Jump to content
Frequently Asked Questions About Celiac Disease Read more... ×
  • Sign Up

Search the Community

Showing results for tags 'cases'.



More search options

  • Search By Tags

    Type tags separated by commas.
  • Search By Author

Content Type


Forums

  • Diagnosis & Recovery, Related Disorders & Research
    • Calendar of Events
    • Celiac Disease Pre-Diagnosis, Testing & Symptoms
    • Post Diagnosis, Recovery & Treatment of Celiac Disease
    • Related Disorders & Celiac Research
    • Dermatitis Herpetiformis
    • Gluten Sensitivity and Behavior
  • Support & Help
    • Coping with Celiac Disease
    • Parents' Corner
    • Gab/Chat Room
    • Doctors Treating Celiac Disease
    • Teenagers & Young Adults Only
    • Pregnancy
    • Friends and Loved Ones of Celiacs
    • Meeting Room
    • Celiac Disease & Sleep
    • Celiac Support Groups
  • Gluten-Free Lifestyle
    • Gluten-Free Foods, Products, Shopping & Medications
    • Gluten-Free Recipes & Cooking Tips
    • Gluten-Free Restaurants
    • Ingredients & Food Labeling Issues
    • Publications & Publicity
    • Traveling with Celiac Disease
    • Weight Issues & Celiac Disease
    • International Room (Outside USA)
    • Sports and Fitness
  • When A Gluten-Free Diet Just Isn't Enough
    • Food Intolerance & Leaky Gut
    • Super Sensitive People
    • Alternative Diets
  • Forum Technical Assistance
    • Board/Forum Technical Help
  • DFW/Central Texas Celiacs's Events
  • DFW/Central Texas Celiacs's Groups/Organizations in the DFW area

Blogs

There are no results to display.

There are no results to display.

