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Dermatitis Herpetiformis Summary A dermatologist who is experienced at recognizing dermatitis herpetiformis should do the biopsy. The biopsy is taken of one of the blisters or the skin at the edge of the lesion. The biopsy should not be taken from the lesion, but from the edge or just near the lesion - it can be misdiagnosed as herpes if taken from the lesion. An iodine patch can be used to bring about a blister. If one has dermatitis herpetiformis, a blister will form; if not, one does not have dermatitis herpetiformis. A positive dermatitis herpetiformis biopsy will show IgA antibodies. The lab should be looking for IgA deposits in a granular line at a specific location in the skin. Some dermatologists use an immunofluorescence method of examination. dermatitis herpetiformis usually appears where pressure is applied to the body, but can appear anywhere. If the biopsy is not taken correctly you can get an incorrect negative. This is a positive method of diagnoses.

The following report was prepared by Ann Whalen, celiac, and editor/publisher of Gluten-Free Living , which is a bimonthly newsletter for celiacs - Gluten-Free Living, PO Box 105, Hastings-on-Hudson, NY 10706. On March 10th, more than 20 members of the celiac community and celiac disease specialists (see list at end) attended a meeting of the Digestive Diseases Intra-agency Coordinating Committee, a part of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The meeting, held to update the current status of Celiac Disease, was chaired by Jay Hoofnagle, M.D., Director of the Division of Digestive Diseases and Nutrition at the NIDDK. At the meeting, presentations were made by Martin Kagnoff, M.D., Joseph Murray, M.D., Alessio Fasano, M.D., and Frank Hamilton, M.D. Dr. Kagnoff is a gastroenterologist and Professor of Medicine at the University of California, San Diego. He spoke about his research into the genetics of Celiac Disease, focusing on the pathogenesis. Dr. Kagnoff is well known for his research into the genetics of Celiac Disease, and several of his studies have been funded by the NIH. Dr. Murray, Associate Professor of Medicine and clinician at the University of Iowa Hospitals and Clinics, described his experience with Celiac Disease both in Iowa and in Ireland, noting that his interest in celiac disease is clinical. He emphasized what he called the Classic II symptoms, meaning the actual symptoms patients have today and not the Classic symptoms many doctors may be familiar with. He said the rate of diagnosis is proportional to suspicion. Dr. Murray described the celiac disease experience at the University of Iowa from 1985 to 1997, presenting statistics that indicated a steep increase in diagnosis. At our institution, Celiac Disease is an adult disease, he said, and is now seen as frequently as Crohns Disease. Anticipating the question, Why look for Celiac Disease?, Dr. Murray gave his reasons: preventing lymphoma and osteoporosis, as well as resolving fatigue and nonspecific symptoms and shortening the current significant delays in diagnosis. Dr. Fasanos presentation was called Where Have All the American Celiacs Gone? He described what has happened in the field of celiac disease in various parts of the world, including some parts of the United States, but emphasized the European experience. Dr. Fasano noted that plans are already underway in Italy to screen all seven-year-olds in 1999. Dr. Fasano explained why an epidemiology study is critically needed in this country. He pointed out the benefits of such a study for four groups: The American health care community: lower health care costs, increased awareness of celiac disease and more knowledge of its protein manifestations in the US Participating physicians: publications, more patients and increased credibility. The American people: the prevalence will be established and celiac disease will be diagnosed more quickly. Celiac Patients: free screening of first-degree relatives, federal support for dietary and drug regulations, an improved food supply, stronger local support groups and more funding for celiac research. Dr. Fasano added that such a study, whatever its findings, would end in a win-win situation for everyone. If the study shows that celiac disease is underestimated in this country, patients will benefit as physicians begin looking for the problem with the knowledge that they might well find it. If the study shows celiac disease is indeed rare in the United States, its even more exciting because we will be able to figure out why. Dr. Hamilton, chief of the Digestive Diseases Program Branch at the NIDDK, briefly described the celiac disease research, to date, that has already been funded by the NIH. He said $1.4 million has been granted for such research, adding that over the last five years, we have seen growth in the funding of Celiac Disease. He said he was pleased funding has increased, and felt a lot of work has to be done. Dr. Hamilton ended by saying, Todays meeting will serve as an impetus for a partnership between the National Institutes of Health, academe, and the lay groups to foster more research. He added that it was important for the investigators and support group representatives present at the meeting to get the word out, referring to information about Celiac