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  1. This article appeared in the Winter 2007 edition of Celiac.coms Scott-Free Newsletter. Celiac.com 04/26/2007 - My fingernails were shredding and I was a bit out of it mentally, missing obvious things. I’ve had to stop eating many foods because I have intolerances to almost everything I used to eat before I went gluten-free, and I wondered if I had dropped some essential nutrients when I cleared all of those foods out of my diet. So I checked my diet for nutrient deficiencies, using the USDA nutrients database at www.nal.usda.gov/fnic/foodcomp/search. I’m sure there’s software that works with this database but I wrote a little computer program to analyze my diet. I have an electronic food scale, so weighing food is easy. The most important thing I found is that I’m low on vitamin D. You can get vitamin D from food, or from a supplement, and from the ultraviolet B in sunlight; many of us, like me, may get almost none from any of those sources. And—this is important for a lot of us—vitamin D deficiency can cause a lot of symptoms including immune system problems! I went looking on Medline and it was mentioned as having anti-inflammatory properties, as preventing cancers such as colon cancer and lymphoma; preventing infections, and helping with autoimmune diseases. Gluten intolerance is less common in the middle east and more common in northern Europe. I’ve seen this explained as the result of evolution, since wheat has been used for longer in the Middle East. But I wonder if people in the north are also more likely to be gluten intolerant (an autoimmune disease) because they don’t get as much vitamin D. It may also explain why people get more colds during the winter season when there’s less sunlight. Vitamin D deficiency is best known for causing rickets in children and osteomalacia (softened bones, muscle weakness and pain, tender sternum) in adults. Osteomalacia is often misdiagnosed as fibromyalgia, because the symptoms are similar. Rickets is increasing in the U.S., especially among black children. Most post-menopausal bone loss in women occurs during the winter. It can take months of increased vitamin D intake to correct the health problems caused by deficiency. There are only a few significant dietary sources of vitamin D. In the U.S., almost all milk is fortified with vitamin D to 100 IU per cup, so you should get the recommended daily intake of 400 IU if you drink 4 cups of milk per day. However, milk often doesn’t have as much vitamin D as is claimed on the label. Some cereals, like Kellogg’s Cornflakes, have small amounts of added vitamin D. Typically, 10 cups of fortified cereal would give you the RDI. The government encourages fortification of milk and cereal so that fewer children will develop rickets. Otherwise—you would get the RDI from nine oysters, or about 4 ounces of fatty fish like salmon or tuna, or a teaspoon of cod liver oil. Many other kinds of fish have only small amounts. You’d have to eat 2 pounds of cod to get the RDI. The only natural vegan source of vitamin D is Shiitake mushrooms. Just like people, mushrooms make vitamin D when they’re exposed to ultraviolet. About 13 sun-dried shiitake mushrooms contain the RDI. And that’s it. Many of us on gluten-free diets are also not eating dairy or fortified cereals, so unless we have a passionate love-affair with fish or oysters or shiitake, we would be getting almost no vitamin D from food. You can get vitamin D the natural way, from the sun. It takes exposure to sunlight outside (not under glass) on your hands and feet for about fifteen minutes a day. I was not sure what was meant by “direct sunlight”. I read someplace that ultraviolet is scattered over the whole sky. Unlike visible light, the whole sky shines with ultraviolet. Clouds would filter out some of it. People with dark skin require more time in the sun, so many black people develop a deficiency. Using even low-SPF sunscreen prevents your body from making vitamin D. The farther from the equator you live, the less UVB there is in the winter sunlight, because the sun is closer to the horizon in the winter and the sunlight filters through more atmosphere before it gets to you. At the latitude of Boston, and near sea level, there isn’t enough UVB radiation between November and February for one’s body to make vitamin D. You have probably heard the public health advice to wear sunscreen—the same ultraviolet B that generates vitamin D in your body