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Found 1,243 results

  1. On Thursday, 16 November 1995 14:46:57 -0500, The SPRUENIK AFD had: Dr. Alexander: In reviewing the syllabus for the Baltimore conference, there are some points that I wonder about. The syllabus suggests the frequency of celiac disease (celiac disease) may be 1 in 250 people. Perhaps it is in Ireland and certain other locations where there is a homogenous population this may be true. But could it really be 1 in 250 people in Italy, which is practically synonymous with pasta? You would expect there to be an epidemic of complications. Perhaps the definition of celiac disease used in these studies is less stringent than it is here. If the studies are based on symptoms or positive blood tests, they could be including a lot of false positives in their statistics. Or perhaps the studies are based on relatives of celiacs, in which case you would pick up a higher percentage of celiacs than you would from the general population.
  2. William Dickey Department of Gastroenterology, Altnagelvin Hospital, Londonderry, Northern Ireland, UK Scandinavian Journal of Gastroenterology 1998; 33: 612-5. Abstract Background: Coeliac disease may present with dyspepsia or reflux. There are characteristic duodenal appearances associated with villous atrophy (mosaic pattern mucosa and loss, reduction in number or scalloping of duodenal folds) which may prompt small bowel biopsy during routine upper gastrointestinal endoscopy. These appearances were sought in patients referred by their general practitioners for open access endoscopy (OAE), to determine the prevalence and significance of coeliac disease as a cause of symptoms. Methods: Five hundred consecutive patients undergoing OAE by one consultant gastroenterologist were studied. Forceps biopsies from the distal duodenum were taken if appearances were suggestive. If villous atrophy was confirmed, the response of symptoms to dietary gluten exclusion was assessed. Results: Ten patients had suspicious endoscopic appearances of whom 8 had villous atrophy, giving a prevalence of coeliac disease of 1.6% (1:63). All 8 had mosaic pattern mucosa with three also having reduction of duodenal folds, and four having scalloped folds. All had serum endomysial antibodies (EmA). Apart from diarrhea, described by one patient, there were no symptoms of typical coeliac disease at diagnosis: three patients were overweight. After dietary gluten exclusion, all reported symptomatic improvement with disappearance of EmA in 5 patients to date. Conclusions- There is a high prevalence of coeliac disease among patients undergoing OAE, which is relevant to their clinical symptoms and which can be identified by careful endoscopic inspection of the duodenum.
  3. W. Dickey, S.A. McMillan, D.F. Hughes Scandinavian Journal of Gastroenterology 1998; 33: 491-3 Departments of Gastroenterology and Histopathology, Altnagelvin Hospital, Londonderry; Regional Immunology Service, Royal Group of Hospitals, Belfast; Northern Ireland, UK Background: Coeliac disease is common yet often undiagnosed because symptoms may be trivial, non-specific, or non-gastrointestinal, or because of lack of clinician awareness. Serum IgA class endomysial antibodies (EmA) have high specificity for coeliac disease and may facilitate case-finding by clinicians other than gastroenterologists. We assessed the appropriateness and diagnostic yield of requests for EmA by primary care general practitioners in a defined geographical area of Northern Ireland. Methods: We identified patients who had EmA requests by their general practitioners during 1994-1996. Individual patient questionnaires were posted to the general practitioners concerned, seeking information on indications for testing, management following the result and final diagnosis. We compared new patient diagnosis rates in two catchment areas, one served by a large district general hospital with a medical gastroenterology facility and the other by smaller hospitals without. Results: A total of 239 patients had coeliac profile testing by 69 of 177 general practitioners in the area. Data were available for 181 patients not previously known to have coeliac disease of whom 20 (11%) had EmA. All EmA +ve patients were referred to hospital where 19 underwent small bowel biopsy, which confirmed coeliac disease in all 19. Only 7 (35%) of the 20 had diarrhea and there was no significant difference in EmA prevalence among patients tested with and without diarrhea. Although the mean number of new patients (per 100,000 population per annum) diagnosed by biopsy was 11 at the large hospital compared with 5 elsewhere, the numbers identified by EmA in general practice for the two catchment areas were similar (2, 3). Conclusion: General practitioners have an important role in the identification of patients with coeliac disease, particularly where there is no local medical gastroenterology facility, which is facilitated by EmA testing.