Categories

  • Celiac.com Sponsors
  • Celiac Disease
  • Safe Gluten-Free Food List / Unsafe Foods & Ingredients
  • Gluten-Free Food & Product Reviews
  • Gluten-Free Recipes
    • American & International Foods
    • Gluten-Free Recipes: Biscuits, Rolls & Buns
    • Gluten-Free Recipes: Noodles & Dumplings
    • Gluten-Free Dessert Recipes: Pastries, Cakes, Cookies, etc.
    • Gluten-Free Bread Recipes
    • Gluten-Free Flour Mixes
    • Gluten-Free Kids Recipes
    • Gluten-Free Recipes: Snacks & Appetizers
    • Gluten-Free Muffin Recipes
    • Gluten-Free Pancake Recipes
    • Gluten-Free Pizza Recipes
    • Gluten-Free Recipes: Soups, Sauces, Dressings & Chowders
    • Gluten-Free Recipes: Cooking Tips
    • Gluten-Free Scone Recipes
    • Gluten-Free Waffle Recipes
  • Celiac Disease Diagnosis, Testing & Treatment
  • Miscellaneous Information on Celiac Disease
    • Additional Celiac Disease Concerns
    • Celiac Disease Research Projects, Fundraising, Epidemiology, Etc.
    • Conferences, Publicity, Pregnancy, Church, Bread Machines, Distillation & Beer
    • Gluten-Free Diet, Celiac Disease & Codex Alimentarius Wheat Starch
    • Gluten-Free Food Ingredient Labeling Regulations
    • Celiac.com Podcast Edition
  • Celiac Disease & Gluten Intolerance Research
  • Celiac Disease & Related Diseases and Disorders
    • Lists of Diseases and Disorders Associated with Celiac Disease
    • Addison's Disease and Celiac Disease
    • Anemia and Celiac Disease
    • Anorexia Nervosa, Bulimia and Celiac Disease
    • Arthritis and Celiac Disease
    • Asthma and Celiac Disease
    • Ataxia, Nerve Disease, Neuropathy, Brain Damage and Celiac Disease
    • Attention Deficit Disorder and Celiac Disease
    • Autism and Celiac Disease
    • Bacterial Overgrowth and Celiac Disease
    • Cancer, Lymphoma and Celiac Disease
    • Candida Albicans and Celiac Disease
    • Canker Sores (Aphthous Stomatitis) & Celiac Disease
    • Casein / Cows Milk Intolerance and Celiac Disease
    • Chronic Fatigue Syndrome and Celiac Disease
    • Cognitive Impairment and Celiac Disease
    • Crohn's Disease and Celiac Disease
    • Depression and Celiac Disease
    • Dermatitis Herpetiformis: Skin Condition Associated with Celiac Disease
    • Diabetes and Celiac Disease
    • Down Syndrome and Celiac Disease
    • Dyspepsia, Acid Reflux and Celiac Disease
    • Epilepsy and Celiac Disease
    • Eye Problems, Cataract and Celiac Disease
    • Fertility, Pregnancy, Miscarriage and Celiac Disease
    • Fibromyalgia and Celiac Disease
    • Flatulence (Gas) and Celiac Disease
    • Gall Bladder Disease and Celiac Disease
    • Gastrointestinal Bleeding and Celiac Disease
    • Geographic Tongue (Glossitis) and Celiac Disease
    • Growth Hormone Deficiency and Celiac Disease
    • Heart Failure and Celiac Disease
    • Infertility, Impotency and Celiac Disease
    • Inflammatory Bowel Disease and Celiac Disease
    • Intestinal Permeability and Celiac Disease
    • Irritable Bowel Syndrome and Celiac Disease
    • Kidney Disease and Celiac Disease
    • Liver Disease and Celiac Disease
    • Lupus and Celiac Disease
    • Malnutrition, Body Mass Index and Celiac Disease
    • Migraine Headaches and Celiac Disease
    • Multiple Sclerosis and Celiac Disease
    • Myasthenia Gravis Celiac Disease
    • Obesity, Overweight & Celiac Disease
    • Osteoporosis, Osteomalacia, Bone Density and Celiac Disease
    • Psoriasis and Celiac Disease
    • Refractory Celiac Disease & Collagenous Sprue
    • Sarcoidosis and Celiac Disease
    • Scleroderma and Celiac Disease
    • Schizophrenia / Mental Problems and Celiac Disease
    • Sepsis and Celiac Disease
    • Sjogrens Syndrome and Celiac Disease
    • Skin Problems and Celiac Disease
    • Sleep Disorders and Celiac Disease
    • Thrombocytopenic Purpura and Celiac Disease
    • Thyroid & Pancreatic Disorders and Celiac Disease
    • Tuberculosis and Celiac Disease
  • The Origins of Celiac Disease
  • Gluten-Free Grains and Flours
  • Oats and Celiac Disease: Are They Gluten-Free?
  • Frequently Asked Questions
  • Journal of Gluten Sensitivity
    • Autumn 2018 Issue
    • Summer 2018 Issue
    • Spring 2018 Issue
    • Winter 2018 Issue
    • Autumn 2017 Issue
    • Summer 2017 Issue
    • Spring 2017 Issue
    • Winter 2017 Issue
    • Autumn 2016 Issue
    • Summer 2016 Issue
    • Spring 2016 Issue
    • Winter 2016 Issue
    • Autumn 2015 Issue
    • Summer 2015 Issue
    • Spring 2015 Issue
    • Winter 2015 Issue
    • Autumn 2014 Issue
    • Summer 2014 Issue
    • Spring 2014 Issue
    • Winter 2014 Issue
    • Autumn 2013 Issue
    • Summer 2013 Issue
    • Spring 2013 Issue
    • Winter 2013 Issue
    • Autumn 2012 Issue
    • Summer 2012 Issue
    • Spring 2012 Issue
    • Winter 2012 Issue
    • Autumn 2011 Issue
    • Summer 2011 Issue
    • Spring 2006 Issue
    • Summer 2005 Issue
  • Celiac Disease Support Groups
    • United States of America: Celiac Disease Support Groups and Organizations
    • Outside the USA: Celiac Disease Support Groups and Contacts
  • Celiac Disease Doctor Listing
  • Kids and Celiac Disease
  • Gluten-Free Travel
  • Gluten-Free Cooking
  • Gluten-Free
  • Allergy vs. Intolerance
  • Tax Deductions for Gluten-Free Food
  • Gluten-Free Newsletters & Magazines
  • Gluten-Free & Celiac Disease Links
  • History of Celiac.com
    • History of Celiac.com Updates Through October 2007
    • Your E-mail in Support of Celiac.com 1996 to 2006

Find results in...

Find results that contain...


Date Created

  • Start

    End


Last Updated

  • Start

    End


Filter by number of...

