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Found 18 results

  1. Celiac.com 06/25/2003 - The Neuropathy Association -- On May 27, 2003 a link between Peripheral Neuropathy and Celiac Disease was reported by physicians at the Weill Medical College of Cornell University and New York Presbyterian Hospital, according to The Neuropathy Association. Peripheral Neuropathy, which affects up to 20 million people in the U.S., can cause pain, numbness and weakness in the arms and legs and, when left untreated, can progress to debilitation. In an article published in todays Neurology, five percent of all patients with neuropathy were found to also have celiac disease, which results from an allergy to gluten in bread and other wheat products, and is estimated to affect one out of every 150 people. Based on the diagnosis, we are now able to treat a substantial number of patients with neuropathy who previously could not be helped, said Dr. Russell Chin, the first author of the paper. In addition, patients with celiac disease tended to have a type of neuropathy called small fiber neuropathy which often causes severe burning, stinging, and electric-shock like pains, but is often misdiagnosed as it is undetectable with routine tests used by neurologists to diagnose neuropathy. Approximately 16% of all patients with small fiber neuropathy were found to have celiac disease. Many of our patients were told that there was nothing physically wrong with them, and were advised to seek psychiatric care for presumed anxiety or depression, noted Dr. Norman Latov, Medical and Scientific Director of The Neuropathy Association, and senior author of the study. You too would be anxious and depressed if you were in constant pain, and no-one believed you or offered to help. Celiac disease is known to run in families, and in several of the cases, other family members were affected. Some were erroneously diagnosed with Charcot-Marie-Tooth disease, an inherited form of neuropathy due to genetic mutations. Not all familial cases of neuropathy are due to Charcot-Marie-Tooth disease, noted Dr. Latov. Peripheral neuropathy can also occur in association with other causes for neuropathy that run in families, such as diabetes or autoimmunity, for example. The article also notes that one third of the celiac neuropathy patients did not have any gastrointestinal symptoms such as malabsorption, abdominal pain or diarrhea, which are associated with celiac disease. What many people dont realize, notes Dr. Peter Green, Director of the Celiac Disease Center at the New York Presbyterian Hospital, and co-author of the paper, Is that 50% of adults with celiac disease have few or no gastrointestinal symptoms, and present with other manifestations such as anemia, or as in this case, peripheral neuropathy. Treatment consists of eliminating gluten or wheat containing foods in the diet. At present, patients with neuropathy are not routinely tested for celiac disease. Based on the new study, however, patients and physicians should be aware that anyone with unexplained neuropathy or pain should be tested for celiac disease regardless of whether or not they have the classic gastrointestinal symptoms. About The Neuropathy Association: The Neuropathy Association is a public, non-profit, charitable organization, founded by patients with neuropathy and their friends and families, whose mission is to provide support and education, and fund research into the causes and treatments of neuropathy. It is a rapidly growing, broad based organization, with over 70,000 members, and over 200 support groups and chapters throughout the US. For more information about peripheral neuropathy and The Neuropathy Association, visit our web site at http://www.neuropathy.org, or contact us at 60 E. 42nd St, Suite 942, New York, N.Y. 10165, Tel: 212-692-0662, e-mail: info@neuropathy.org. Contact information: Media Contact: Jeanne Abi-Nader Tel: 212-484-7954 E-mail: jabi-nader@rlmnet.com Norman Latov, M.D., Ph.D., Professor of Neurology and Neuroscience, Weill Medical College of Cornell University, and Medical and Scientific Director, The Neuropathy Association. Tel: 212-888-8516 E-mail: nol2002@med.cornell.edu.
  2. Hi! My almost 4 yr old son has recently been tested for celiac. He is very small for his age and as I review his growth he has dropped in percentile over the past 2 years from 40-30th down to 5-10th percentile. He's always have had stomach "issues" alternating constipation and diarrhea and frequent Bms. He has also had canker sores several times and he has eczema. He had a celiac panel and his labs were all within normal except Ttg Igg. It was "7" and the normal range was between (0-5). I dont know what his CBC was but I plan to find out this week. Could this mean he is celiac or gluten intolerant? When I "Google" the labs it means a "weak positive" but I'm confused as to whether another lab needs to be positive or not. Are there other labs that need to coordinate with Ttg igg to be considered positive? His doctor said his labs were "normal" but my gut tells me there is something going on. I've been attempting to keep him gluten free to see if there is a difference. Any advice would be great!! Thanks!
  3. Celiac.com 05/11/2012 - Horses are susceptible to inflammatory small bowel disease, and the condition effects horses in much the same way as it effects humans. As with its human counterpart, equine inflammatory small bowel disease (ISBD) is an idiopathic pathologic condition that seems to be growing more and more common. A research team recently conducted a study to examine the possibility that gluten may play a role in equine ISBD. The researchers were J.H. van der Kolk, L.A. van Putten, C.J. Mulder, G.C. Grinwis, M. Reijm, C.M. Butler, B.M. von Blomberg of the Department of Equine Sciences, Medicine Section, Faculty of Veterinary Medicine at the University of Utrecht, in Utrecht, in the Netherlands. For their study, the team assessed antibodies that are known to be important in the diagnosis of human celiac disease: IgA antibodies to human recombinant and guinea pig tissue-transglutaminase (TGA), native gliadin (AGA), deamidated-gliadin-peptides (DGPA), and primate and equine endomysium (EMA). The team measured these antibodies using blood samples from three different groups of horses: Twelve ISBD affected horses on a gluten-rich diet, along with two control groups. The first control group included 22 horses on a gluten-rich diet, and the second included 25 horses on a gluten-poor diet. The researchers measured differences (p < 0.05) in the groups using the Wilcoxon test. They found that both ISBD-affected horses and gluten-rich control group had significantly (p < 0.0004) higher hrTGA titers than gluten-poor control group. However, ISBD horses did not show significantly higher levels of any of the celiac disease related antibodies when compared to gluten-rich controls. Still, They found significantly higher antibody levels (TGA, EMA and DGPA) in one of the ISBD horses. They put that horse, 14-year-old stallion, on a gluten-free ration for 6 months. They then reassessed his antibodies and found a significant reduction of antibody levels, along with clinical recovery associated with improved duodenal histopathology. The researchers write that this is the first such study assessing gluten-related antibodies in horses and that the results suggest a potential pathogenic role of gluten in at least some cases of equine ISBD. These clinical results suggest that further study into the immunologic basis of possible gluten-sensitive enteropathy in horses might have important implications for the human manifestation of the disease. Source: Vet Q. 2012 Apr 10.