Disease. These talks were followed by a round table discussion, between the members of the committee and the presenters. Later, audience comment was invited. The committee showed an interest in the current adult nature of the disease, the changing symptoms, current testing methods, and identification of the most critical research needs. Patients who spoke were anxious to let the committee know what they felt were the important concerns in the real world. At the end of the meeting, Dr. Hoofnagle said his division will prepare a short, pithy plan, then present it to Drs. Kagnoff, Murray and Fasano. He noted that the important issues are pathogenesis, delivering the message to physicians, clinical research issues and pediatric health concern. Some Quotes from the Meeting Elaine Monarch: There is a general lack of knowledge, awareness and interest in Celiac Disease among the medical profession. We celiacs can go for years with substantial symptoms but not diagnosis...The cost to the medical community is enormous. Joseph Murray, M.D.: There is more than one gene involved in Celiac Disease. Most Europeans are homogenous. Here we have a mongrelized population. What happens when you mix? How much does it change? Our mongrelized population may be at risk at a later age. Martin Kagnoff, M.D.: The issue of other genes is not at all clear. Like Joe (Dr. Murray), I see adult celiacs. Their time delay to diagnosis is not exaggerated, but what is striking is the lack of knowledge of doctors, even at the University of California. They really are not aware of this disease. Alessio Fasano, M.D.: We receive 10-15 calls a day. The vast majority are self diagnosed. They say, I know more than my gastroenterologist. Peter Green, M.D.: We need to emphasize education of gastroenterologists. At my institution (Columbia-Presbyterian Medical Center in New York City), doctors are not used to looking at the duodenum...We need to educate many levels of the medical community and tell them, If you dont recognize something, take a biopsy. Sue Goldstein: Im concerned about the people who have not yet been diagnosed and the reasons why a physician wont consider Celiac Disease. It all boils down to, its rare and you cant have it. In addition to the speakers, the following were among those who attended: Phyllis Brogden, celiac, founder and chairperson of the Greater Philadelphia Celiac Sprue Support Group. Winnie Feldman, celiac, Celiac Disease Foundation Kenneth Fine, M.D., gastroenterologist/ researcher at Baylor University Medical Center in Dallas. Al Fornace, M.D., celiac, National Cancer Institute Sue Goldstein, celiac, founder and advisor, Westchester Celiac Sprue Support Group Peter Green, M.D., clinician/researcher at Columbia-Presbyterian Medical Center in New York City. Joanne Hameister, celiac, former chairperson, Western New York Gluten-Free Support Group Ivor Hill, M.D., clinician/researcher at Bowman Gray School of Medicine, Winston-Salem, North Carolina. Beth Hillson, celiac and proprietor of the Gluten-Free Pantry. Karoly Horvath, M.D., clinician/researcher at the University of Maryland School of Medicine in Baltimore. Marge Johanamen, celiac, CSA Kentucky state coordinator Pam King, University of Maryland Bob Levy, Celiac Research Foundation Ruth Levy, spouse Jax Lowell, celiac and author of Against the Grain Elaine Monarch, celiac, founder and Executive Director of the Celiac Disease Foundation Selwyn J. Monarch, Board of Directors, CDF Diane Paley, celiac, governing board CSA/USA Michelle Pietzak, M.D., pediatric gastroenterologist at Childrens Hospital, Los Angeles Connie Tur, celiac, president Greater Louisville Celiac Sprue Support Group

Celiac.com 07/02/2002 (Summary prepared 06/05/2002) - I'm here at the 10th International Celiac Disease Research Conference, in Paris, and three days of intense meetings and reports have just concluded. I didn't want to wait to share with you some of the most interesting and exciting developments in celiac disease--so I'm in a cyber cafe in Paris sending this e-mail. First of all, many of you know that there are two main types of medical research--work that is done in a laboratory, with test tubes and equipment, and research that is done using human participants, called clinical research. There were many presentations on laboratory research at this meeting, which is a subject that tends to be pretty complicated (for me at least!). Laboratory Research Presentations: Many of the presentations on this area of research were focused on answering the following question, so neatly outlined by Dr. Fasano: How do environmental factors (like gluten) reach the immune system (which is primed by genetic predisposition) to cause a response (the development of disease)? The wall of the intestine is designed to prevent this from happening, he said. There are many theories as to why this occurs. Some theorized that gluten actually penetrates epithelial cells (they are the ones that line the intestine) and come out the other side. Other researchers showed evidence that the bonds between epithelial cells break down and opens a pathway for gluten to enter the intestine. Interestingly, another researcher, Dr. Bana Jabri from Princeton has focused her research on the role of immune killer cells that are activated in celiac disease, and gliadin does not have to be