-
Welcome to Celiac.com!
You have found your celiac tribe! Join us and ask questions in our forum, share your story, and connect with others.
-
Celiac.com Sponsor (A1):
Celiac.com Sponsor (A1-M):
-
Get Celiac.com Updates:Support Our Content
Search the Community
Showing results for tags 'esophagus'.
-
Celiac.com 03/23/2022 - There's not much solid data, and no clear consensus, on the connection between eosinophilic esophagitis and celiac disease. There seems to be no clear pattern to the conditions in which they occur together in patients. A team of researchers recently set out to investigate rates of esophageal eosinophilia and eosinophilic esophagitis in a large group of children with celiac disease, and to prospectively follow the group over an eleven year period. The research team included Fernanda Cristofori; Fulvio Salvatore D’Abramo; Vincenzo Rutigliano; Vanessa Nadia Dargenio; Stefania Castellaneta; Domenico Piscitelli; Davide De Benedittis; Flavia Indrio; Lidia Celeste Raguseo; Michele Barone; and Ruggiero Francavilla. They are variously affiliated with the Interdisciplinary Department of Medicine, Pediatric Section “B. Trambusti”, University of Bari “Aldo Moro” in Bari, Italy; the Department of Emergency and Organ Transplantation, Section of Gastroenterology, University of Bari “Aldo Moro” in Bari, Italy; the Department of Emergency and Organ Transplantation, Section of Pathology, University of Bari “Aldo Moro” in Bari, Italy; the Department of Information Engineering, University of Pisa, Largo L. Lazzarino in Pisa, Italy; and the Department of Medical and Surgical Science, University of Foggia, Viale L. Pinto, 71122 Foggia, Italy. The team used data from a prospective observational study performed between 2008 and 2019. They used ESPGHAN criteria to make celiac disease diagnosis. They sampled at least four esophageal biopsies in patients who underwent endoscopy. The team defined esophageal eosinophilia as at least 15 eosinophils/HPF seen on esophageal biopsy. They diagnosed eosinophilic esophagitis using the International Consensus Diagnostic Criteria for Eosinophilic Esophagitis. The team diagnosed a total of 465 children with celiac disease. A total of three hundred and seventy patients underwent endoscopy, while the team found esophageal biopsies for 313 of those. The rate of esophageal eosinophilia in children with celiac disease was 1.6%. Just a single child was diagnosed with eosinophilic esophagitis, for which the team calculated a prevalence rate of 0.3%. Overall, the team saw eosinophilic esophagitis in celiac patients at a rate at least 6.5 times higher than in the general population. According to the team, eosinophils over 15/HPF do not have a clinical implication or warrant intervention in celiac patients, so they do not recommend esophageal biopsies beyond what may be clinically indicated. This is one of the first studies to put some hard numbers on the connection between eosinophilic esophagitis and celiac disease. The idea that people with celiac disease don't generally need to worry about eosinophilic esophagitis is one less thing to deal with in the often confusing world of living with celiac disease. Read more: Nutrients 2021, 13(11), 3755
-
- celiac disease
- eosinophilia
- (and 3 more)
-
Celiac.com 12/17/2021 - Gastro-esophageal reflux disease, or GERD, is the focus of considerable medical attention at the moment. This very old problem has gotten some new attention as it has recently been recognized as a significant factor in some pulmonary diseases(1) and esophageal malignancies(2). While some sufferers have few or no symptoms of reflux disease, most of us feel at least some degree of discomfort when a mixture of food particles and stomach acids are pushed back up the esophagus where there is less protection from harsh stomach acid. The protection diminishes the further up the esophagus the acid rises as there is some mucous produced in the lower reaches of the esophagus nearer the stomach. The unprotected tissues further up the esophagus are burned, often causing pain, and sometimes, permanent damage(2). We need only turn on our television sets to see the frequent and expensive advertising campaigns for the various products available to treat this widespread problem of indigestion and heartburn. If you regularly experience heartburn or indigestion, you may take one of the many drugs that are often prescribed to reduce production of stomach acid. Or you may just take one or more of the over-the-counter remedies such as Tums, Gaviscon, Rolaids, Mylanta, etc. But all of these products, whether prescribed or not, simply mask the symptoms of GERD without addressing the underlying cause. Many of us who have gluten-induced disease have experienced some degree of relief from GERD symptoms after beginning a gluten-free diet. Prior to my diagnosis of celiac disease, I not only took prescription medications in a vain attempt to control the acidity in my stomach and throat, I also ate a huge quantity of Tums and/or Rolaids every day, all day long. The lucky ones among us experience complete, long-lasting relief from indigestion and heartburn. For those of us who aren’t so