also causes skin cancer and ages skin. The small amount of exposure to sunlight required is probably only a very small cancer risk and would cause little photo-aging of the skin. Unfortunately I wasn’t able to find quantitative information about how carcinogenic fifteen minutes’ daily sun exposure would be. There are also vitamin D lights, which are probably also a healthful choice. I have severe immune system problems. I tested positive for 53 inhalant allergies—my body had developed allergies to almost all the allergens around. I get sick for days if I eat almost any of the foods that I ate while I was eating gluten. I even get sick from a couple of foods that, so far as I can remember, I only started eating on a gluten-free diet. So I live on an exotic-foods diet. I’ve had a hellish time trying to get allergy shots. At a concentration of 1 part in 10 million they make me sick for a couple of days while the normal starting concentration for allergy shots is 1 in 100,000. I’m plagued by bladder infections. With cranberries being one of my intolerances, I can’t even use them to help prevent the infections. I’ve certainly been short of vitamin D. I live in the north, and I’m always careful to use high-SPF sunscreen when I go outdoors. I can’t eat milk, fish, shellfish or mushrooms, so I can’t get a significant amount of vitamin D from food. I haven’t been taking any vitamin supplements, because almost all have traces of protein from some food that makes me sick. It would be lovely if vitamin D deficiency turned out to be part of the cause of my very burdensome immune problems. I’m skeptical because I was getting vitamin D from a supplement and/or from my diet up until 2 years ago, when I found I had a vast number of hidden food intolerances, and I started having reactions to vitamin pills. Fortunately there is a vitamin D supplement that I can take—vitamin D3 made by Pure Encapsulations. The ingredients in the capsule are made from wool and pine trees. I’ll find out if it helps over the next few months. Vitamin D causes disease when taken in large amounts, so if you think you are deficient, don’t take too much to make up for it. Vitamin D is a hormone—it’s not something to take in mega-doses, any more than, hopefully, one would take a mega-dose of estrogen or testosterone. If your doctor recommends a high dose, they should do regular blood tests to keep track of your vitamin D level. It’s pretty safe to take up to 2000 IU per day on your own. Dr. Michael Holick, a vitamin D researcher at Boston University and author of The UV Advantage, believes that people need about 1000 IU per day. I asked a family doctor, who said they suggest 400-800 IU per day for middle-aged women. However, it might be a good idea for gluten intolerant people to take more, about 1000 - 2000 IU per day, since we may have difficulties absorbing vitamins and celiac disease is an autoimmune disease. Vitamin D is very important, just as all the vitamins are. But we are conditioned by the media, and tend to think more about vitamins C and E, which get a lot of attention because they’re antioxidants. Vitamin D was the absolutely last one I looked at. Then I found that it was my most serious deficiency! And nutrient deficiencies are not a trendy topic, so the possibility of developing deficiencies is something people tend to forget while trying to improve their diets. Many people who avoid gluten also have other food intolerances, or are on some other kind of special diet, and it would be an excellent idea to go to the USDA database and find out whether their new diet is giving them enough vitamins and minerals. It certainly helped me. I feel more cheerful and alert, like my mind woke up on a sunny day. It’s best to get as much as possible from one’s diet, too. Whole foods have a lot in them that’s good for the body that research hasn’t yet identified, and if your diet gives you the RDA of all the vitamins and minerals, it will also be giving you other healthful nutrients that will do you a lot of good. This might also be true of vitamin D. Maybe it’s better to get a small amount of ultraviolet, like an iguana sitting under a UV lamp, instead of taking pills. UVB might be healthy in ways we don’t yet know about. Vitamin D is a bit like stored-up sunlight. You can catch it for yourself from the sun when it’s high in the sky, you can eat the sunlight the fish have gathered for you, or you can take a supplement and keep packed sunlight on your shelf.