present for them to react and create celiac disease! Several researchers discussed the toxic areas of the gliadin protein, and how they are activated in the presence of immune molecules like IL 15. One interesting but complicated note--in a study of numerous patients (using biopsy samples) all of the intestinal samples recognized different toxic fragments of gluten--meaning that there are dozens of ways that celiac disease can develop at the cellular level. These researchers are studying the earliest events in the body that may lead to celiac disease. It is hoped that if we can better explain the series of events (like a row of dominos that fall, one at a time) we can develop treatments to stop these events and prevent celiac disease. Did you know there was more than one kind of tTG (tissue Transglutaminase)?...I didn't! There is an epidermal transglutaminase that is present in dermatitis herpetiformis...this difference may indicate why people with DH are much more sensitive to gluten than those with celiac disease. Clinical Research and Screening Studies: Dr. Joe Murray presented a retrospective analysis of the incidence of celiac disease in the county that includes Rochester, Minnesota and the Mayo Clinic. In his analysis, which goes back decades, he found that the average age of diagnosis is 45-64, and the incidence of celiac disease was more common in women by 3 to 1. He found that celiac disease was more common in this county than ulcerative colitis and more common than Type1 diabetes. Dr. Carlo Catassi, currently in residence at the Center for Celiac Disease Research in Baltimore but native to Italy, presented an overview of the differences between celiacs in the United States and Europe. Some interesting and not surprising information--Europeans are diagnosed younger as adults (34 years of age) when compared to Americans. In Europe, children are diagnosed on average by the age of 4, while many American children are school-age by the time they reach a diagnosis. Surprisingly, Catassi reported that US celiacs tend to have more diarrhea than their European counterparts. Catassi also reported that Europeans have more atypical forms of celiac disease than Americans. He presented the celiac disease screening prevalence figures for the US: 2,121,212 people are projected to have celiac disease in America. There are 140 unknown celiacs for every diagnosed celiac in the US. Dr. Michele Pietzak, in California, did a prevalence study of at-risk conditions in children and found that 14% of children with iron-deficiency anemia had celiac disease. A group in Salt Lake found that 10% of children with Downs Syndrome had celiac disease, and the Childrens Hospital of Milwaukee found that 7% of children with type 1 diabetes have celiac disease. This is a strong case for screening all children with these conditions. Speaking in reference to children, Dr. Catassi said that weaning practices in the US and other countries are having a bigger role in the development of celiac disease than previously thought. Osteopathy: a South American researcher has looked at the issue of fractures in people with silent celiac disease as compared to people with symptomatic celiac disease. He found that people who had symptomatic celiac disease were more likely to suffer fractures than those with silent celiac disease. In all cases, the fractures were less severe in nature. More confirmation with regard to bone mass deficiency in children-the gluten-free diet alone will repair the deficit, and there is generally no need for other medical interventions. Another area of research concerned gluten-related ataxia (a complicated condition that I dont fully know how to describe, but includes muscle weakness and confusion). Overall, it was reported that 6-10% of celiac patients may develop neurological problems (of which gluten-related ataxia is only one). This is another case where celiacs with ataxia may produce different antibodies (like in DH) which lead to the development of ataxia. Most importantly, ataxia does not develop as a result of a nutrient deficiency. There was a great deal of information presented about autoimmune disorders, and I want to make sure I get it right, so Ill summarize that section more in detail (along with other topics) when I return to the office. However, one interesting item related to children with celiac disease and their risk for developing autoimmune disorders was presented: In a study of 74 children diagnosed with celiac disease before the age of 5, Italian researchers found that after 10 years, their risk of developing autoimmune disorders was no greater than that of the general population. Yet another reason for early intervention! Another important area of research presented was in the area of refractory sprue and the development of lymphomas. Im also going to give this area a bit more thought before I post anything, but I will reassure everyone that the risk of lymphomas is very rare. One more thing: I apologize for the incompleteness of my e-mail if any researcher or physician finds that I have not best described their work--I'm summarizing my notes after a very long three days of meetings and my brain cells may be a bit dysfunctional. I will clarify any information and send abstracts to anyone who would like them, just send me your snail mail address. Au Revoir!