Joined

  • Start

    End


Group


AIM


MSN


Website URL


ICQ


Yahoo


Jabber


Skype


Interests


Location

Found 18 results

  1. Celiac.com 10/20/2017 - Are doctors even getting close to diagnosing the actual number of cases of celiac disease? Or are they missing the vast majority? Researchers have said for some time that there are far more people with celiac disease than are being diagnosed, and that the vast majority of cases go undiagnosed. So, just how far are we from the actual number? Well, if a new study by Canadian nutrition researchers is any indication, doctors are very far from diagnosing most cases. The team studied the blood work of nearly 3,000 people, and their conclusions are stunning. They say that ninety percent of celiac cases go undiagnosed. How could this be? One reason is that even classic celiac disease symptom, such as abdominal pain, bloating, gas, diarrhea, anemia and weight loss can mimic other conditions. Less classic symptoms such as fatigue, low vitamin C, D and calcium levels can be misleading. Ahmed El-Sohemy, a professor of nutritional science at the University of Toronto, wanted to see whether celiac disease results in subpar nutrition because of poorer absorption of vitamins and minerals. But to find out, he needed Canadian data on the frequency of undiagnosed celiac disease. To that end, El-Sohemy and his colleagues checked blood samples from more than 2,800 individuals in Toronto. One group had an average age of 23, and the other 45. Among their findings is likely ~1%, with 87% of cases being undiagnosed. These findings suggest the need for better screening in high genetic risk groups. Source: BMJOPEN.com
  2. Celiac.com 10/17/2017 - Are primary care physicians under-testing for celiac disease in patients with iron deficiency anemia? A new survey of primary care doctors indicates that they are. It's fairly common for people with celiac disease to develop iron deficiency anemia (IDA), but researchers don't know much about the frequency with which primary care physicians test for celiac disease in patients with IDA. A team of researchers recently set out to describe how primary care doctors approach testing for celiac disease in asymptomatic patients with IDA. The research team included Marisa Spencer, Adrienne Lenhart, Jason Baker, Joseph Dickens, Arlene Weissman, Andrew J. Read, Seema Saini, and Sameer D. Saini. They are variously affiliated with the Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America; the Department of Internal Medicine, Henry Ford Health System, in Detroit, Michigan, United States of America; the Department of Statistics, University of Michigan, Ann Arbor, Michigan, United States of America; the Research Center at the American College of Physicians, in Philadelphia, Pennsylvania, United States of America; Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America, Ambulatory Care, Veterans Affairs Medical Center, Ann Arbor, Michigan, United States of America. For their study, the team began by electronically distributing a survey to primary care doctors who are members of the American College of Physicians. The survey asked whether doctors would test for celiac disease, either by serologic testing, referral for esophagogastroduodenoscopy [EGD], or referral to GI) in hypothetical patients with new IDA, including: (1) a young Caucasian man, (2) a premenopausal Caucasian woman, (3) an elderly Caucasian man, and (4) a young African American man. The team chose the scenarios to assess differences in testing for celiac disease based on age, gender, and race. They used multivariable logistic regression to identify independent predictors of testing. Testing for celiac disease varied significantly according to patient characteristics, with young Caucasian men being the most frequently tested (61% of respondents reporting they would perform serologic testing in this subgroup (p Interestingly 80% of doctors surveyed said they would definitely or probably start a patient with positive serologies for celiac disease on a gluten-free diet prior to confirmatory upper endoscopy, which is contrary to guideline recommendations. This survey indicates that primary care doctors are under-testing for celiac disease in patients with IDA, regardless of age, gender, race, or post-menopausal status. The majority of primary care doctors surveyed do not strictly adhere to established guidelines regarding a confirmatory duodenal biopsy in a patient with positive serology for celiac disease. Clearly, even with all of the advances in celiac disease awareness and with more refined protocols, primary care doctors have some work to do when it comes to testing IDA patients for celiac disease, and even more work to do in following proper referral guidelines before putting patients on a gluten-free diet. Source: PLOSONE