  2. Celiac.com 02/26/2003 - The subject of cardiology-related symptoms of celiac disease and celiac disease-associated cardiological disease has not been reviewed. So, here I attempt to summarize readings of research papers and abstracts of research papers dealing with the topic. My interest in cardiac related issues in association with celiac disease is related to a familial history of hypertrophic cardiomyopathy which like celiac disease can be missed and some times before a person is found to have it he/she may experience an episode of sudden cardiac arrest, or syncope (fainting). End stage hypertrophic cardiomyopathy can look like dilated cardiomyopathy. Dilated cardiomyopathy has been associated with celiac disease. Celiac disease and Cardiomyopathy and Heart Failure A study of 642 patients who were candidates for heart transplant in Italy found that 1.9% had anti-endomysial antibodies (AEA) (compared to 0.35% of 720 healthy controls) and that 2.2% of 275 patients with dilated cardiomyopathy were AEA-positive (compared to 1.6% in the remaining transplant candidates) (Prati D, et al, 2002, Am J Gastroenterol 97:218; Prati D, et al, 2002, Dig Liver Dis 34:39). Although an association was found, there was no way to assess cause and effect. The AEA-positive patients and AEA-negative patients presented with similar cardiologic criteria and had similar 2-year post-transplant survival. Similar, but more limited findings were described in preliminary data (Curione M, et al, 1997, Lancet 354: 222). The authors suggest a study of whether a gluten-free diet improves cardiac function in such patients. A study in Italy found that 5% of 60 elderly (over 65 years) celiac disease patients died during the study due to heart failure (Gasbarrini G, et al, 2001, Gerontology 47:306). The authors determined that this was significantly higher than the non-celiac disease population, but dont give a non-celiac disease rate. Furthermore, 0.4% of 226 non-elderly adult celiac disease patients died with heart failure as the cause and this rate was not significantly higher than the comparable non-celiac disease population. Other cardiological symptoms and disorders were not assessed. Common Causes? In a case study, similar cellular changes were found in both the intestinal microvilli and the heart muscle of a patient who had both idiopathic congestive cardiomyopathy and celiac disease (Chuaqui B, et al, 1986, Pathol Res Pract 181:604). While this was a limited study and the molecular causes of each were not evaluated, it is an intriguing find. In another case study, a celiac disease patient also had recurrent hemoptysis and developed heart block (Mah MW, et al, 1989, Can J Cardiol 5:191). The authors hypothesize that there is a common cause of the symptoms above. The cause is undefined by the authors. Similarly, a patient who had chronic anemia, cardiomyopathy, and heart block but did not have digestive symptoms was found to have anti-gliadin antibodies (AGA), AEA, and anti-reticulin antibodies (ARA) as well as the typical celiac biopsy (Rubio JLC, et al, 1998, Am J Gastroenterol 93:1391). The authors found that after 1 year of gluten-free diet, blood tests and biopsy were normal and confirm celiac disease as a diagnosis; but they do not mention whether or not the cardiomyopathy and heart block resolved. Celiac Disease and Autoimmune Myocarditis In an Italian study, 187 patients, including 110 with heart failure and 77 with arrhythmias, diagnosed with myocarditis were tested for celiac disease (Frustaci A, et al, 2002, Circulation 105:2611). Thirteen patients had IgA tissue transglutaminase antibodies (tTGA); all had anemia. Nine of the thirteen were AEA-positive; these patients also had abnormal biopsies. Thus, 4.4% of myocarditis patients had celiac disease (they compare this to 0.6% in the non-myocarditis population; this was statistically significant. Eight of the nine myocarditis patients with celiac disease had HLA DQ2-DR3, the other patient had DQ2-DR5/DR7. Five of the nine myocarditis patients with celiac disease had heart failure and were treated with immunosuppression and gluten-free diet. The other four myocarditis patients with celiac disease had heart arrhythmias and were treated with gluten-free diet. All nine patients markedly improved in cardiologic features and were tTG- and AEA-negative post-treatment (8-12 months) . Other Cardiologic Diseases Celiac Disease and Ischemic heart disease: In a report made in 1976, celiac disease was associated with