  4. Celiac.com 01/02/2012 - To properly diagnose celiac disease doctors must observe classic histological changes to small bowel mucosa. Success rates can vary among clinics and practitioners. A clinical team recently compared biopsy interpretation between different pathology practice types. A research team recently assessed variability in small bowel histopathology reporting between different pathology practice settings, and its impact celiac disease diagnosis. The researchers included Carolina Arguelles-Grande, Christina A. Tennyson, Suzanne K. Lewis, Peter H. R. Green, and Govind Bhagat. The team used a pathologist to blindly assessed biopsies from community hospitals (n=46), university hospitals (n=18) and commercial laboratories (n=38) for differences in histopathology reporting and agreement in diagnosis of celiac disease and degree of villous atrophy (VA) by k analysis. Data showed very good agreement for primary diagnosis between the authors and university hospitals (k=0.888), but only moderate agreement compared with community hospitals (k=0.465) or commercial labs (k=0.419). The review showed that diagnosis varied in 26 (25%) cases, leading to a 20% increase in celiac disease diagnosis after review. The 49 patients diagnosed with celiac disease by both institutions showed fair agreement in degree of VA (k=0.292), with moderate agreement between the authors and commercial laboratories (k=0.500) and fair agreement with university hospitals (k=0.290) or community hospitals (k=0.211). In 27% of cases, the degree of VA was upgraded, while VA was downgraded in just 2% of cases. Data also showed poor agreement for Marsh score categories 1 and 2 (k<0.0316), with both missed at other centers, and just fair or moderate agreement for Marsh scores 3a and 3b. They found that data on the degree of VA and intraepithelial lymphocytosis were lacking in 26% and 86% of reports, while non-quantifiable descriptors, such as ‘blunting’ or ‘marked atrophy’ were common. The data show that community-based hospitals and commercial pathology labs are under-diagnosing celiac disease-related histological changes. To combat variations in biopsy interpretation and reduce under-diagnosis of celiac disease, the team calls for greater celiac disease awareness and uniformity in small bowel biopsy reporting among pathologists. Source: Journal of Clinical Pathology (2011). doi:10.1136/jclinpath-2011-200372
  5. Dig Liver Dis. 2002 Dec;34(12):846-50. Celiac.com 07/12/2004 – In a study designed to determine the causes of continued gastrointestinal problems in celiacs who are on a gluten-free diet, Italian researchers looked at 15 celiac patients who continued to experience symptoms even after 6-8 months on a gluten-free diet. Histology improved in all patients after this time so refractory celiac disease was excluded as the cause. The scientists performed AGA and EMA tests, stool examination, EGD with histological examination of small bowel mucosa, and sorbitol-, lactose-, and lactulose H2-breath tests to determine a possible cause of the patients persistent symptoms. The researchers found that one patient who had Marsh II lesions was fully compliant with his diet but had mistakenly taken an antibiotic that contained gluten. Two of the patients had lactose malabsorption, one had Giardia lamblia, and one had Ascaris lumbricoides infestation. Ten patients were found to have small intestinal bacterial overgrowth (SIBO) by lactulose H2-BT. The doctors prescribed a diet without milk or fresh milk-derived foods to the patients with lactose malabsorption; and treated the patients with parasite infestation with mebendazole 500 mg/day for three days for two consecutive weeks. The SIBO patients were treated with rifaximin 800 mg/day for one week. All of the patients were re-evaluated one month after treatment, and all were symptom-free. The researchers conclude that SIBO affects most celiacs who have persistent gastrointestinal symptoms after going gluten-free.