  3. Celiac.com 01/16/2017 - Cerebellar ataxias can be caused by a wide range of disease processes, either genetic or acquired. Establishing a clear diagnosis requires a methodical approach with expert clinical evaluation and investigation. A team of researchers recently published a description of the causes of ataxia in 1500 patients with cerebellar ataxia. The research team included M Hadjivassiliou, J Martindale, P Shanmugarajah, R A Grünewald, P G Sarrigiannis, N Beauchamp, K Garrard, R Warburton, D S Sanders, D Friend, S Duty, J Taylor, and N Hoggard. They are variously affiliated with the Academic Department of Neurosciences, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK; Sheffield Diagnostic Genetics Service, Sheffield Children's NHS Foundation Trust, Sheffield, UK; the Department of Gastroenterology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK; and the Department of Neuroradiology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK. All patients in the study were referred to the Sheffield Ataxia Centre, UK, and underwent extensive examination, including, where appropriate genetic testing using next-generation sequencing (NGS). The team followed-up patients on a 6-month basis for reassessment and further investigations, as needed. The team assessed a total of 1500 patients over 20 years. Twenty per cent of those patients had a family history of ataxia, with the remaining having sporadic ataxia. The most common cause of sporadic ataxia was gluten ataxia at 25%. They found a genetic cause in 156, or 13% of sporadic cases, with alcohol excess causing 12% and a cerebellar variant of multiple system atrophy causing 11% of sporadic cases. Using NGS, they obtained positive results in 32% of 146 patients tested. The most common ataxia they found was EA2. A total of 57% of all familial ataxias were supported by genetic diagnosis. The most common genetic ataxias were Friedreich's ataxia (22%), SCA6 (14%), EA2 (13%), SPG7 (10%) and mitochondrial disease (10%). The diagnostic yield following attendance at the Sheffield Ataxia Centre was 63%. Immune-mediated ataxias are common. Advances in genetic testing have significantly improved the diagnostic yield of patients suspected of having a genetic ataxia. Making a diagnosis of the cause of ataxia is essential due to potential therapeutic interventions for immune and some genetic ataxias. Gluten is a culprit is 25% of sporadic ataxia cases, and clinicians should keep this in mind when diagnosing patients, as many of these cases can be reversed with a gluten-free diet. Source: J Neurol Neurosurg Psychiatry. doi:10.1136/jnnp-2016-314863
  4. Celiac.com 05/19/2016 - Using a prospective cohort study, a team of researchers recently set out to assess the outcomes of the latest celiac diagnosis guidelines from the European Society of Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) and British Society of Paediatric Gastroenterology, Hepatology and Nutrition (BSPGHAN). The research team included Elisa Benelli, Valentina Carrato, Stefano Martelossi, Luca Ronfani, Tarcisio Not, and Alessandro Ventura. They are variously affiliated with the Department of Medical, Surgical and Health Sciences, University of Trieste in Trieste, Italy, and the Institute for Maternal and Child Health IRCCS 'Burlo Garofolo' in Trieste, Italy. The study was conducted at the Institute for Maternal and Child Health IRCCS Burlo Garofolo in Trieste, Italy. For the study, the team prospectively enrolled children diagnosed with celiac disease without a duodenal biopsy (group 1), following the last ESPGHAN and BSPGHAN guidelines, and children diagnosed with a duodenal biopsy, matched for sex, age and year of diagnosis (group 2). All of this was done over a 3-year period. The team made sure all patients were on a gluten-free diet (gluten-free diet) and then followed them for clinical conditions and laboratory testing at 6 months every year since diagnosis. The average follow up period was just under two years. Their analysis looked at resolution of symptoms, body mass index, levels of hemoglobin and anti-transglutaminase IgA, adherence to a gluten-free diet, quality of life, and supplementary post-diagnosis medical consultations. Out of 468 patients, the team found 51 patients (11%) who were diagnosed without a duodenal biopsy (group 1; median age 2.1 years), and matched those patients to 92 patients diagnosed with a biopsy (group 2; median age 2.4 years). At the end of follow-up the two groups showed statistically comparable clinical and nutritional status, anti-transglutaminase IgA antibody levels, quality of life, adherence to a gluten-free diet, and number of supplementary medical consultations. This study indicates that celiac disease can be reliably diagnosed without a duodenal biopsy in approximately 11% of cases. At least during a medium-term follow-up, this approach has no negative consequences relating to clinical remission, adherence to diet, and quality of life of children with celiac disease. Source: Arch Dis Child 2016;101:172-176. doi:10.1136/archdischild-2015-309259