a decrease in ischemic heart disease in 77 members of the Coeliac Society of England and Wales (Whorwell PJ, et al, 1976, Lancet 2:113). In another study with 653 celiac disease patients, the authors found no decrease in ischemic heart disease or stroke for celiac disease patients (Logan RF, et al, 1989, Gastroenterology 97:265). A recent study examined the risk factors for ischemic heart disease in dermatitis Herpetaformis patients (Lear JT, et al, 1997, J Royal Soc Med 90:247). The authors found that, compared to the normal population, dermatitis Herpetaformis patients had lower cholesterol, lower triglycerides, lower apolipoprotein B, lower fibrinogen, higher HDL2, smoked less, and were generally of higher social class. Pericarditis Dermatitis herpetiformis has also been found to be associated with recurrent pericarditis (Afrasiabi R, et al, 1990, Chest 97:1006). The authors found IgG, IgA, and complement in the pericardium, thus demonstrating similarities with the skin deposition of IgA in dermatitis Herpetaformis lesions. Summary While there hasnt been a comprehensive review by a celiac disease researcher, the research papers summarized here point to a correlation of celiac disease with cardiomyopathy, heart arrhythmias, and heart failure. The authors of the articles summarized here often point to a probable association of autoimmune disease in both celiac disease and related heart diseases. Glossary of terms: Cardiomyopathy: aberrant heart muscle structure. Congenital: non-inherited, usually referring to what is considered a "birth defect." Heart block: blockage of the conduction of the heart electrical signaling system which regulates the heart beat. Hemoptysis: spitting blood, usually due to lesions to the respiratory tract or voice box. Idiopathic: often used to describe something whose origin is unknown. Ischemic heart disease: heart damage due to insufficient blood flow to the heart (i.e., via the coronary arteries). Myocarditis: inflammation of the heart muscle. Pericarditis: inflammation of the pericardium, a sac which encloses the heart.
  3. Celiac.com 09/30/2002 - The Canadian Medical Association Journal (Hoey, 2002;166:479-80) published the following, Irritable Bowel Syndrome: Could it be Celiac Disease?, as excerpted below. This was an analysis of a Lancet article (Sander et al, 2001;358:1504-8) called, Association of Adult Coeliac Disease with Irritable Bowel Syndrome: A Case-Control Study in Patients Fulfilling Rome II Criteria Referred to Secondary Care. Here are the CMAJ excerpts: Irritable Bowel Syndrome is found in 10% to 20% of people with the use of standard diagnostic tools such as the Rome II criteria. Rome II criteria is specified below: At least 12 weeks, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that has 2 out of 3 features: Relieved with defecation Onset associated with a change in frequency of stool Onset associated with a change in form (appearance) of stool Symptoms that cumulatively support the diagnosis of irritable bowel syndrome: Abnormal stool frequency (more than 3 bowel movements per day or fewer than 3 bowel movements per week) Abnormal stool form (lumpy/hard or loose/watery stool) Abnormal stool passage (straining, urgency or feeling of incomplete evacuation) Passage of mucus Bloating or feeling of abdominal distention Question: What proportion of patients who meet the Rome II criteria for irritable bowel syndrome have celiac disease? Case subjects: The article cites that 300 people (214 women, 86 men ranging in age from 18 to 87, (mean 56 years)) met the Rome II criteria out of 686 new patients who were referred by a family physician to a university hospital gastroenterology clinic. Control subjects were healthy people without irritable bowel syndrome. Also, most control subjects were companions of the patients who were matched to case subjects by age (within 1 year) and sex, as well as questioned in the same manner as case subjects. All case and control subjects underwent a wide range of baseline investigations, including full blood count, measurement of erythrocyte sedimentations rate, blood urea nitrogen and serum electrolyte levels, and thyroid function tests. In addition, they were investigated for celiac disease by analysis of serum levels of IgG antigliadin, IgA antigliadin and endomysial antibodies. Most of the case subjects, particularly those older than 45, underwent colonoscopy or sigmoidoscopy and barium enema. Case and control subjects with positive antibody