  6. Celiac.com 12/05/2011 - Class II major histocompatibility molecules are one of the main points of susceptibility for a number of autoimmune disorders, including type 1 diabetes. A team of researchers recently set out to investigate structure-based selection of small molecules to alter allele-specific MHC Class II antigen presentation The research team included Aaron W. Michels, David A. Ostrov, Li Zhang, Maki Nakayama, Masanori Fuse, Kristen McDaniel, Bart O. Roep, Peter A. Gottlieb, Mark A. Atkinson, and George S. Eisenbarth. They are variously affiliated with the Barbara Davis Center for Childhood Diabetes at the University of Colorado Denver, the Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, in Gainesville, FL, and with the Department of Immunohaematology and Blood Transfusion at Leiden University Medical Center in Leiden, The Netherlands. In the NOD mouse model of spontaneous autoimmune diabetes, Human DQ8 and I-Ag7 imparts diabetes risk by modulating presentation of specific islet peptides in the thymus and surrounding area. To define small molecules that could live in specific structural pockets along the I-Ag7 binding groove, the research team made use of an in-silico molecular docking program to review a vast “drug-like” chemical library. They were hoping to either promote or inhibit presentation to T cells of the autoantigen insulin B chain peptide, which consists of amino acids 9–23. By making use of both murine and human cells, the team's results show that small molecules can in fact influence specific TCR signals in the presence of cognate target peptides, based upon the targeted structural pocket. The effect of a compound on TCR response varied among targeted pockets, with pocket 1 and 6 compounds inhibiting TCR response, and molecules targeted at pocket 9 promoting peptide responses. It takes just nanomolar levels of the inhibitory molecules to block the insulin B chain peptide, which consists of amino acids 9–23, endogenous insulin, and islet-stimulated T cell responses. At concentrations as low as 10 nM, Glyphosine, a pocket 9 compound, enhances insulin peptide presentation to T cells, upregulates IL-10 secretion, and prevents diabetes in NOD mice. These studies offer a new way to identify small molecules that can both stimulate and inhibit T cell responses, thus offering a potential for future therapeutic treatment options. Source: Journal of Immunology doi: 10.4049/​jimmunol.1100746
  7. Celiac.com 12/22/2010 - A recent evaluation of the safety and efficacy of small intestinal release mesalamine (SIRM) for symptom relief in refractory celiac disease (RCD) shows that SIRM seems to be a safe and effective treatment option, though larger tests are needed to know for certain. The research team conducting the evaluation included Shailaja Jamma, MD, Daniel A. Leffler, MD, Melinda Dennis, RD, Robert M. Najarian, MD, Detlef B. Schuppan, MD, Sunil Sheth, MD, and Ciaran P. Kelly, MD, They set out to evaluate the safety and efficacy of small intestinal release mesalamine (SIRM) for symptom relief in refractory celiac disease. There are currently no adequate clinical therapies for patients with refractory celiac disease and corticosteroid and/or immunosuppressants treatments are of limited use due to side effects. SIRM has been shown to reduce local inflammation, and it is well tolerated. For the study, the team looked at records of the refractory celiac disease patients who received SIRM in an open-label therapeutic trial. Data included patient demographics, disease characteristics, dose and duration of SIRM therapy, and patient response. The team then categorized each response as complete, if symptoms resolved completely, partial if symptoms improved at least 50%, and non-responsive if symptoms improved less than 50%. The team treated four patients with SIRM alone and six patients with a combination of SIRM and oral budesonide. After four weeks, half of the patients showed complete response, while 10% showed a partial response. Two of the six patients were able to discontinue budesonide. One patient discontinued SIRM after complaining of headaches. These initial results indicate that SIRM seems to be a safe and efficacious treatment option in patients with refractory celiac disease, though a larger, more comprehensive study is needed to confirm these results. Source: J Clin Gastroenterol 2010 Sep 24. doi: 10.1097/MCG.0b013e3181f42401
  8. American Journal of Clinical Pathology, April 2000 - A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, by Kenneth Fine, M.D. and Frederick Ogunji Ph.D (Celiac.com 07/09/2000) Patients with gluten sensitivity should be evaluated for nutrient malabsorption because if present, this means there is small intestinal damage and institution of a gluten-free diet is imperative to prevent osteoporosis and other nutrient deficiency syndromes. Furthermore, a test at the time of diagnosis serves as a baseline to be compared to later if needed. For more than 50 years, the primary method used to assess for the presence of small intestinal damage and nutrient malabsorption in patients with celiac disease has been a 72-hour quantitative stool collection. However, because this method requires that patients accurately collect all the stools they pass for 3 days (missed stools lead to falsely low results), the test is logistically difficult for medical centers unaccustomed to the procedure, and the voluminous specimens usually are abhorred by patients and laboratory technicians. It poses obvious problems for children who cannot or will not collect all their stools, as well as for patients with chronic diarrhea, who may have bowel movement frequencies reaching 15 or more per day and/or fecal volumes as high as 2 or 3 liters per day. For these reasons, physicians evaluating patients with suspected or proven gluten sensitivity often avoid tests for intestinal malabsorption altogether. Recently, researchers at the Intestinal Health Institute in Dallas, Texas have developed a new method for quantitating fecal fat excretion that requires collection of only a single stool specimen. Development of this method was based on the fact that as more fat is malabsorbed, the fat globules in stool become more numerous and larger. In a study published in the April 2000 issue of the American Journal of Clinical Pathology entitled A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, Kenneth Fine, M.D. and Frederick Ogunji Ph.D. tested 180 patients and found a highly statistically significant linear correlation between quantitative fecal fat microscopy (the new method) and chemically measured fecal fat output (the old method). They also showed that their microscopic analysis of just one stool gives comparable results to analysis of an entire 3-day collection. These researchers have, thus, shown that a dedicated quantitative analysis of one stool under a microscope can detect the rise in fecal fat due to intestinal malabsorption (or pancreatic maldigestion) as accurately as 3-day stool collections, making this latter test a thing of the past for most patients. This new stool test for intestinal malabsorption and other celiac-testing is available for order online from a laboratory set up by Drs. Fine and Ogunji to serve the needs of celiac patients. It is called EnteroLab and can be accessed at http://www.enterolab.com/.