  5. Celiac.com 01/11/2016 - Is celiac disease a disability under the federal Americans with Disabilities Act? The Department of Justice says not necessarily. On the heels of a federal lawsuit that claiming that restaurants are violating federal disability laws by charging more for gluten-free food than for non-gluten-free counter parts, a Department of Justice spokesperson has stated that a 2012 civil rights settlement on behalf of Lesley University students with celiac disease does not make the condition a disability in all cases. DOJ public affairs specialist, Patrick Rodenbush, said settlement at Leslie University did not set a legal precedent, because the "…settlement enforces the rights of students whose food allergies were disabilities, [but] it doesn't necessarily make celiac disease a disability in all cases." This is relevant to a case in California, where federal judge recently denied a motion to dismiss a class action lawsuit alleging P.F. Chang's violates the Americans with Disabilities Act because it charges more for gluten-free items. In the P.F. Chang's case, Judge Ronald Whyte denied P.F. Chang's motion to dismiss because, he wrote, that, although the court had not found specific information proving that celiac disease constituted a disability under the ADA, the "plaintiff has pled sufficient facts to support her claim that she has a disability that impacts a major life activity." Whyte noted "on a more complete factual record, the court might reach a different conclusion." He also stated that it may be difficult, or impossible for Phillips to prove her claims. "The ultimate question is whether P.F. Chang's, in providing gluten-free meals, is providing different products or whether the price differential with regular meals is a pretext for discrimination against those with celiac disease," Whyte wrote. At stake is whether or not food vendors, such as P.F. Chang's can charge higher prices for gluten-free foods than they do for non-gluten-free items. The results of this case are being watched closely by celiacs and by restaurant companies, because a ruling that establishes that people with celiac disease are covered under the federal Americans with Disabilities Act could conceivably have a serious impact on how the restaurant industry approaches gluten-free food. Stay tuned for new developments. Source: legalnewsline.com
  6. Celiac.com 04/26/2016 - Vice President Dan Quayle famously stated: "what a waste it is to lose one's mind, or not to have a mind is being very wasteful, how true that is," when speaking to people involved in the United Negro College Fund (1). While it is entertaining to read and ponder, this statement evokes some ideas I have about senility, which is increasing, along with many other modern diseases, at a frightening speed. The prospect of losing my mind, my memory, my sense of connection with friends and loved-ones, and even my sense of identity and personal hygiene is a frightening spectre. Can you separate your memories and experiences, along with what you think and feel, from who you are? I can't. I'm not sure I would want to be able to do so. My identity is tied to my memories, experiences, and how I responded and continue to respond to them. I remember looking at my son's tiny hands and feet when we first brought him home from the hospital. My daughter, born prematurely, had even smaller digits. They seemed impossibly tiny yet they were all perfectly formed and quite beautiful. It seemed miraculous to me. It still does. I can't imagine anything that I'd be willing to accept in exchange for those memories. Neither would I willingly surrender my memory of the joy I felt at my first convocation or my first car. Yet those lost memories form the prison in which many people already find themselves. It appears that many more will follow. One segment of this problem, the epidemic of Alzheimer's disease (AD), already effects 5.4 million Americans and 30 million people throughout the world (2). Parkinson's disease, which is a neurological ailment that, in its later stages is often accompanied by dementia, is a similar ailment that is rapidly increasing both in absolute numbers and as a percentage of the population (3). Vascular dementia is yet another condition in which brain mass and mental acuity wane with advancing years (4). Perhaps this trend is partly due to the large number of aging baby boomers from the World War II era. But the relevant research suggests otherwise. Although we may be living longer and that may contribute to a small part of the growth of these devastating ailments, the biggest contributors appear to be lifestyle choices that include low daily activity levels, consumption of highly glycemic and inflammation-promoting refined carbohydrates and grain products, inadequate sleep duration, and exposure to toxic substances. As most students of celiac disease have long been aware, there is a powerful and potentially devastating component of brain and neurological damage associated with this ailment as a result of gluten grain consumption. In addition to the behavioral changes identified by Gibbons in 1889 (5), attention deficits identified by Reichelt (6), Neiderhofer (7, 8), and others (9 - 11), subsequent reports have connected increased incidence of seizure disorders(12-17), reductions of brain size (17 -20), a variety of neurological movement disorders (21 -23), a range of mood disorders (24, 25), and several psychiatric ailments (26, 27) including schizophrenia (28, 29), and signs of learning disabilities have been reported to improve quite dramatically and quickly on a gluten-free diet (30). Sleep disorders are also common among people with celiac disease (31). With emerging research into non-celiac gluten sensitivity over the last two