test results were offered duodenal biopsy to confirm the possibility of celiac disease. Of the 66 case subjects who had positive antibody test results, 49 had elevated levels of only IgG antigliadin 4 of only IgA antigliadin and 6 of only endomysial antibodies Fourteen of the 66 were subsequently found to have histologic evidence of celiac disease; 11 of the 14 were positive for endomysial antibodies. Nine of the of 66 case subjects were lost to follow-up or refused duodenal biopsy; 1 of them was positive for endomysial antibodies. Of the 44 control subjects who had positive antibody test results, 41 had elevated levels of only IgG antigliadin 1 of only IgA antigliadin and 2 of IgG antigliadin and endomysial antibodies Only the last 2 subjects elected to undergo duodenal biopsy, and both were found to have histologic evidence of celiac disease. Commentary: The authors found that a high proportion of patients (about 5%) who were referred to a university hospital gastroenterology clinic and who met the Rome II criteria did have celiac disease. In addition, the clinic specialists uncovered other organic abnormalities in almost 20% of the referred patients. The study had several weaknesses. For instance, although most of the case subjects underwent extensive investigations of the lower gastrointestinal tract, the control subjects did not. Thus, some of the case subjects who were lost to follow-up or refused investigation and many of the age-matched control subjects might have been found to have irritable bowel disease, celiac disease or other gastrointestinal abnormalities. The authors conclude from their findings that patients who meet the Rome II criteria for irritable bowel syndrome and who are referred to a secondary care centre should be investigated routinely for celiac disease. In an editorial accompanying the Lancet article, a gastroenterologist cautioned that more studies are needed. He noted an earlier study in which 121 consecutive patients were referred for investigation of irritable bowel syndrome. Using Rome I criteria and similarly extensive investigation, the researchers detected no cases of celiac disease. Because of the findings from the Lancet study, the editorialist has decided to further lower his threshold for screening for celiac disease among patients referred for investigation of irritable bowel syndrome. Perhaps other gastroenterologists would be wise to do the same. I verified the five percent as cited in the CMAJ as 14 out of the 300 patients who met the Rome II criteria also had celiac disease. The CMAJ also cites the following, Studies in Europe have shown that up to 1% of the adult population may have celiac disease. We can make our own conclusions from this study in Lancet and we might agree that 1% may be understated but further studies have to be performed to corroborate a higher percentage of undiagnosed celiacs; I hope this definitely encourages closer scrutiny of IBS patients like myself who was diagnosed with IBS in 1997 with only a symptom of left side tenderness below my rib cage and a sigmoidoscopy which revealed no abnormalities except a hemorrhoid. Then, in the summer of 2001, I was diagnosed with lactose intolerance and IBS once more before discovering from medical research and my food dairy taken since May 2001, along with corroboration by an allergist in October 2001, that it may be celiac disease, as my malabsorption symptoms grew worse.
  4. Celiac.com 09/01/2002 - Patients with celiac disease are 20 times more likely than the general population to have epilepsy and often have associated cerebral and cerebellar calcifications imaged by CT and MRI. Depression, dementia, and schizophrenia are all also common in persons with untreated celiac disease. Cerebellar degeneration with resulting ataxia (gluten-associated ataxia) is a known entity in Europe, and the National Institutes of Health (NIH) is currently recruiting subjects with ataxia to examine them for gluten sensitivity and celiac disease. Focal white matter lesions in the brain recently have been reported to occur in children with celiac disease and are thought to be either ischemic in origin as a result of vasculitis or caused by inflammatory demyelination. Parents of children with celiac disease have reported behavioral changes such as irritability, separation anxiety, emotional withdrawal, and autistic-like behaviors that all seemed to improve on a GFD. Although not scientifically validated, the GFD is now also being advocated