  9. Research indicates that rod-shaped bacteria, of the species Clostridium, Prevotella, and Actinomyces, in the proximal small intestine may contribute to some cases of celiac disease in children. Recent data builds on previous research by the team from 1985 to 1996, which proved that rod-shaped bacteria were present in the proximal small intestine of Swedish children with celiac disease, but not in those without celiac disease. For the current study, Sten Hammarström and colleagues from Umeå University in Sweden used an electron microscope to scan proximal small intestine biopsies from 45 children with celiac disease taken between 2004 and 2007, and 18 without the condition. To identify the bacteria, they used 16S ribosomal DNA sequencing in DNA extracted from biopsies washed with solution containing an agent that enriches bacteria attached to the epithelial lining. In healthy children with no celiac disease, Streptococcus and Neisseria bacteria are most common of the normal, mucosa-associated microbial flora of the proximal small intestine, along with a limited number of other genera, including Veillonella, Gemella, Actinomyces, Rothia, and Hemophilus. Surprisingly, the researchers found that microbial flora of the proximal small intestine in biopsies from celiac disease patients differed only slightly from that of the control subjects. Only a single biopsy tested positive for rod-shaped bacteria. This finding made the team to look more closely at the microbial flora of nine frozen celiac disease samples that showed the presence of rod-shaped bacteria. In these samples, microbial flora were substantially richer in Clostridium, Prevotella, and Actinomyces compared with biopsies lacking rod-shaped bacteria. The researchers also note that all three types of bacteria could be found in two current celiac disease biopsies taken from children born during the celiac disease epidemic in Sweden in 1985–1996, when the earlier study was carried out. During this time, rates of celiac disease in children younger than 2 years of age increased four-fold. “We hypothesize that the increased frequency of rod-shaped bacteria in the jejuna mucosa of celiac disease children at least partly was due to the changes in infant-feeding practice during that time,” write the researchers. The changes resulted from new national feeding recommendations for infants to delay the introduction of gluten-containing foods from 4 to 6 months. This meant that many more children consumed their first gluten without the protective benefits of breastfeeding, the researchers write. The recommendation was later reversed. The study by Hammarström and co-workers supports their conclusion that these rod-shaped bacteria may contribute to celiac disease in genetically susceptible individuals by uptaking and transforming gluten into large immunogenic peptides, which can then cross with the bacterium through the epithelium, or interfere with the barrier action of the epithelium to permit the passage of gluten into the under-laying tissue. “Such bacteria could be seen as an adjuvant promoting T-cell activation,” they say. “Whether the identified bacteria have any of these properties remain to be elucidated.” Am J Gastroenterol 2009; 104: 3058–3067
  10. Celiac.com 01/17/2010 - A team of researchers based in the Netherlands and in Germany recently found that abnormal T-Lymphocytes in refractory celiac disease may occur beyond small intestinal intraepithelia. The research team was made up of W.H.M. Verbeek, B.M.E. von Blomberg, V.M.H. Coupe, and S. Daum, C.J.J. Mulder, and M.W.J. Schreurs. The team members are associated with the Departments of Gastroenterology, Pathology, Epidemiology and Biostatistics at VU University Medical Centre, Amsterdam, The Netherlands, and with the Department of Medicine I, Gastroenterology, Infectious Diseases & Rheumatology at Charite Universitatsmedizin, Campus Benjamin Franklin, in Berlin, Germany. Refractory celiac disease (RCD) is characterized by persistent mucosal pathology despite a strict gluten free diet. Patients with RCD type II show phenotypically abnormal (CD71CD3-CD4/8-cytoplasmicCD31) T-lymphocytes within the intraepitelial lymphocyte (IEL) population in the small intestine, with 50–60% of these patients developing an enteropathy associated T-cell lymphoma (EATL). The goal of the study was to determine whether abnormal T-lymphocytes in RCD II can be detected in other parts of the small intestinal mucosa besides the intraepithelial compartment. Additionally, the presence of aberrant T-lymphocytes was analyzed in two RCD II patients that developed atypical skin lesions. Researchers conducted multi-parameter flow cytometric immunophenotyping on both IEL and lamina propria lymphocyte (LPL) cell suspensions, isolated from small bowel biopsy specimens of RCD II patients (n 5 14), and on cutaneous lymphocytes isolated from skin-lesion biopsy specimens of RCD II patients (n 5 2). They also carried out immunofluorescence analysis of frozen RCD II derived small intestinal biopsies. The results clearly show that abnormal T-lymphocytes may develop in both the IEL and the LPL compartments of RCD II derived small intestinal biopsies. Indeed, even though the highest percentages are always found in the IEL compartment, abnormal LPL can exceed 20% of total LPL in half of patients with RCD II. Interestingly, cutaneous lymphocytes isolated from atypical skin lesions that developed in some RCD II patients showed a similar abnormal immunophenotype as found in the intestinal mucosa. In RCD II, the abnormal T-lymphocytes may also manifest in the sub-epithelial layer of the small intestinal mucosa, in the lamina propria, or even in locations completely outside the intestine, including the skin. Whether this finding indicates a passive overflow from the intestinal epithelium or active movement towards other anatomical locations remains to be determined. Source: Cytometry Part B (Clinical Cytometry) 76B:367–374 (2009)