  4. The following was written by Dr. Kalle Reichelt who is a leading celiac disease researcher at the Pediatric Research Institute in Oslo, Norway. Please direct any questions regarding this article to him at: K.L.Reichelt@rh.uio.no What most people ignore is that both peptides and trace (biologically significant amounts) amounts of proteins are taken up across the gut mucosa (1,2). Because one molecule of gluten contains at least 15 opioid sequences it is quite clear that this could cause a problem. Increased peptide excretion is found in the urine of celiacs before treatment (3) (Reichelt et al in prep). This is confirmed by a series of papers that demonstrate intact food proteins in mothers milk (4-7). A Canadian group has confirmed that gluten does change a brain enzyme and monoamine levels in cats (8). Their findings a significant even though cats are not gluten eating animals. There is increasing evidence that components from food can indeed cause serious psychiatric (9-12) and neurological (13-16) diseases. Even rheumatoid arthritis may have a link to food proteins (17), and it well established that stress increases gut permeability. Nobody denies the possibility of reactive depression, but there is little reason why this could not be made worse by dietary factors. Because antibodies are indeed induced by peptides it may even be so that dietary peptides by mimicry to endogenous cell surface peptide sequences, may be responsible for many autoimmune diseases (18). References: Gardner MLG (1994) Physiology of the gastrointestinal tract. Edit: LR Johnson. Raven press 3rd edit. pp 1795-1820. Husby S et al (1985) Scand J Immunol 22:83-92. Klosse JA et al (1972) Clin Chim Acta 42:409-422. Kilshaw PJ and Cant AJ (1984) Inter. Arch Allergy Appl Immunol 75:8-15. Axelsson I et al (1986) Acta paed Scand 75:702-707. Stuart CA et al (1984) Clin Allergy 14:533-535. Troncone R et al (1987) Acta paed Scand 76:453-456. Thibault L et al (1988) J Clin Biochem Nutr. 4:209-221. Hallert C et al (1982) Psychic disturbances in adult celiac disease III.Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol 17:25-28. Singh MM and Kay SR (1976) Wheat gluten as a pthogenic factor in schizophrenia. Science 191:401-402. Dohan FC and Grasberger JC (1973) relapsed schizophrenics: earlier discharge from the hospital after cereal-free, milk-free diet. Amer J Psychiat 130:685-686. Reichelt KL et al (1990) The effect of gluten free diet on glycoprotein attached urinary peptidee excretion and behaviour in schizophrenics. J Orthomol Med 5:223-239. Gobbi G et al (1992) Celiac disease, epilepsy and cerebral calcifications. The Lancet 340:439-443. Paul K-D et al (1985) EEG-Befunde Zoeliakikranken Kindern in Abh{ngigkkeit von der Ern{hrung. Z Klin Med 40:707-709. Kahn A et al (1987) Difficulty of initiating sleep associated with cows milk allergy in infants. Sleep 10:116-121. Hadjivassiliou M et al (1996) Does cryptic gluten sensitivity play a part in neurological illness? The Lancet 347:369-371. Kjeldsen-Kragh J et al (1991) Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. The Lancet 338:899-902. Karjalainen J et al (1992) Bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. New Eng J Med 327:302-307.