for children with autism by several groups. Whether or not children with autism are at a higher risk for celiac disease or celiac children have a higher incidence of autism remains to be proven. However, children with Down syndrome, who often have autistic-like behaviors, are at higher risk for celiac disease. It has been hypothesized that gluten may be broken down into small peptides that may cross the blood-brain barrier and interact with morphine receptors, leading to alterations in conduct and perceptions of reality. The serologic tests can be divided into 4 different types of antibodies: antigliadin (AGA), antireticulin, antiendomysium (AEA), and antitissue transglutaminase (tTG). Each antibody varies widely in its sensitivity, specificity, and positive and negative predictive values (Table 2). Table 2 (from Pietzak et al, 2001, compiled data from multiple studies) Test Sensitivity Specificity PPV NPD AGA IgG 57-100 42-98 20-95 41-88 AGA IgA 53-100 65-100 28-100 65-100 AEA IgA* 75-98 96-100 98-100 80-95 Guinea pig tTG† 90.2 95 Human tTG† 98.5 98 * Patients older than 2 years of age. † IgG +IgA antibodies. The AEA IgA immunofluorecent antibody is an excellent screening test for celiac disease, with both a high sensitivity and specificity. This antibody was discovered in the early 1980s and rapidly gained use as part of a screening celiac panel by commercial laboratories in combination with AGA IgG and AGA IgA. Its major drawbacks are that it may be falsely negative in children under the age of 2 years, in patients with IgA deficiency, and in the hands of an inexperienced laboratory. Also, the substrate for this antibody was initially monkey esophagus, making it expensive and unsuitable for screening large numbers of people. Recently, the human umbilical cord has been used as an alternative to monkey esophagus. However, the subjective nature of the AEA assay may lead to false-negative values and unacceptable variability between laboratories. Because tTG had been first described as the autoantigen of celiac disease in 1997, it has been used to develop innovative diagnostic tools. The tTG IgA ELISA test is highly sensitive and specific, using either the commercially available guinea pig tTG or human recombinant tTG. The tTG assay correlates well with AEA-IgA and biopsy. However, it represents an improvement over the AEA assay because it is inexpensive and rapid (30 minutes), is not a subjective test, and can be performed on a single drop of blood using a dot-blot technique. Therefore, this test is ideally suited for mass screenings and in the future could be performed in the general practitioners office, much like the now routine finger-stick hematocrit. For the reasons outlined above, the IgA class human anti-tTg antibody, coupled with the determination of total serum IgA, currently seems to be the most cost-effective way to screen for celiac disease. AEA should be used as a confirmatory, pre-biopsy test, whereas AGA determinations should be restricted to the diagnostic work-up of younger children and patients with IgA deficiency, using the guidelines in Table 3. Table 3 Probability of celiac disease based on three antibodies in combination AEA IgA AGA IgA AGA IgG Interpretation + + + Celiac disease 99% probable + - + probable + + - Celiac disease probable + - - Celiac disease probable - + + Celiac disease less likely* - - + Celiac disease less likely* - + - Celiac disease less likely - - - Celiac disease very unlikely+ * If patient is IgA sufficient: AGA IgG > 100 warrants work-up of enteropathy. + If patient is on a gluten-containing diet. Celiac disease: AEA, antiendomysium antibodies: AGA, antigliadin antibodies.
  5. Dr. Kelly, who is a refractory sprue specialist, had interesting insights into Celiac Disease. He first described once having a patient say to him that eating at a restaurant or food take out is the gastronomic equivalent of promiscuous and unprotected sex because (you) dont know where food has been, who else its been with, and what you might get from it. Dr. Kelly explained that his job when seeing a patient with possible Refractory Sprue is to first confirm that the patient really has Celiac Disease and is adhering to a gluten-free (gluten-free) diet. He explained that some patients would rather prefer an iron shot than adhere to a gluten-free diet and that sensitivities vary which removes another drive to say gluten-free; however, if symptomatic, he has found that the patient has the motivation to adhere. Hes