lucky, the problem may be caused by one or more of several factors such as smoking, excessive alcohol consumption, or allergic reactions to the foods we are eating. If you struggle with excess acid production and/or esophageal reflux, it may be the result of your immune system reacting to the contents of your stomach. When such immune reactions are mounted, histamine is released into the stomach which triggers excessive secretion of gastric acid. If there isn’t enough food in the stomach to absorb the acid produced, we begin to feel uncomfortable. We may eat more food to get temporary relief or we may take one or more of the remedies listed above. Weight gain and obesity are predictable results of eating more and more to control stomach acid production. Prescription and non-prescription anti-acid strategies pose a host of other health problems—from inducing vitamin deficiencies— to compromising the immune protection provided by stomach acids. Whatever we choose, GERD is likely to continue until we address the underlying problem by eliminating allergenic foods from our diet. The first step in this elimination process is to identify the foods that are triggering an immune response. There are simple, convenient IgG antibody blood tests available to help identify the specific foods that are causing your discomfort. If you are following a gluten-free diet and you continue to experience GERD, you may benefit from this testing. However, if you have been free of gluten for more than a few months, you should not expect these tests to identify any of the gluten grains (Also, such negative results should not be taken to imply that it is safe to return to eating gluten). Once the allergenic foods have been identified, they should be strictly removed from your diet for at least six months. You can try re-introducing the offending foods after that time, but some immune reactions may last many years. Even six years after my own IgG food allergy testing, I must still avoid eggs, dairy proteins, and several other foods that were identified back then. The lab that did my testing (Immuno Labs, Ft. Lauderdale) provided information on the strength of the immune reaction to each allergenic food. From weak to strong, the reactions were numbered +1 to + 4. This has been very helpful because I was able to re-introduce most of the foods marked +1 and +2 after about six months. Whether you follow a gluten-free diet or not, if you are experiencing heartburn and/ or indigestion, food allergy testing may be just what you need. It has proven very helpful to my family and me. References: Katz PO. Gastroesophageal reflux disease and extraesophageal disease. Rev Gastroenterol Disord. 2005;5 Suppl 2:31-8. Suzuki H, Iijima K, Scobie G, Fyfe V, McColl KE. Nitrate and nitrosative chemistry within Barrett’s oesophagus during acid reflux. Gut. 2005 Nov;54(11):1527-35.
- 2 comments
-
- esophagus
- food allergy
- (and 8 more)
-
Celiac.com 06/24/2010 - Scientists have previously seen a nuclear fluorescence reactivity (NFR) pattern on monkey esophagus in sections which were exposed to celiac disease patients that were sera positive for anti-endomysium antibodies (EMA). Because of this prior knowledge, scientists created a new study to illustrate the NFR, to study NFR positive results in connection with gluten withdrawal, and also to assess the possible role of NFR in celiac disease follow-up's. For twelve months, scientists closely evaluated twenty untreated celiac patients, eighty-seven treated celiac patients, and fifteen healthy control subjects. Scientists incubated the sera of all 122 patients on monkey esophagus sections. The goal was to evaluate the existence of NFR by indirect immunofluorescence analysis. To asses the rate of NFR in culture supernatants, duodenal mucosa samples from treated celiac patients were challenged with gliadin peptides. Scientists evaluated the reactivity of NFR immunoglobulins (Igs) response to the nuclear extract of human intestinal cells. What they found was that serum NFR was visible in all untreated celiac patients and it persisted for up to 151 +/-37 days from gluten withdrawal. It reappeared in treated celiac patents when they did not stick to their dietary restrictions. Serum NFR was also present in two of the healthy control subjects. NFR presented itself before EMA, in culture supernatants of celiac intestinal mucosa that was challenged with gliadin peptides. The Igs responsible for NFR were labeled as, “IgA2 Subclass”. The NFR had different results than the EMA and anti-nuclear antibodies, although they reacted with two nuclear antigens of 65 and 49 kDa. Thus, a new auto-antibody named NFR, which is related to celiac disease, was depicted. In conclusion, the studies of NFR have demonstrated that NFR detection has potential to be used as a beneficial tool in monitoring compliance of a gluten-free diet, as it has the ability to diagnose slight dietary shifts pertaining to gluten. Source: Clinical and Experimental Immunology
-