  5. The following is a list of citations where you can find more information on the relationship between hypothyroidism and celiac disease: The American Family Physician web page (http://www.aafp.org/afp) has an article (March 1, 1998) on detecting Celiac in a patient. It says that autoimmune thryroid diseases were found in 5.4% of celiacs. In the Feb 15,1998 issue there is an article entitled Subclinical Hypothyroidism: Deciding When to Treat. Cole DE, et al. [see Related Articles]. Neonatal severe hyperparathyroidism, secondary hyperparathyroidism, and familial hypocalciuric hypercalcemia: multiple different phenotypes associated with an inactivating Alu insertion mutation of the calcium-sensing receptor gene. Am J Med Genet. 1997 Aug 8; 71(2): 202-210. PMID: 9217223; UI: 97360195. Corazza GR, et al. [see Related Articles] Propeptide of type I procollagen is predictive of posttreatment bone mass gain in adult celiac disease. Gastroenterology. 1997 Jul; 113(1): 67-71. PMID: 9207263; UI: 97350887. Shaker JL, et al. [see Related Articles] Hypocalcemia and skeletal disease as presenting features of celiac disease. Arch Intern Med. 1997 May 12; 157(9): 1013-1016. PMID: 9140273; UI: 97285000. Moran CE, et al. [see Related Articles] Bone mineral density in patients with pancreatic insufficiency and steatorrhea. Am J Gastroenterol. 1997 May; 92(5): 867-871. PMID: 9149203; UI: 97293150. Corazza GR, et al. [see Related Articles] Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult celiac disease. Bone. 1996 Jun; 18(6): 525-530. PMID: 8805992; UI: 96399521. Keaveny AP, et al. [see Related Articles] Bone remodeling indices and secondary hyperparathyroidism in celiac disease. Am J Gastroenterol. 1996 Jun; 91(6): 1226-1231. PMID: 8651176; UI: 96237643. Wrong O. [see Related Articles] A woman with bone pain, fractures, and malabsorption. Lancet. 1996 Mar 23; 347(9004): 829. No abstract available. PMID: 8622356; UI: 96180154. Kumar V, et al. [see Related Articles] Celiac disease and hypoparathyroidism: cross-reaction of endomysial antibodies with parathyroid tissue. Clin Diagn Lab Immunol. 1996 Mar; 3(2): 143-146. PMID: 8991626; UI: 96265434. Bertoli A, et al. [see Related Articles] A woman with bone pain, fractures, and malabsorption. Lancet. 1996 Feb 3; 347(8997): 300. No abstract available. PMID: 8569366; UI: 96158642. Rude RK, et al. [see Related Articles] Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int. 1996; 6(6): 453-461. PMID: 9116391; UI: 97183181. Molteni N, et al. [see Related Articles] Intestinal calcium absorption as shown by stable strontium test in celiac disease before and after gluten-free diet. Am J Gastroenterol. 1995 Nov; 90(11): 2025-2028. PMID: 7485015; UI: 96048763. Pratico G, et al. [see Related Articles] [Calcium-phosphorus metabolism in celiac disease in children]. Pediatr Med Chir. 1995 Sep; 17(5): 403-406. Italian. PMID: 8684993; UI: 96286520. Corazza GR, et al. [see Related Articles] Bone mass and metabolism in patients with celiac disease. Gastroenterology. 1995 Jul; 109(1): 122-128. PMID: 7797010; UI: 95317529. Gonzalez D, et al. [see Related Articles] Body composition and bone mineral density in untreated and treated patients with celiac disease. Bone. 1995 Feb; 16(2): 231-234. PMID: 7756052; UI: 95275602. Mazure R, et al. [see Related Articles] Bone mineral affection in asymptomatic adult patients with celiac disease. Am J Gastroenterol. 1994 Dec; 89(12): 2130-2134. PMID: 7977227; UI: 95067822. Wortsman J, et al. [see Related Articles] Case report: idiopathic hypoparathyroidism co-existing with celiac disease: immunologic studies. Am J Med Sci. 1994 Jun; 307(6): 420-427. PMID: 8198149; UI: 94256518. Bolla G, et al. [see Related Articles] [Tertiary hyperparathyroidism revealing celiac disease in adults]. Presse Med. 1994 Feb 19; 23(7): 346. French. No abstract available. PMID: 8208699; UI: 94269013. Lindh E, et al. [see Related Articles] Screening for antibodies against gliadin in patients with osteoporosis. J Intern Med. 1992 Apr; 231(4): 403-406. PMID: 1588266; UI: 92268780. Caraceni MP, et al. [see Related Articles] Bone and mineral metabolism in adult celiac disease. Am J Gastroenterol. 1988 Mar; 83(3): 274-277. PMID: 3257843; UI: 88147922
  6. Collin P et al. (1994) Celiac disease - associated disorders and survival. Gut vol 35 (9):1215 1218. Abstract: The associated diseases in 335 celiac patients diagnosed 1980-1990 were compared with age and sex matched control patients with various gastrointestinal symptoms. Endocrine disorders were found in 11.9% of celiac and 4.3% of control patients (p=0.0003). Celiac patients had insulin dependent diabetes mellitus significantly (p=0.0094) more often (5.4%) than control patients (1.5%). Connective tissue diseases were found in 7.2% of celiac and 2.7% of control patients (p=0.011). Sjogrens syndrome occurred in 3.3% of celiac patients and 0.3% of controls (p = 0.0059). Autoimmune thyroid diseases were found in 5.4% and asthma in 3.6% of celiac patients but also in 2.7% and 3.6%, respectively, among control patients. The incidences of malignant disease and the survival rate in celiac patients were compared with those in the Finnish population. Ten celiac patients developed a cancer during the follow up (mean 5.3 years, range 1-12) but none had a lymphoma. The risk of malignant disease did not differ from that in the Finnish population in general. Eleven celiac patients died during the follow up. The five year survival rate of celiac patients did not differ from those in the general population. At least 83% of the celiac patients adhered strictly to the gluten free diet, which may explain the favorable outcome.