even had to recruit and train dieticians to take an interest in Celiac Disease. He said that Celiac Disease or Gluten Sensitive Enteropathy is driven by activated lamina propria T-cells to whom gliadin is being presented through their T-cell receptors. In Refractory Sprue, he said that the cells are evident at intraepithelial lymphocytes rather than lamina propria lymphocytes and they no longer require gluten in order to be driven. So, theyre on auto-pilot. He emphasized that this is a rare disease and advised that doctors get a competent dietician to help patient adhere to diet. If the concern is that the patient is adhering but is not responding, Dr. Kelly advised doctors to think of other disorders masquerading as Celiac Disease, especially if patient is IgA, EmA (anti-endomysial) negative or if not HLA DQ2 or DQ8 (common Celiac genes) positive. He added that not every flat mucosa consistent with Celiac Sprue is Gluten Sensitive Enteropathy but that there can be a differential diagnosis such as cow protein intolerance. He said that there are unusual immunologic disorders that can be mistaken for sprue or refractory sprue. He said that doctors should consider these if the patient was not IgA endomysial or human tTg (transglutaminase) antibody positive at diagnosis. He explained that the positive predictive value of those tests are so strong that really its in some ways has a higher positive predictive value than even biopsy that you dont get very, very if any false positives at least by the immunofluorescence assay. So, if theyre negative at diagnosis considering other possibilities and this is one instance where HLA typing actually may be clinically useful if you have a patient you think has Celiac Sprue but isnt behaving or responding as you would expect with a gluten free diet and you ask do they really have Sprue. If they are HLA DQ2/DQ8 negative, then the likelihood of them having gluten sensitive disease is much, much lower. He said that serology (blood tests) were helpful but not be relied upon. He said that IG antibody levels against gliadin, or tissue transglutaminase tend to drop fairly quickly usually within 2 to 3 months provided they (patient) were positive to begin with. ...The IgG takes much longer so it tends to be less useful and of course, if they are IgA deficient, they wont be IgA positive to begin with and you cant use then. Even if their antibody levels are high to begin with, and remain high, that to me means that theyre still exposed to the antigen and they still have T-cells. Their lamina propia T-cells are still being driven by the antigen. But if theyre negative, Im afraid that its not particularly sensitive and low levels of gluten exposure may result in symptoms and poor response would not necessarily be identifiable by antibody.... Dr. Kelly said that patients with subtle manifestations of Celiac Sprue who have been previously diagnosed with irritable bowel or host of other disorders are now being more frequently seen. He said that there has been a lot of discussion in the past year about Celiac Sprue being misdiagnosed as Irritable Bowel Syndrome. Dr. Kelly also described the circumstance that patients with Celiac Sprue show improvement both serologically (blood) and histologically (biopsy) but their symptoms persist. He said that doctors need to be aware that just because a patient has gluten sensitive enteropathy doesnt mean they cant get another gastrointestinal disorder. He gave examples such as microscopic colitis and what he called a classical association, hyperthyroidism, or something else which could also cause diarrhea and weight loss. Dr. MacDonald, a celiac specialist, discussed new insights into the pathogenesis of Celiac Disease. Dr. MacDonald discussed primarily the role that other factors besides the DQ2 (gene) molecule, control the T-cells in the gut mucosa which produce the lesion or flat mucosa. In the genesis of the lesion, he explained how the T-cell immune response in the gut wall results in a gut shape of tall villi and short crypts which results in an increase in mucosa volume with flat mucosa and an increase in mucosa thickness. My husband, a PhD immunologist, interpreted this for me; He said that imagine the villi are the hill and the crypts are the valley. The valley is where things grow. The oldest cells are at the tip of the hill and as cells mature, they get transported up the hill. As damage occurs, the hill gets chopped down, valleys get deeper making more area