bet and pSTAT1 expressions in peripheral blood and whether such up-regulation may be associated with celiac disease activity. The research team was made up of G. Frisullo, V. Nociti, R. Iorio, A. K. Patanella, D. Plantone, A. Bianco, A. Marti, G. Cammarota, P. A. Tonali, and A. P. Batocchi of the Department of Neurosciences at the Catholic University in Rome, Italy. The team used flow cytometry to analyze T-bet, pSTAT1 and pSTAT3 expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes from peripheral blood of 15 untreated and 15 treated celiac disease patients and 30 controls, and longitudinally in five celiac patients before and after dietary treatment. The team measured the results using enzyme-linked immunosorbent assay (ELISA), interferon (FN)-gamma, interleukin (IL)-17 and IL-10 production by peripheral blood mononuclear cell (PBMC) cultures. Patients with untreated celiac disease showed higher T-bet expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes and IFN-gamma production by PBMC, than either treated celiac patients or control subjects. CD4(+)T cells, B cells and monocytes from untreated celiac patients showed higher pSTAT1 expression than either treated celiac patients or controls. Only in monocytes from untreated patients showed increased pSTAT3 compared with treated celiac patients and controls. Data from longitudinal evaluation of transcription factors corroborated these findings. Flow cytometric analysis of pSTAT1 and T-bet protein expression in peripheral blood mononuclear cells could be useful and sensible markers in the follow-up of celiac disease patients to evaluate disease activity and response to dietary treatment. Being able to spot celiac disease early is key to achieving optimal outcomes for celiac patients. The development of simple, reliable, low-cost tests is key to that effort. Stay tuned for more developments regarding celiac disease testing, screening and diagnosis. Source: Clinical & Experimental Immunology, Volume 158 Issue 1, Pages 106 - 114
  6. Br J Dermatol. 2004 Oct;151(4):891-4 Celiac.com 11/09/2004 – A study carried out by Irish researchers to determine whether there is an association between celiac disease antibodies and psoriasis activity found that the presence of Antigliadin antibodies (AGA) did increase the severity of the disease. The researchers looked at 130 patients with psoriasis and screened them for serum IgG and IgA AGA, IgA antitransglutaminase and IgA antiendomysial antibodies. The patients were invited to undertake an endoscopy with duodenal biopsy. They found that a significantly higher proportion of psoriasis patients had elevated celiac disease associated antibody levels, and those with elevated antibodies had previously required systemic immunosuppressants or psoralen plus ultraviolet A phototherapy. Out of the 130 patients one new case of celiac disease was diagnosed. The researchers conclude that the presence of celiac disease associated antibodies in psoriasis patients correlates with greater psoriasis activity.
  7. Celiac.com 04/23/2007 - A study published in a recent issue of the journal Gut suggests that wheat gliadin might trigger pathological development in mucosal cells that are already abnormal, but otherwise tolerated, within the intestinal tracts of individuals with celiac disease. Researchers at the Universita degli Studi di Napoli Federico II in Naples, Italy, led by Dr. Salvatore Auricchio looked at the effects of gliadin peptides on various cell lines and celiac mucosal cells in culture. More specifically, the study evaluated the effects of gliadin and affiliated toxic peptides such as A-gliadin P31-43 on endocytosis, cell proliferation, apoptosis, cytoskeleton rearrangements, and activation of epidermal growth factor receptor (EGFR). The researchers report that gliadin peptides induce EGF-like effects across a wide range of cell types. Actin rearrangements and cell proliferation are examples of these effects. Also, they state that gliadin peptides act not as ligands of the EGF receptor, but that they actually inhibit EGFR endocytosis. According to the research team, these observations of gliadin-induced delay of EGFR endocytosis, along with S-phase entry of epithelial intestinal cells, clearly indicate that EGFR plays a role in celiac disease. Dr. Auricchio proffers that a genetic factor in celiacs may bring about deregulated activity in the endocytotic pathway that is compensated in the absence of gliadin. The study concludes that wheat gliadin slows receptor deactivation of Epidermal Growth Factor. This may explain how wheat gliadin and related cereal prolamines trigger rapid increase in cell growth and associated disease activity in people with celiac disease. Gut 2007;56:480-488.
  8. TI- Disaccharidasen-Aktivitaten als Beurteilungskriterium der Dunndarmschleimhaut. AU- Stern M; Plettner C JN- Monatsschr Kinderheilkd; 131 (5) p264-8 PY- May 1983 AB- Activities of lactase, sucrase, and maltase were determined in small intestinal biopsies of 125 children with Coeliac disease, cows milk protein intolerance, transient gluten intolerance, nonspecific enteropathies, and controls. Four cases of primary disaccharidase deficiencies could be identified. In the enteropathies, morphometric data were more closely correlated to the degree of the mucosal lesion (r = -0.92 for crypt depth) than were disaccharidase activities (r = 0.61 for lactase). In a stepwise discriminate analysis of the patient groups, based upon immunological, morphometric, and biochemical variables, lactase activity was a valuable secondary criterion, ranking third among the variables used.
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