  7. The following was taken from a lecture given by Dr. Joseph Murray in October, 1996. It was published by the Sprue-Nik Press (Published by the Tri-County Celiac Sprue Support Group, a chapter of CSA/USA, Inc. serving southeastern Michigan) Volume 5, Number 9, December 1996. Dr. Joseph Murray, one of the leading USA physicians in the diagnosis of celiac disease (celiac disease) and dermatitis herpetiformis (DH). Dr. Murray (murray.joseph@mayo.edu) of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease: Q: Can you touch on bone pain? A: The most common cause of severe bone pain with untreated celiac disease is osteomalacia, which is malformation of the bones due to lack of Vitamin D and calcium. It affects mostly the hips, and sometimes the shoulders and back. It usually gets better with specific treatment, which includes the gluten-free diet for celiacs and sometimes includes Vitamin D supplementation and other interventions. Another cause of bone pain is osteoporosis. It can often cause pain in the back, due to vertebrae which have become shortened and have begun squeezing the nerves. This condition is very painful and is not going to get better; once the vertebrae have shortened they are not going to stretch back up to their original size. Muscle pain can also occur, due to Vitamin D deficiency. I have seen some leg pains as the initial presentation of celiac disease which cleared up with the gluten-free diet.
  8. Of the many immune related disorders linked with the celiac condition, the best established connection is with Type I diabetes (mellitus). Type I diabetes occurs at a rate of about 0.5% in the general population, but at a rate estimated at 5-10% among celiacs. Normally the diabetes is diagnosed first, both because this form of diabetes tends to strike early in life and its diagnosis is certain. No connection has been found with the more common form of diabetes (mellitus= honey , from the sugar laden urine when uncontrolled), Type II which occurs at a rate of 2-2.5% in the general population. In Type I diabetes, the insulin producing cells of the pancreas are destroyed by the immune system, perhaps in overreaction to some kind of infection (The incidence of Type I is highest in the winter.) Normally, insulin is released into the blood for distribution to nearly all cells in the body so glucose can be burned for energy. There are indirect connections with protein and fat metabolism as well which give rise to some of the poisons that build up in the absence of insulin. For glucose, cells have an insulin receptor on the surface: once insulin is bound there, glucose can enter and hence be metabolized. At diagnosis, the Type I presents itself with a better defined form of malnourishment than celiac disease: hyperglycemia (high blood sugar), weight loss, excessive thirst, excessive urination laden with (un-metabolized) sugar and protein, a fruity smell to the breath and little or no insulin in the blood. Treatment consists of 1-3 subcutaneous injections of insulin a day and control of carbohydrate intake. The recommended diet for diabetes, long before it was recommended for everyone, consisted of less fat and protein and more carbohydrate. Complex carbohydrates (less quickly metabolized) were recommended to cut down the peak in blood glucose that occurs about two hours after eating. It was, and is, a perfect Jane Brody diet - lots of fresh fruit and vegetables, hence with lots of fiber. The restriction on sugar is indirect: only the total carbohydrates must be controlled. So, if you have some sugar, you must eliminate something else (less carbohydrates probably), and have to put up with less on the plate. Control of Type I is certainly more of a nuisance than celiac disease, but also one with much better information readily available. Food labels are nearly adequate for controlling carbohydrate intake; the risks of the various long term complications versus average blood glucose are well known; relatively inexpensive, reliable home monitoring of blood glucose is possible to even out the daily