for cells to replicate. Dr. MacDonald assumed that because the epithelium is turning over so fast in Celiac Disease that the lamina propria, the shape of the gut itself would be turning over, but actually the data says otherwise. The flat mucosa isnt turning over at all, ... a rather stable shape, its not really dynamic, its remodeled. He said that putting Celiacs on a gluten free diet may take them a long time to get better, because it takes a long time for this to go back because this is actually stable, its remodeled.... Dr. MacDonald explained that gliadin peptides associate with DQ2 and DQ8 molecules putting themselves into the grooves to be seen by T cells. However, he gave an instance where a particular gliadin peptide doesnt fit well into the pockets of DQ2 to be seen by T cells. Tissue Transglutaminase or Ttg deamidates (removes chemical groups on certain amino acids and allows peptide to bind to DQ2) this peptide in terms of glutamine into glutamic acid, gives a negative charge, fits very well into pocket, and binding increases 100 fold. Tightness of the binding ... controls the specificity and strength of the T-cell response. Dr. MacDonald also described the case of a woman with cancer who was treated with interferon. He said that she had the endomysial antibodies, was DQ2 positive, and had Celiac Disease; however, he cited that the reason why the Celiac Disease was not found earlier was that interferon alpha/gamma used to treat the cancer may have precipitated clinical Celiac Disease. He added that her son was later diagnosed with Celiac Disease as well. It was also eluded to that a viral infection like a gastrointestinal flu would stimulate or produce interferon alpha. Dr. Alessio Fasano from the Center for Celiac Research at the Univ. of Maryland also explained that its not just the gluten antigen and genes (i.e., HLA DQ2 or DQ8) but an added element like that alluded to by Dr. MacDonald such as a viral infection which can result in Celiac Disease. Dr. Fasano described a study performed on North African children who were thought to have symptoms resembling infectious disease with symptoms like anemia and diarrhea were found to have Celiac Disease at the rate of 1 in 18. He said because they have a high consumption of grains and seem to carry a high frequency of the genetic elements, he felt that non-profit organizations may intervene to help institute a gluten-free diet in this Celiac population. Dr. Fasano mentioned a study performed in Southern California which found Celiac Disease in 2 to 4% of people with symptoms or associated diseases and 5% in family members of Celiacs. Dr. Fasano stated that the overall prevalence is 1 in 266 which he said on a global scale, by far this is the most frequently genetic disease of human kind. Fasano said that in the 1970s, it was thought Celiac Disease was confined to the pediatric population but that since 1998 there has been a surge in adult versus child cases. He believes that the disease may have been overlooked in adults because adults have more atypical symptoms like anemia, osteoporosis, abortion that would NOT see a Gastroenterologist but would see an internist, reproductive OBGyn, endocrinologist, etc. Dr. Fasano said that if the iceberg idea is diarrhea, weight loss, abdominal symptoms, you will surely crash into the iceberg, but he proposed, what about the people who have joint pain, constipation, fatigue, and so on. He said that if you are willing to see the monument of the problems, you have to get down under the water because in the vast majority of cases, Celiacs will not see a Gastroenterologist and that doctors must be aware of those under the water. Dr. Fasano during the question and answer session listened to a doctor in the audience describe a patient with diarrhea and schizophrenia whose diarrhea and schizophrenia resolved when put on a gluten-free diet. The doctor didnt know what to do with the patient but explained that the patients background, being of Irish descent, gave him a red flag into the possibility of Celiac Disease. Dr. Fasano in response described how there can be a change in behavior such as attention deficit disorder, depression, and schizophrenia. He described a theory that the epitopes of gluten could cross the intestinal barrier, cut into the bloodstream, and cross the blood brain barrier. He believes that there is a clear association between Celiac Disease and change in behavior.
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