Dr. Joseph Murray, of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease. He gave a talk entitled Celiacs in the 90s at a conference hosted by the American Celiac Society on June 10-11, 1994. What follows are highlights of Dr. Murrays talk. Dr. Murray comes from Ireland, where Celiac Sprue (CS) is much more common. In Ireland, people have a much easier time dealing with the gluten-free (gluten-free) diet, whereas in the US it is almost as though it were considered unpatriotic to not eat wheat. You can reach Dr. Murray at: murray.joseph@mayo.edu. Dr. Murray believes that ALL Dermatitis Herpetiformis (DH) patients also have Celiac disease, whether they realize it or not. This celiac disease is often latent or silent. Earlier reports of patients with DH who did not have enteropathy (small intestinal damage) may not have counted milder forms of the celiac disease damage. (Editors note: Dr. Alexander, our physician advisor, believes most, but not all DH patients have Celiac disease.) Not every Celiac patient suffers weight loss or has diarrhea. One of his patients is a woman who weighed 400 lbs. when she was diagnosed. Her symptoms included nocturnal pain, and constipation. After checking the stomach and some other testing, they did a small intestine biopsy. When they found the classic flat villi, they suspected a lab mix-up because the womans symptoms were so atypical. In this case, the woman was suffering from cravings that caused her to greatly overeat. She was nutritionally over- compensating for the small intestine damage. After being diagnosed, the patient went on the gluten-free diet, lost some of these cravings, and promptly lost 50 lbs. Symptomatic Celiacs can be split into two groups: Those that have the classical CS symptoms and those that have atypical symptoms or only one of the classical symptoms. Patients in the first group are usually (though not always) diagnosed correctly by a gastroenterologist. Those in the second group, which make up about 2/3 of Dr. Murrays patients, are much more difficult to diagnose. Another factor is variable histology, which basically means that the villi are not always completely flat. The average adult has more than 20 feet of small intestine, and often, only the very front part gets severely damaged. Often, the remaining portion of the small intestine is able to compensate for what the damaged section is not absorbing. Dr. Murray believes that we are seeing fewer diagnosed Celiacs in the US than in Ireland because our diets are very calorie-dense. This means that even with malabsorption you are still getting a lot of nutrients so that you absorb enough to not lose weight and not fully develop other symptoms. Gluten causes damage that makes the gut leaky. This can lead to exposure of the bodys immune system to foreign allergens it would not otherwise see. This explains why Celiacs tend to have more allergies than the general population. Dr. Murray believes there are several triggers that can activate Celiac disease in genetically susceptible people: A sudden change to a low fat diet, which usually means a sudden increase in starches, which usually means a dramatic increase in wheat-based products. A woman is susceptible during postpartum, when the immune system is adjusting to the changes after delivery. Surgery, particularly GI (gall bladder, etc.) can be a trigger. Certain viral infections. Also, there is some suspicion that certain antibiotics can be triggers, though in these cases it could also be the infection that the antibiotics are fighting. Dr. Murray believes CS is not an allergy; it is an auto immune disease (Allergy vs. Intolerance). For Celiac disease to develop, two conditions must be met: There must be a genetic predisposition towards Celiac disease. This involves very specific genetic factors. The auto immune system must be triggered in some way. CS tends somewhat to run in families. The incidence in first degree relatives (parents, siblings, children) of a Celiac is about 10%. Anyone who has both a parent and a child with CS should be tested themselves for CS. CS is not entirely genetic. Among identical twins, if one has CS, about 70% of the time the other will also have CS. If the disease were entirely genetic, then the incidence in identical twins would be 100%. Among siblings