peaks and valleys; a longer term blood test reliably measures average blood glucose for sufficient monitoring of longer term risks. Like celiac disease, Type I diabetes is more common in those of northern European extraction. Like celiac disease, it is highly linked to the so-called HLA markers of the immune system (those marking white blood cells). Celiacs are likely to be positive for both HLA-B8 and HLA-DR3; Type Is are most linked to HLA-B8 and either HLA-DR3 or HLA-DR4. An English study several months ago found that multiple genes were linked to Type I reflecting the fact that parents of a Type I are often diabetes free (the interpretation being that genes were required from both sides). The recent request for celiac siblings for a study of genetic typing intends to duplicate the study which looked for celiac genes. Reference: Gluten Intolerance Group of North America newsletter, V. 13, Issue 2, 1987; New York Times, Sept. 13, 1994, genetics study by Dr. John Todd at Oxford
  9. Scott Adams

    Dr. Ivor D. Hill on Celiac Disease

    Celiac disease is a permanent (lifelong) condition which affects genetically predisposed individuals who are exposed to gluten and related products from rye, barley and oats. Once the diagnosis has been confirmed there is absolutely no indication for periodically undertaking a gluten challenge. It is well known that patients with celiac disease who start ingesting gluten again after having been on a gluten free diet may go for years without apparently having any symptoms. Despite this there will be ongoing histological damage to the intestines. It was this apparent prolonged symptom free state that led doctors in the past to believe that people could grow out out of the condition. This is no longer accepted as correct. Dr. Ivor Dennis Hill left the University of Baltimore and is now in North Carolina. He is the Chief of the Division of Pediatric Gastroenterology and Nutrition, Bowman Gray School of Medicine, Winston-Salem. His new phone number is (910) 716 4431. As such he will be very involved in all aspects of Clinical Pediatric Gastroenterology. Dr. Hill has every intention of continuing his work with celiac disease and sees this as an opportunity to open another center of interest. Colleagues at Duke and Chapel Hill are keen to join Dr. Hill in a Pediatric Gastroenterology Group.
  10. Bardella MT, Minoli G, Radaelli F, Quatrini M, Bianchi PA, Conte D Gastrointest Endosc. 2000 Jun;51(6):714-716 Background: Loss or reduction of duodenal folds, scalloping of Kerkring folds and a micronodular or mosaic duodenal mucosal pattern have been described in celiac disease (celiac disease), endoscopic findings that are considered reliable in the diagnosis of this disorder. However, most data have been obtained in patients with suspected or certain disease. We assessed the accuracy of the above markers in diagnosing celiac disease in patients with non-ulcer dyspepsia. Methods: In this prospective study, in 705 consecutive dyspeptic patients (284 men, 421 women, mean age 51 +/- SD 15.8 years) duodenal biopsies were obtained only in the presence of typical endoscopic markers, whereas in another 517 (207 men, 310 women, mean age 49.9 +/- SD 16 years) duodenal biopsies were done irrespective of macroscopic findings. celiac disease was diagnosed histologically and on the basis of positive antiendomysium antibody. Results: Endoscopic markers were found in 4 patients of the first group but celiac disease was ruled out. In the second group 5 patients had an endoscopic pattern that was consistent and celiac disease was diagnosed in 3, whereas 3 others with normal endoscopic findings were eventually diagnosed as having celiac disease. Endoscopic markers had a sensitivity of 50% and a specificity of 99.6% (95% CI [11.8, 88.2 and 98.6, 99.9], respectively) with positive and negative predictive values of 60% and 99.4%, respectively. Conclusion: The accuracy of endoscopic markers in the diagnosis of celiac disease must be reevaluated in relation to the characteristics of the population studied.