  11. Celiac.com 01/20/2009 - Refractory celiac disease is a serious condition that occurs when celiac symptoms and intestinal damage continue even when the patient consumes a gluten-free diet. There are two types of refractory celiac disease (RCD). In RCD type I, immuno-phenotype of intraepithelial lymphocytes (IELs) are normal and polyclonal, while RCD) type II, is noted for the presence of an abnormal intraepithelial lymphocyte (IEL) population (CD7+ CD3− CD4/8-cytoplasmic CD3+). More than half of people with this condition develop enteropathy-associated T-cell lymphoma (EATL), a rare but virulent form of cancer with high mortality rates. A team of doctors recently set out to examine the relationship between lymphoma development and intraepithelial gamma/delta T-lymphocytes in the small intestine of patients with all types of celiac disease, as compared to the general population. The team was made up of Wieke H.M. Verbeek, M.D., B. Mary E. von Blomberg, Ph.D., Petra E.T. Scholten, B.Sc., D. Joop Kuik, M.Sc., Chris J.J. Mulder, M.D. Ph.D., and Marco W.J. Schreurs, Ph.D., all from Amsterdam’s VU University Medical Center. A certain type of IELs called TCRγ/δ+ IELs may play an important role in repairing mucosa, maintaining homeostasis, and guarding against tumor development. TCRγ/δ+ IELs in the human intestine have recently shown promise in the regulation of uncomplicated celiac disease. In the study, the research team wanted to see if patients with RCD II had fewer TCRγ/δ+ IELs than either RDC I, or celiac disease, an thus provide a possible explanation for ongoing mucosal damage and inflammation, and the development of abnormal T cells that tend to morph into EATL. The team used a method called multi-parameter flow cytometric immuno-phenotyping on IELs obtained from recent small bowel biopsy specimens from a fairly large, distinct celiac disease and control groups (N = 87). Patients with RCD II showed a much lower ratio of TCRγ δ+ IELs compared to either RCD I or celiac disease patients. Whereas, patients with uncomplicated celiac disease showed significantly higher numbers of TCRγ δ+ IELs than were found in the control group. The results showed the relationship between TCRγ δ+ IELs and aberrant IELs to be negative. It is interesting to note that TCRγ δ+ IELs numbers do rise in RCD II patients after effective treatment. The negative relationship between TCRγ δ+ and abnormal IELs, together with their known role in regulating uncomplicated celiac disease, suggests that TCRγ δ+ IELs may play a crucial role in helping the body to repair mucosa, maintain homeostasis and possibly even guard against tumor development. These cells may serve as important markers, along with the abnormal T cells, to help distinguish between types of celiac disease, and to gage the effectiveness of treatment efforts. Am J Gastroenterol 2008;103:3152–3158
  12. Celiac.com 06/03/2008 - As you travel and experience the sites of the world you are going to have to stop at a restaurant or destination that has a small kitchen. Let me tell you a little bit about myself so you can understand that I also started in a small kitchen. Chef Daniel P's Autobiography I started working at the age of 13 and began my work in a very small tourist town and was promoted up from busboy to dishwasher. I was so fast at washing the dishes that I was promoted up within a month to cook. I went from the buffet type restaurant to an ala cart restaurant and buffet line. At the age of 17 I was completely in charge of the kitchen—this included all ordering, menu making, staff hiring and firing, and every task a person would do to run a successful kitchen. I didn’t know how to cook though—at least not compared to what I learned later. Yes I could do the basic menus but I wanted more and I left to climb the ladder of a big kitchen—so I set my sites on gourmet food. At that time I saw that Prince Charles from England was visiting Palm Beach Florida. I saw that he visited two places while he was in Palm Beach—the Palm Beach Polo Ground and he also visited the Breakers Resort. I applied at both places when I came to Florida and both wanted to hire me. Every one has to start somewhere and you as the traveler are the ones who are going to train the future cooks or chefs. Yes you—the cook is going to learn from you as celiac patrons, so you need to do the right training. Let’s use the example of eating on a train that cooks for their patrons as they travel across the country. I like to think of a small boat or train as two of the most difficult places to prepare a gluten-free meal. They both are going to be small, and both have the potential to get bumpy while the cook is preparing food. This means there is a good chance an accident can happen and of course cross-contamination. These kitchens probably keep their fires contained in the stove or flat top burners. By keeping the flame for cooking contained in a box, this means they have less chance of a fire starting and that is very important if you are on a river or going down the train tracks. The cooks are going to use sauté pans, hard top grills, ovens, steam boxes and possibly microwaves. If you know that you are going ahead of time to these types of restaurants you should see if they can send you the menu ahead of time so that you can look it over. Hint: If you know your destination for any of your trip, see if you can get the menu before you arrive, as most places always have their menus prepared ahead of time. If you get the menu you can make up your Chef Daniel P Restaurant Form before you go. I would try to spell out your entire meal in great detail. I also use this technique for all mom and pop restaurants. You are not insulting a cook or chef by asking them to prepare your meal a certain way. Every day the cook receives orders from the waitress on how to prepare a particular meal. Just because you are giving the instructions yourself only means to the chef that you are very serious about how your food is prepared. What to Eat And How to Cook Your Meal In these type of restaurants that are small and have limited space you have to try to eliminate any mistakes that the cook might make. How…you ask? Try some of these ideas: Notify them ahead a time if you can. Let the train, boat or any restaurant know that you are coming. Make sure you tell them the date, time and how many people will be receiving special meals. Don’t be upset if you get there and no one knows that you are coming, it is just part of the business. Have their phone number available so when you arrive in the city you can call a few hours before you arrive to eat. Just remind them again that you are planning on eating at their restaurant and ask them when their slowest time is. If it is a train or boat ask if you can eat at the last seating time (unless they indicate that an earlier time is slower). Feel them out to see when the best time is for you to order a specially prepared meal. During your phone call, ask who you should ask for when you do arrive for your meal. Make sure you arrive with your Chef Daniel P Restaurant Form and a pen or pencil. When you arrive ask for the manager or the