decades, we have also begun to see evidence of similar connections between gluten consumption and most of these neurological/brain ailments. This added dimension of non celiac gluten sensitivity and its impact on human neurological health, were previously obscure and, in the case of amyotrophic lateral sclerosis (ALS) (26, 32), was thought to be rapidly deadly and incurable (33). Most recently, Bredesen reported that the gluten-free diet, or a low grain diet, forms one significant part of their multi-modal protocol for reversing several dementias among a small group of those who experienced recent symptom onset, including Alzheimer's disease, objectively identified disruptions in memory function or subjective, self-reported symptoms of dementia (2). Of the ten subjects studied in this latter investigation, nine showed substantial recovery in the form of symptom reversal along with either a return to work or improved performance at work (2). Harnessing the gluten-free diet makes sense, of course, because of the many neurological dimensions of gluten's harmful impact on human neurological tissues. Over the last 20 years, Dr. Marios Hadjivassiliou and colleagues, at the University of Sheffield and the Royal Hallamshire Hospital, have been reporting a wide range of neurological ailments in association with elevated anti-gliadin antibodies ( both with and without celiac disease) afflicting a large portion of their patients with neurological diseases of unknown origin (34 -37). Further, Dr. Joe Murray and colleagues have also reported on a group of thirteen patients experiencing moderate cognitive decline, three of whom experienced stabilized or improved cognitive function on a gluten-free diet alone (38). However, the protocol reported by Bredesen is aimed at correcting a greater number and broader spectrum of converging metabolic processes that are shaped, in large part, by our modern lifestyle, and are increasingly thought to be at the root of the current epidemic of dementias, including Alzheimer's disease (2). Gluten is only an important part of the overall picture. Dr. Suzanne de la Monte and colleagues have also identified a dynamic which they call type 3 diabetes at work in the brains of many patients with Alzheimer's disease (39). Insulin resistance, in the brain and elsewhere, is also a multi-factorial condition (40) which mostly involves disrupted metabolic processes, either through depletion of insulin production or, more likely, increased cellular resistance to insulin's movement of glucose into the cell. Dr. Dale Bredesen has argued that "in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one" (2) This is the rationale that underlies his enormously broad therapeutic approach employed in his protocol. Please consider each of the following facets of Bredesen's therapeutic protocol: 1. Serum testing was conducted and subsequent supplement recommendations were made, aimed at improving vitamin, mineral, amino acid, and herb supplements to achieve optimal values. All of the foregoing is aimed at harnessing their putative anti-oxidant function, supporting various facets of metabolism, and making use of their reported anti-inflammatory properties. Chelation therapy was also used to correct heavy metal (mercury, lead, cadmium) toxicity. Non-farmed fish, vegetables, and fruits were emphasized, while meat consumption was either discouraged or patients were encouraged to eat only organic and free range meat. 2. Patients were given their choice of several low glycemic, low inflammatory, low grain diets. By this description, such a diet would exclude or severely limit gluten consumption. 3. Patients were encouraged to engage daily in strategies, including meditation and listening to music, toward reducing their stress levels, which would reduce their cortisol production. Cortisol is a hormone that triggers increased release of glucose into the bloodstream, suppresses the immune system, and inhibits bone formation. In addition to excluding or treating sleep apnea, patients were prescribed melatonin at 0.5 mg daily, toward achieving at least eight hours of sleep each night, thereby reducing production of hunger-inducing ghrelin hormones in the stomach and increasing hunger-suppressing leptin hormones which are produced in the fat cells. Each carries its message to the brain. Reductions in cortisol and ghrelin secretion in combination with increasing leptin production would have a net effect of reducing inflammation while aiding weight loss and reducing blood glucose levels to normal fasting levels and targeting reduction of hemoglobin A1c levels to below 5.5, further reducing inflammation. Optimum levels of thyroid hormones, along with progesterone and pregnenolone were also pursued, along with reductions of free homocysteine to below 7 mg/L by prescription of vitamin B6, B12, and folic acid supplements, to reduce vascular damage and blockage that can be caused by elevated free homocysteine levels. Twice daily dietary supplementation with medium chain triglycerides (MCTs) also provides strategy for altering hormone production aimed at improved cognitive function. In humans, medium chain fatty acids resist storage. They must either be converted to ketone bodies in the liver, or rapidly utilized for energy. Because MCTs can induce the liver to increase ketone production, it provides an alternative energy source for many of the brain's cells, without requiring insulin to usher these ketones into the cells, as glucose does. In essence, adequate ketone production provides an alternative fuel both for many brain and other cells throughout the body. The liver mostly produces the ketone called beta-hydroxybutyrate. This acts not only as a fuel source, but is also a powerful anti-oxidant that does not require insulin to enter the cell, unlike vitamin C, which does require insulin to enter cells. 