  11. Vijay Kumar, MD, Research Associate Professor at the University of Buffalo and President and Director of IMMCO Diagnostics I enjoyed reading J. Murrays comments related to the diagnosis of celiac disease and agree that taking multiple biopsies is still the gold standard of diagnosing celiac disease. However, I am sure he will agree that there are limitations in the histopathological methods of diagnosing celiac disease. As we know, histological features occur in continuum, with flat lesions at one end of the spectrum and a mucosa with normal villous and crypt architecture but abnormally high density or count of villous intraepithelial lymphocytes at the other, which may be reported normal. In addition, patients with silent, atypical or occult celiac disease may exhibit normal or mild villous atrophy and histopathology may not be diagnostic. The best example would be patients with dermatitis herpetiformis (DH). As we know, all DH patients have gluten sensitive enteropathy, but only 60-70% of DH patients exhibit characteristic histopathology diagnostic of gluten sensitive enteropathy. In this regard, there has been a constant effort to put forth a simple serological method that is a specific and sensitive indicator of gluten sensitive enteropathy. There are basically three antibody markers (ARA, AGA and EMA) that could be used for diagnosing celiac disease and DH. Our studies indicate and corroborate with the others that the AGA test is a sensitive but not very specific marker of celiac disease. On the other hand, ARA is very specific but not sensitive. We described in 1984 the endomysial antibody test and we felt very comfortable reporting that this EMA test has >99% specificity and sensitivity for gluten sensitive enteropathy. We reported cases of DH who were biopsy negative but EMA positive in which the histopathological changes consistent with celiac disease could be induced on an increased gluten intake indicating thereby the sensitivity of EMA tests. The following table is a summary of our studies on the utility of various serological methods of diagnosing celiac disease. Comparison of Sensitivity, Specificity, Positive and Negative Predictive Value of AGA, ARA, and EMA in Active Celiac Disease: % of Sensitivity % of Specificity Predictive Value % Pos Predictive Value % Neg EMA (Endomysium) 97% 98% 97% 98% ARA (Reticulin) 65% 100% 100% 72% IgG AGA 88% 92% 88% 92% IgA AGA 52% 94% 87% 74% I shall be glad to discuss the utility of serological methods in diagnosing celiac disease with anyone interested.
  12. IgA class Reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. IgA class endomysial antibodies are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patient with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than either reticulin or gliadin antibodies for diagnosis of celiac disease. Antibody titers are found to parallel morphological changes in the jejunum and can also reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge. The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet, and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten-free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative. The reverse is also true. That is, a patient with celiac disease who has been on a gluten-free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The test results you reported are consistent with a patient who is conforming to a gluten-free diet.
  13. The following was received on March 5, 1998 from Kathryn K. Harden, Ph.D., k-harden@UIUC.EDU, Assistant Editor, The Journal of Nutrition, University of Illinois, Urbana-Champaign. The latest issue of the American Journal of Clinical Nutrition contains two articles concerning celiac disease. It is encouraging to see research papers concerning celiac disease in important basic research and clinical journals. The citations are: Reversal of low bone density with a gluten-free diet in children and adolescents with celiac disease. S. Mora, G. Barera, A. Ricotti, G. Weber, C. Bianchi and G. Chiumello. AJCN 67: 477-481, 1998. The authors conclude that in children and adolescents with low bone mineral density (BMD) due to celiac disease, a gluten free diet promotes a rapid increase of BMD that leads to a complete recovery of bone mineralization. Due to the severe consequences of low BMD, the authors emphasize the need for early diagnosis and treatment of celiac disease. Nutritional status of newly diagnosed celiac disease patients before and after the institution of a celiac disease diet - association with the grade of mucosal villous atrophy. T Kemppainen, V-M Kosma, E Janatuinen, R Julkunen, P Pikkarainen, M Uusitupa. AJCN 67: 482-487, 1998. Authors found that celiac disease patients with 3 levels of intestinal villous atrophy (partial, subtotal, total) did not differ in the nutritional status variables measured except erythrocyte folate and serum ferritin concentrations. The following was received from J.C. Trevett JCTrevett@aol.com on September 28, 1998: Two articles I would like to add to your list if you dont already have info. Journal of Pediatrics, August 1998 article entitled, Celiac disease: A Reappraisal, by David Branski, MD and Ricardo Troncone, MD. Dr. Branski is Dept. of Pediatrics, Shaare Zedek Medical Center, P. O. Box 3235, Jerusalem, Israel. It is a good five page article referring to the tip of the iceberg again - at least all the experts are in agreement all over the world that we are not diagnosing enough celiac disease. This is a good article - there is some technical stuff about the DB MOLECULE, which I will never understand, but I gave a copy to my gastroenterologist and he seemed to appreciate it. Tufts University, Medford, MA, Tufts Health & Nutrition Letter - September, 1998 - Volume 16, Number 7. Good article for average layperson on Coping with Celiac Disease - mentions CSA/USA, Inc. and its many (80) support groups throughout the country. Also mentions Gluten Intolerance Group, Energy Foods and Dietary Specialties. To quote part of the article: In one survey, 43 percent of those with the condition said that theyd been diagnosed with an assortment of ailments - such as anemia, stress, ulcers, and nerves before finding out that celiac disease was responsible for the symptoms.