person you talked to on the phone. Tell the manager in great detail about your special diet request. Let them know you will be writing out your request that will specifically tell them how to prepare your meal. Ask if there is anything you should know about the kitchen or the chef—anything that could help you in preparing your meal and making it as safe as possible. You might have to ask the manager how they cook their food. Some are going to use a flat-top grill, broiler, steamer or even a microwave oven. Once you find this out it is time to create your meal instructions and present them to the manager so he can deliver them to the cook.How the Cook Prepares Your Food: Sautéing: To me is one of the safest ways to have your food prepared. No matter if the cooks are in a small or large kitchen. This is how I might write it down for the cook to see: “Sauté 1 whole chicken breast in olive oil, make sure the pan is very clean and does not have a crumb on it.” When asking to sauté you can ask for them to make a quick sauce in the pan. That is what I do, even if it is just to squeeze a lemon on your food, this can add some fresh flavor. Hard Top Grill: I don’t recommend using this unless you are the very first ones to arrive. During the day when they cook on the grill pieces of food stay on the grill for the whole day. You can ask them to use the razor blade to scrape the grill. Even using the razor blade it is not 100% and food from other meals may get on your food. Steamer: This is a good way to cook as long as your food is the only one in the steamer. You can ask them to wrap the food and this will keep all crumbs off of your food. Example: “Please wrap a piece of salmon up with some saran wrap. Place it on a holey pan so the steam can circle salmon." Microwave: This is great for potatoes or vegetables and a good way to keep food safe. I always ask for my veggies to be micro-waved. This is a great way to get a baked potato. Even some fish and other entrees can be cooked in the microwave. Example: “Could you please cook a potato and my vegetables in the microwave. Put them in a dish then cover with saran wrap.” Fryer: You must stay away from a fryer in small kitchens (unlike fast food chains and some bigger restaurants). They use the fryer for everything and that means that everything could be in it. When they cook your French fries, the crumbs from the chicken nuggets could get on your food. Boiling: This is another great way to cook food. You must ask them to only cover the food product that they are cooking. Some fishes, vegetables and other meats can be cooked this way. If they have a steamer I would ask for that first since they don’t have to wait for it to get hot. Example: “I would like two eggs boiled or poached in just enough water to cover the entrée so it won’t take so long. You could have the cook put a small amount of water then cover the pan and steam it.” Broiler: Sometimes small kitchens that are moving are not going to have a broiler. It is the fear of the open fire that could cause a fire in the kitchen. If they do have one you could ask for this example: “I would like a piece of salmon on a metal plate. Cook it until it is done, then splash it with white wine before plating.” The main idea you take into small kitchens is this: It is a lot like cooking at your home (unless you have a huge kitchen). Those kitchens are made small but can put out large amount of meals if needed. Those menus are made to accommodate the small amount of storage also. You need to really know your menu and the ingredients they are using. Unlike a large kitchen you might not have the extra supplies that a big kitchen has. They just don’t have the room and you need to think of that. So if it is a river boat or a train, when you look at the menu some of the items will be canned products, because canned products are so much easier to store than refrigerated items. As you look at the menu take the item you would like and ask them if they can cook it in a sauté pan or maybe in the oven. This is a very safe way to have your food prepared. When I was employed at the resort and we would often have banquets for over 200 people. If the meal was New York strip steak we would put the steaks on the broiler and mark the diamond char marks in order to get the steaks cooked exactly at the same time. We would then pull the steaks off and put them on large sheet pans. Just before we needed the steak, we would put them in the ovens and cook them until they were the proper temperature. The customers never knew that the steaks were cooked in the oven and not the broiler. The char marks on the steak made everyone believe that it was broiled. The point is that you can have your food baked as long as you don’t get sick—for me that is the most important thing. When I do eat out, I don’t care too much about the taste or temperature of the meal—my number one goal is that I get a gluten-free meal and that the restaurant doesn’t ruin my vacation. Also, you have to be very careful when you send your food back. Just remember how busy the cooks are and whether or not they are going to remember your specially ordered meal when it comes back to them. If they are busy in the back and the waitress says to the cook, “Cook it more,” what do you think happens—will they take as much time as they did the first time? These are the types of questions that you have to ask yourself when you are sitting at your table and thinking about sending your meal back. I know that we all expect a perfect meal when we pay for it. Sometimes it is just easier to ask them to only warm it up in the microwave. Something to think about is that the microwave is like a closed room where it is not likely that your food will get contaminated. Most kitchens, especially smaller ones, have a microwave like the one that you use at home. If you do need your meal cooked more, try to explain it to the manager and remind him that you will get very sick if it gets contaminated—ask the manager nicely if you can watch and see if the cook does it right. Another thing to remember when you are eating in these types of restaurants is that they are small and that means the kitchens are small too. The cooks are going to be right next to each other—only arms and shoulders apart. Remember; if you don’t think they will be able to feed you properly always have a plan B, so you can still eat. Plan your meal to be as simple as possible for them to prepare and you will be able to conquer the Gluten Monster and have a wonderful train or boat experience! Chef Daniel P.