The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada. There is much evidence linking untreated celiac disease with malignancy. I have recently been notified of publication of a report I have written on that connection, which is promised for the September, 1997 issue of Medical Hypotheses (1). In that report, I combine a review of the literature with an outline of a possible biochemical pathway whereby psychoactive peptides derived from the pepsin digests of wheat, rye and barley may down-regulate the activation of natural killer cells, the bodys first line of defense against malignancy. This is not a postulation that glutinous grains are carcinogenic. Humankind has been exposed to carcinogens throughout its ~ two million year evolution. But it is only in recent centuries that malignancy has increased exponentially, and has struck so many children and adolescents. This is clearly a counter-evolutionary trend when youngsters are afflicted, because the incidence should be decreasing over time, as these youngsters genes are being pruned from the gene pool. There is some evidence that has come to light since my aforementioned report, which will be of interest to celiacs and members of their families. M. Stanislas Tanchou, a truly visionary physician, and campaigned with Napoleon Bonaparte, presented a paper to the Paris Science Society in 1843, which was a complex statistical examination of malignancy, offering evidence of increased malignancy with increased civilization (2). One of the prime indicators of a civilizing trend was a diet that included cereal grains. The greater the consumption of these foods, the greater the incidence of malignancy (3). Dr. Chris Reading, an orthomolecular psychiatrist, in Australia, has documented the treatment of five cancer patients for depression (4). His testing for food allergies, and subsequent treatment of depression with dietary exclusion of cereal grains resulted in total remission of the cancers (which were also given conventional treatments) in all five patients he reports treating. One of these patients did die, but that was from the cancer treatment. There are also two reports in the Journal of Clinical Gastroenterology (5) Lancet (6) that I cite in my Medical Hypotheses article. These reveal a total remission of malignancy in each patient. One report then recants the original diagnosis, and identifies the correct diagnosis as lymphadenopathy. In the other report, which spurs a heated debate, the original diagnosis is supported by a resected section of malignant bowel, and there can be no doubt as to the correct diagnosis. Further, in a 1977 report, in Nutrition and Cancer (8), from Stanford University, all the children suffering from radiation and chemotherapy damage to the small bowel recovered fully from their chronic enteritis, and suffered no relapse of either the bowel obstruction or the disease. The treatment they were given was a gluten-free, dairy-free, low fat, low residue diet. In an obscure Czech journal, a report has recently indicated that one or more of the gliadins, a sub-set of proteins in gluten, may also interfere with natural killer cell activation in peripheral blood (9). They tested the levels of natural killer cell activation in normal, and in treated celiacs, and found no significant difference. BUT, after 30 minutes exposure of the celiacs blood to gliadin, there was a reduced activation of natural killer cells. For the last hundred years, billions of dollars have been spent identifying carcinogens. Most of what we encounter in our environment appears to have some measure of carcinogenic potential. Unfortunately, we have failed to reconcile that Humanity has been exposed to most of these carcinogens throughout its evolution. Conventional wisdom has pointed to the increasing levels of chemical pollution and environmental damage. And I do not doubt that these factors are contributing to the current epidemic of malignancy. What I do doubt is that segment of the population, variously reported at 20% to 30%, which has the HLA factors which predispose to celiac disease and many other autoimmune diseases, can mount an adequate immune response, with natural killer cells, against malignancy. References: Hoggan R, Considering Wheat, Rye, and Barley Proteins as Aids to Carcinogens in press Medical Hypotheses, 1997. Tanchou S, Statistics of Cancer London Lancet 1843; Aug 5, 593. Audette R, personal communication. Reading C, Meillon R, Your Family Tree Connection, Keats; New Canaan, Conn.: 1988. Wink A, et. al. Disappearance of Mesenteric Lymphadenopathy with Gluten-Free Deit in Celiac Sprue, J. Clin. Gastroenterol, 1993; 16(4): 317-319. Wright DH, et. al. Celiac disease and Lymphoma, Lancet 1991; 337:1373. Wright DH, et. al. letter Lancet 1991; 338: 318-319. Donaldson SS, Effect of Nutrition as Related to Radiation and Chemotherapy, Nutrition and Cancer, Winick ed. 1977; Wiley & Sons, NewYork, 137153. Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H, Natural Killer Cell Activity in Celiac Disease: Effect of in Vitro Treatment on Effector Lymphocytes and/or Target Lymphoblastoid, Myeloid and Epithelial Cell Lines with Gliadin, Folia Microbial, 1995 (Praha) 40; 6: 615-620.
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8-M):
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8):
Celiac.com Sponsor (A8-M):