  14. The following was taken from THE SPRUE-NIK PRESS, September 1995. The University of Maryland School of Medicine sponsored a conference on July 14-15, 1995 entitled Celiac Disease: The Dark Side of the Gastrointestinal Planet, by Salvatore Auricchio, MD, summarized by Jim Lyles. Dr. Auricchio is Professor and Chairman of Pediatrics at the University Frederico II in Naples, Italy. celiac disease manifests itself in the small intestine. A distinct pattern of abnormalities has been observed [comments in braces have been added by Jim Lyles]: Villous atrophy [partial or complete flattening of the finger-like projections in the small intestine] Hyperplasia of the crypts of Lieberkuhn [the crypts under the villi become highly elongated when compared with normal crypts] Increased plasma cell and lymphocyte infiltration of the lamina propria [more lymphocytes under the epithelial or outer layer of the villi. Lymphocytes are the cells that fight off viruses, etc.] Increased intraepithelial lymphocytes [more lymphocytes within the epithelial cells. The epithelial cells form the outer layer of the intestine and allow nutrients to pass through from the intestine into the bloodstream] Abnormalities in the epithelial cells which become flattened, cuboidal, and pseudo- stratified [layered].
  15. This information came to me from Michael Walker (xix25@dial.pipex.com) of Genesis Diagnostics Ltd. Press Release: Genesis Diagnostics Ltd, Cambridge, UK have announced the development of a new and sensitive test for celiac disease. The test will be available through hospital laboratories. The test is based on detecting antibodies to an enzyme called transglutaminase in blood. The new test is more specific for celiac than currently available tests and should result in speedier diagnosis. Genesis Diagnostics is a manufacturer of ELISA based kits for autoimmune diagnosis. We already produce kits for gliadin IgG and IgA antibodies, which have been used for the past 5 years as the main test for celiac disease. The new test for transglutaminase was an obvious development of our experience in this area. We will continue to develop and improve blood tests in this area. We will be seeking FDA approval for the transglutaminase test kit in 1999. In the mean time it can be used for research only.
  16. Authors Rivabene R. Mancini E. De Vincenzi M. Source Biochimica et Biophysica Acta - Molecular Basis of Disease. 1453(1):152-160, 1999 Jan 6. Abstract: Coeliac disease (celiac disease) is an inflammatory disorder of the upper small intestine in which gluten acts as an essential factor in its pathogenesis. Although it is generally accepted that cereal protein activation of the immune system is involved in celiac disease progression, a non-immunomediated cytotoxic activity of gliadin-derived peptides on the jejunal/duodenal tract cannot be excluded. In this work, considering that (a) little has been reported about the intracellular metabolic events associated with gliadin toxicity, and ( an important role for free radicals in a number of gastrointestinal disease has been demonstrated, we investigated the in vitro effects of gliadin-derived peptides on redox metabolism of Caco-2 intestinal cells during a kinetic study in which cells were exposed to peptic-tryptic digest of bread wheal up to 48 h. We found that the antiproliferative effects displayed by gliadin exposure was associated with intracellular oxidative imbalance, characterized by an increased presence of lipid peroxides, an augmented oxidized (GSSC)/reduced (GSH) glutathione ratio and a loss in protein-bound sulfhydryl groups. Significant structural perturbations of the cell plasma membrane were also detected. Additional experiments performed by using the specific GSH-depleting agent buthionine sulfoximine provide evidence that the extent of gliadin-induced cell growth arrest critically depends upon the basal redox profile of the enterocytes. On the whole, these findings seem to suggest that, besides the adoption of a strictly gluten-free diet, the possibility for an adjuvant therapy with antioxidants may be considered for celiac disease patients. © 1999 Elsevier Science B.V. All rights reserved. [References: 38]
  17. Scott Adams

    What is celiac disease?