  13. Celiac.com 10/28/2005 - Alba Therapeutics Corporation (Alba) today announced successful completion of its first Phase I trial for the drug candidate AT-1001, and that the FDA has granted Fast Track designation to AT-1001 for treatment of celiac disease. We are pleased to have concluded our first human study of oral AT-1001 and delighted that the FDA has granted fast track status to AT-1001. These two events are important additional milestones in our efforts to help those suffering from celiac disease, a disease for which there is no effective treatment, said Blake Paterson, MD, President and CEO of Alba. Alba plans to begin a proof of concept study demonstrating efficacy of AT-1001 in celiac patients within the next few months. Fast track process is designed to facilitate development and expedite the review of new drugs with the potential to address significant unmet medical needs for the treatment of serious or life-threatening conditions. Potential fast track benefits include FDA input into development, submitting new drug applications in sections rather than all at once and the option of requesting Accelerated Approval. About Celiac Disease Celiac disease is a T-cell mediated auto-immune disease that occurs in genetically susceptible individuals and is characterized by small intestinal inflammation, injury and intolerance to gluten. Gluten is a mixture of proteins found in common food grains such as wheat, rye and barley. According to the NIH, celiac disease affects approximately 3 million Americans, although the diagnosis is rarely made. The only treatment for celiac disease is complete elimination of gluten from the diet, which results in remission for some patients. About Zonulin Zonulin is an endogenous signaling protein that transiently and reversibly opens the tight junctions (tj) between the cells of epithelial and endothelial tissues such as the intestinal mucosa, blood brain barrier and pulmonary epithelia. Discovered by Alba co-founder Dr. Alessio Fasano, zonulin appears to be involved in many disease states in which leakage occurs via paracellular transport across epithelial and endothelial tight junctions (tj), and thus may play an important potential role in the treatment of auto-immune diseases. About Alba Alba Therapeutics Corporation is a privately held biopharmaceutical company based in Baltimore, Maryland. Alba is dedicated to commercializing disease-modifying therapeutics and drug delivery adjuvants based on the zonulin pathway. Albas lead molecule, AT-1001, is targeted towards the treatment of Celiac Disease and Type 1 Diabetes. Contact: Dr. Blake Paterson Alba Therapeutics Corporation 410-522-8708
  14. Eur J Gastroenterol Hepatol. 2004 Oct;16(10):961-8. Celiac.com 07/12/2005 - In an effort to determine the role of T-cells in celiac disease, researchers in Ireland examined the cells taken from the duodenal biopsies of both treated and untreated celiac disease patients. An assessment was made of the samples cell yields, and analyses were done to determine their viability and flow cytometric characteristics to quantify CD8 expression in the CD4CD8 T-cells. The researchers were surprised to find that T-cell yields in the epithelial layer were not elevated in active, untreated celiac disease, although enterocyte counts decreased significantly, which gave the appearance of T-cell infiltration. There was a dramatic decrease in the number of CD4CD8 T-cells in untreated patients in both the epithelial layers and in the lamina propria regions, and the levels of CD8 expression by CD4CD8 T-cells in the epithelial layer were also significantly decreased—and these levels did not return to normal even after treatment with a gluten-free diet and the return to normal of their intestinal architecture. According to the researchers: "No increase of intraepithelial lymphocytes in the celiac lesion may require us to reconsider the definition of celiac disease as an inflammatory condition. Low CD4CD8 populations in treated as well as untreated coeliac patients indicate that these T-cells are inherently absent in individuals genetically predisposed to celiac disease." The reduced levels of CD4CD8 T-cell populations could be the initial trigger of oral gluten tolerance in genetically susceptible individuals, and play a key role in the mucosal damage caused by celiac disease. More research in this area is needed to determine the full implications of these findings.
  15. The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada. There is much evidence linking untreated celiac disease with malignancy. I have recently been notified of publication of a report I have written on that connection, which is promised for the September, 1997 issue of Medical Hypotheses (1). In that report, I combine a review of the literature with an outline of a possible biochemical pathway whereby psychoactive peptides derived from the pepsin digests of wheat, rye and barley may down-regulate the activation of natural killer cells, the bodys first line of defense against malignancy. This is not a postulation that glutinous grains are carcinogenic. Humankind has been exposed to carcinogens throughout its ~ two million year evolution. But it is only in recent centuries that malignancy has increased exponentially, and has struck so many children and adolescents. This is clearly a counter-evolutionary trend when youngsters are afflicted, because the incidence should be decreasing over time, as these youngsters genes are being pruned from the gene pool. There is some evidence that has come to light since my aforementioned report, which will be of interest to celiacs and members of their families. M. Stanislas Tanchou, a truly visionary physician, and campaigned with Napoleon Bonaparte, presented a paper to the Paris Science Society in 1843, which was a complex statistical examination of malignancy, offering evidence of increased malignancy with increased civilization (2). One of the prime indicators of a civilizing trend was a diet that included cereal grains. The greater the consumption of these foods, the greater the incidence of malignancy (3). Dr. Chris Reading, an orthomolecular psychiatrist, in Australia, has documented the treatment of five cancer patients for depression (4). His testing for food allergies, and subsequent treatment of depression with dietary exclusion of cereal grains resulted in total remission of the cancers (which were also given