that are HLA-matched to a Celiac sibling, the incidence of CS is about 30%. When not HLA-matched, the incidence rate is much lower. According to Dr. Murray, since CS is an auto immune disease, it follows that there are other auto immune diseases that are associated with it. Rheumatoid Arthritis, Lupus, Type I Diabetes, and some eye problems may occur more frequently in CS patients. This is not because of gluten or CS itself; it is because CS patients are part of a group that is genetically predisposed towards auto immune problems. About 5% of CS patients also have DH. At the University of Iowa, there have been 350 patients diagnosed with DH. Dr. Murray believes these have celiac disease. If these DH patients are only 5% of the Celiacs, then there should be about 7,000 Celiacs in the Iowa area. The number of diagnosed Celiacs is much less than 7,000. Even if this extrapolation is exaggerated, it is still clear that there are many undiagnosed Celiacs out in the general population. Most DH patients are prescribed Dapsone, which treats the symptoms. In most cases, they are told of the gluten-free diet, but it is not stressed and so most DH patients do not follow the diet. Dr. Murray finds this most distressing, because even if these patients dont have GI-related symptoms, there is still continual damage being done to the small intestine. Dermatologists, in general, dont give enough consideration to a GI problem as the source of DH. This places DH patients at an even greater risk of developing lymphoma in the small intestine. Lymphoma in the small intestine is extremely rare in the general population. Untreated Celiacs have a 70 or 80 times greater chance of developing lymphoma. A lifetime of not following the gluten-free diet gives a Celiac about a 7% chance of developing lymphoma. There is also an increased risk of other GI-related and lymphatic cancers. The risk of developing lymphoma immediately begins to decrease when a Celiac patient starts following a gluten-free diet. The risk continues to decrease until, after 3-5 years, it approaches that of the general population. Dr. Murray makes a small intestine X-ray a routine part of the treatment for a newly diagnosed adult Celiac patient, especially those over 40 years of age. Hes looking for lymphoma in the small intestine. It is very difficult to find, but if it is found it can usually be successfully treated. DH is caused by reactions to antibody complexes that, for reasons not totally clear, become deposited under the skin. These DH breakouts can continue for a long time after a gluten-free diet is adopted, because these deposits are not reabsorbed by the body very quickly. In about 70% of the cases, dapsone treatments can be discontinued after 18 months-2 years; for the other 30% it takes longer. How gluten-free should the diet be? Dr. Murray believes that Celiacs should treat gluten the same way they treat rat poison. Celiacs should never eat food if it is known to contain gluten. Accidental ingestion of gluten should be avoided as much as possible. For a Celiac, it is unacceptable for gluten to be ingested more than once a month, accidentally or otherwise. You can NOT judge whether a food has gluten by your reaction to it. Many Celiacs can ingest small amounts of gluten with no symptoms; however, the small intestine is still being damaged. Dr. Murray stressed that once you have Celiac disease, you will always have it; you will never be able to eat wheat or other gluten-containing products again. This is a fact of life that Celiacs simply must accept and live with. Lactose intolerance is not common in white Caucasian adults of northern European descent; probably close to 5%. (Editors note: According to Dr. Alexander, it occurs in about 30% of the adult US population.) A newly diagnosed Celiac may have temporary lactose-intolerance due to the damage in the gut; the intolerance should disappear once the gut heals. If you are lactose-intolerant, you should be aware that while ingesting lactose may make you uncomfortable, it does not damage the intestine. Most newly diagnosed Celiacs can use temporary lactose-intolerance as a way to check on the healing taking place. Once a month, they should drink half a glass of milk on an empty stomach and see if there is a reaction such as gas, cramps, diarrhea, etc. Failure