    Celiac disease (also called coeliac, nontropical sprue, celiac sprue, gluten intolerant enteropathy, or gluten sensitive enteropathy) is a condition in which there is a chronic reaction to certain protein chains, commonly referred to as glutens, found in some cereal grains. This reaction causes destruction of the villi in the small intestine, with resulting malabsorption of nutrients. There is clear evidence of a family tendency toward celiac disease. 5-10% of the first-level relatives (parents, children, and siblings) of diagnosed celiacs may develop celiac disease. The disease affects both sexes, and it can begin at any age, from infancy (as soon as cereal grains are introduced) to later life (even though the individual has consumed cereal grains all along). The onset of the disease seems to require two components: genetic predisposition (two specific genetic markers, called HLA sub-factors, are present in well over 90% of all celiacs in America), and some kind of trigger. The trigger may be environmental (as in overexposure to wheat), situational (perhaps severe emotional stress), physical (such as a pregnancy, an operation), or pathological (a viral infection). Once thought to be a childhood disease that would be outgrown, recent evidence indicates that it is not uncommon for the symptoms of celiac disease to disappear during late childhood or adolescence, giving the appearance of a cure. Unfortunately, damage still occurs during these years of apparent health, and later in life these celiacs may find they have suffered considerable damage to the small intestine, and have for years deprived themselves of important nutrients.
  18. New England Journal of Medicine October 19, 1995 -- Volume 333, Number 16 Celiac.com 10/25/1995 - According to an article published for the week of October 19, 1995 (Vol. 333, No. 16) in the New England Journal of Medicine, it is not a problem for celiacs to eat oats (non-contaminated, of course!). The article is based on a study conducted in Finland by a group of doctors who did very rigorous testing on adult celiacs and concluded that oats can, and should be included on the celiac diet (The lead doctor for the study is also a celiac). The following is a summary of the study: 52 celiacs in remission (on a gluten-free diet for more than a year) were given duodenal-biopsies, and then fed an average of 49.9 grams of oats per day for six months. They were again given biopsies, and none of the subjects were found to have any villi damage. There was also a group of 40 newly diagnosed celiacs who underwent the same procedures, except they were studied for 12 months rather than 6. The initial biopsies with this group showed significant villi damage due to the fact that they were still on a gluten-containing diet until they began the study. This group was fed an average of 46.6 grams of oats per day, and were given biopsies at 26 and 52 weeks. Their biopsies were almost normal at 26 weeks, which means their damaged villi were able to heal while eating oats daily. At the end of the year their biopsies showed no damage to their villi. The study DID NOT test people who had severe cases of celiac disease, and therefore cannot make recommendations with regard to them. Also, three people with dermatitis herpetiformis withdrew from the study because of an increase of itching, but none of them showed any signs of dermatitis. One person withdrew because of abdominal symptoms, but they did not exhibit damaged villi. Their conclusion: Our data suggest that most patients with celiac disease, whether in remission or newly diagnosed, can add moderate amounts of oats to their otherwise gluten-free diets without any harmful subjective side effects or laboratory abnormalities. Furthermore, among the newly diagnosed patients the improvement of mucosal architecture and the disappearance of mononuclear-cell infiltration were similar, regardless of the use of oats. -NEJM There is also an editorial from England which cites positive research which has been done there regarding oats. The NEJM is the Bible of medical research, with extensive peer reviews before publication.
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