conventional treatments) in all five patients he reports treating. One of these patients did die, but that was from the cancer treatment. There are also two reports in the Journal of Clinical Gastroenterology (5) Lancet (6) that I cite in my Medical Hypotheses article. These reveal a total remission of malignancy in each patient. One report then recants the original diagnosis, and identifies the correct diagnosis as lymphadenopathy. In the other report, which spurs a heated debate, the original diagnosis is supported by a resected section of malignant bowel, and there can be no doubt as to the correct diagnosis. Further, in a 1977 report, in Nutrition and Cancer (8), from Stanford University, all the children suffering from radiation and chemotherapy damage to the small bowel recovered fully from their chronic enteritis, and suffered no relapse of either the bowel obstruction or the disease. The treatment they were given was a gluten-free, dairy-free, low fat, low residue diet. In an obscure Czech journal, a report has recently indicated that one or more of the gliadins, a sub-set of proteins in gluten, may also interfere with natural killer cell activation in peripheral blood (9). They tested the levels of natural killer cell activation in normal, and in treated celiacs, and found no significant difference. BUT, after 30 minutes exposure of the celiacs blood to gliadin, there was a reduced activation of natural killer cells. For the last hundred years, billions of dollars have been spent identifying carcinogens. Most of what we encounter in our environment appears to have some measure of carcinogenic potential. Unfortunately, we have failed to reconcile that Humanity has been exposed to most of these carcinogens throughout its evolution. Conventional wisdom has pointed to the increasing levels of chemical pollution and environmental damage. And I do not doubt that these factors are contributing to the current epidemic of malignancy. What I do doubt is that segment of the population, variously reported at 20% to 30%, which has the HLA factors which predispose to celiac disease and many other autoimmune diseases, can mount an adequate immune response, with natural killer cells, against malignancy. References: Hoggan R, Considering Wheat, Rye, and Barley Proteins as Aids to Carcinogens in press Medical Hypotheses, 1997. Tanchou S, Statistics of Cancer London Lancet 1843; Aug 5, 593. Audette R, personal communication. Reading C, Meillon R, Your Family Tree Connection, Keats; New Canaan, Conn.: 1988. Wink A, et. al. Disappearance of Mesenteric Lymphadenopathy with Gluten-Free Deit in Celiac Sprue, J. Clin. Gastroenterol, 1993; 16(4): 317-319. Wright DH, et. al. Celiac disease and Lymphoma, Lancet 1991; 337:1373. Wright DH, et. al. letter Lancet 1991; 338: 318-319. Donaldson SS, Effect of Nutrition as Related to Radiation and Chemotherapy, Nutrition and Cancer, Winick ed. 1977; Wiley & Sons, NewYork, 137153. Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H, Natural Killer Cell Activity in Celiac Disease: Effect of in Vitro Treatment on Effector Lymphocytes and/or Target Lymphoblastoid, Myeloid and Epithelial Cell Lines with Gliadin, Folia Microbial, 1995 (Praha) 40; 6: 615-620.
  16. TI- Disaccharidasen-Aktivitaten als Beurteilungskriterium der Dunndarmschleimhaut. AU- Stern M; Plettner C JN- Monatsschr Kinderheilkd; 131 (5) p264-8 PY- May 1983 AB- Activities of lactase, sucrase, and maltase were determined in small intestinal biopsies of 125 children with Coeliac disease, cows milk protein intolerance, transient gluten intolerance, nonspecific enteropathies, and controls. Four cases of primary disaccharidase deficiencies could be identified. In the enteropathies, morphometric data were more closely correlated to the degree of the mucosal lesion (r = -0.92 for crypt depth) than were disaccharidase activities (r = 0.61 for lactase). In a stepwise discriminate analysis of the patient groups, based upon immunological, morphometric, and biochemical variables, lactase activity was a valuable secondary criterion, ranking third among the variables used.
  17. TI- Proba prowokacyjna u dzieci z nietolerancja biaLek mleka krowiego i glutenu: ocena reakcji klinicznych i zmian w bLonie sluzowej jelita cienkiego. AU- Kaczmarski M CS- Kliniki Chorob Zakaznych Dzieci AM w BiaLymstoku. JN- Pol Tyg Lek; 45 (8-9) p161-5 PY- Feb 19-26 1990 AB- Provocation test (re-introduction of the noxious protein) was carried out in two groups of patients: (a) with intolerance to the cow-milk proteins (41 children) treated with milk-free diet for 6-24 months, and ( with gluten intolerance (26 children) treated with gluten-free diet for 6-36 months. The following parameters were compared: type and frequency of the clinical symptoms seen in these patients prior to the introduction of allergen-free diet. Moreover, the type of observed morphological changes in the small intestine mucosa following provocation test were analyzed in the groups of 7 patients. A two-year elimination of milk from the diet produces milk tolerance in about 61% patients; clinical symptoms in the remaining children are diversified. Re-introduction of gluten with the diet (provocation test) produces recurrence of gluten intolerance in 96% of children treated with gluten-free diet for 2-3 years. Recurrence of the disease was accompanied by the atrophy of the intestinal villi.
  18. AU- Kaczmarski M; Lisiecka M; Kurpatkowska B; Jastrzebska J JN- Acta Med Pol; 30 (3-4) p129-39 PY- 1989 AB- Quantitative estimation of the infiltration by intraepithelial lymphocytes and eosinophils of the mucosa was carried out in 21 children with cows milk and 35 children with gluten intolerance. Before dietary treatment, a statistically significant increase in the infiltration by LIE in children with milk intolerance to the mean value of 34.1 cells and in children with gluten intolerance to 39.0 cells was found, what statistically significantly differed from the mean value of LIE for the control group (19.0 cells/100 epithelial cells). The eosinophilic infiltration in this phase of the disease was noted in 38% of children with cows milk intolerance (16.9 cells/mm2) and in 27% of children with gluten intolerance (28.6 cells/mm2). After 8-24 months of elimination diets--a decrease in the mean value of the LIE infiltration in the mucosa was revealed in both treated groups.
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