to have a lactose reaction means that the gut is healing and the diet is working. For most people, lactose intolerance will disappear within six months of being on a gluten-free diet. Dr. Murray advises Celiac patients against smoking. Newly diagnosed Celiacs, as well as those not following a strict gluten-free diet, already have an increased risk of malignancy. Celiacs cannot afford to increase that risk even further by smoking. Refractory Sprue is a rare complication that generally occurs in older Celiac patients. This is a situation where malabsorption continues to occur even though the patient is on a gluten-free diet. Dr. Murray says the first three things you do when presented with refractory sprue are: Check the diet Check the diet again Check the diet a third time Once you have verified that no hidden sources of gluten are causing the problem, then you recheck the diagnosis, look for enzyme supplements to help with digestion, check for pancreatic problems, lymphoma bacterial overgrowth, etc. Diagnosis of CS in the US is probably lower than it should be due to rigid medical practices and old thinking. One common label applied to people with stomach complaints is Irritable Bowel Syndrome. Dr. Murray calls that an intellectual trash can if it is used too widely and if doctors forget about other possibilities, in that it is occasionally over-diagnosed. It really means, There is something wrong with your stomach, and we dont know what it is. The occurrence of stress-induced bowel dysfunction is a real entity. In the US, CS is an exception to the rule concerning research efforts. It is considered to be a marginal disease. There is very little commercial interest in it. CS is definitely under-represented when compared to other diseases that get far more attention. Dr. Murray believes there are too many different national organizations that deal with CS. He believes these organizations need to unify and become one in order to advance the national agenda. He thinks local support groups such as our TCCSSG are doing a lot of good work; he considers belonging to a support group to be an essential part of the treatment of Celiac disease. Dr. Murray recommends physicians associated with local support groups should read a book that thoroughly explains this disease. The book is Coeliac Disease, by Michael Marsh, Blackwell Scientific Publications, November 1992. It costs about $175, but is well worth the cost if it helps a physician become more interested and learn more about this disease.

Summary prepared by Mardena Waller Here is the Summary on the Bioengineered Foods and Celiac Awareness meeting February 24, 2001 at Caltech, sponsored by CDF - Burbank, Glendale, Pasadena Connections Group. Pasadena (CA) Wild Oats provided free gluten-free foods, and is a stand-out, and nearly stand-alone, market promoting education on gmo-free foods. Let them know you appreciate what they are doing, and tell them you support them. Ask them for a copy of Genetically Engineered Foods - Are They Safe? (Scientists explain health and environmental risks.) Heres an example of what Marshall Crostowski cautioned: Question #1: Are biogeneticists working to reduce or eliminate gluten proteins adversely affecting celiac suffers? Short Answer: Glutens are mainly found in wheat and the related cereals barley, rye and triticale and are important components not only in baked goods but also in a large number of processed food, medicines and cosmetics. Most of the current genetic modifications are to increase the quantity and quality of gluten and to introduce wheat gluten genes into other crops such as barley, maize, sorghum, tobacco, and perhaps rice. There may be some research in Europe toward eliminating or neutralizing wheat gluten or the bodys immunological reaction to it. Gluten Biotech Watch recommends when you e-mail food companies asking about ingredients, tell them you dont want gmo foods, and ask them to go (and label) gmo/gluten-free! Groups and individuals can support companies that do, boycott companies that dont. Make some noise! To help, E-mail GBW at noyodelling@yahoo.com (we DO have a sense of humor!). Robert Jeffers, Ph.D., and Marshall Crostowski will lead GBW to monitor gmo/gluten research.

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.