4. To further promote these values and other facets of wellness arising out of regular activity, patients were asked to exercise for 30 to 60 minutes per day, 4 to 6 days each week. Each and all of the above have been reported somewhere in the literature as valid and valuable as part of reversing dementias, which Bredesen's list of citations supports (2). However, while significant improvements in the dementia symptoms of nine of the ten subjects does argue for the validity of this protocol, wholesale acceptance of all of the concepts here would fail to narrow our focus on those factors that are most likely to contribute to causing the vast majority of the various dementias that are contributing to the emerging epidemic. Bredesen also acknowledges that study participants were encouraged to follow as many instructions as they could. They were not asked or expected to be fully compliant with the instructions they were given. Nonetheless, I would probably err on the side of caution, by implementing as many of these strategies as possible, were I dealing with a loved-one who struggled with dementia. Conversely, I would be most reluctant to accept the interdiction of meats, organic or otherwise. On the other hand, growth promotion using low doses of anti-biotics can result in delivering anti-biotic resistant microbes. Poultry, hogs, and cattle are all high risk meats. Further, grains, especially gluten grains and corn, combine to form the mainstay of feeds used to fatten these animals and birds for market, where weight is the determining factor in the price paid for these meats. Bredesen also pointed, quite rightly, to the small number of subjects as a weakness in his study. However, when 9 of their 10 subjects achieved such remarkable results, especially in the context of the common belief that dementia, at any stage, is irreversible, this study certainly suggests that exploring dementias as a group of metabolic illnesses is a potentially fruitful path. This is a perspective that is enjoying considerable support from a variety of sources. Many researchers have, for the past decade or so, thought of many dementias as type 3 diabetes, with a growing body of support for this perspective amassing in the peer reviewed literature (41). More recently, chronic sleep deprivation has been similarly implicated in several ways. The first is specific to Alzheimer's disease, where beta amyloid deposits or plaques characterize this ailment. New research has shown that during sleep, brain tissues shrink, while the fluids that surround the brain permeate these tissues and inter-cellular structures, assimilating amyloid, which is a group of protein fragments (peptides) that are waste products of daytime brain cell activities (42). Because there is no lymphatic system in the brain, it has long been believed that the brain did not dispose of its waste products. However, another field of brain research has shown that conduits of these fluids form surrounding the blood vessels, carrying waste products into the bloodstream and, ultimately, out of the brain for disposal (42). Since average nightly sleep duration has shortened from nine hours to seven hours, given the above research findings, this reduction in sleep decreases our nightly capacity to remove waste amyloid and other detritus, leading to the formation and growth of amyloid deposits, which characterize at least one form of dementia. This same culture-wide sleep deprivation also induces memory disturbances and memory losses. It does so by a circuitous route. Throughout the day, each of us encodes memories through our hippocampus, a small region of the brain that is also involved in spatial navigation and contributes, with other parts of the lymbic system, to the regulation of many body functions. During sleep, the day's memories are thought to be processed and integrated with prior knowledge, emotions, and impressions in the neo-cortex. Some researchers are now postulating that this integration process is what results in our dreams (43-45). Regardless of whether it is the author of our dreams, Dr. Robert Stickgold and colleagues have shown that sleep helps us to consolidate the day's learning experiences, thus improving our memory retention. He has also shown that inadequate sleep compromises learning (43). The net result is that we not only need sleep to permit the brain to clean out the day's wastes, we also need it to form and preserve learning. Although Bredesen made no mention of it, there is another complicating factor here. Statin drugs are aimed at reducing cholesterol. However, they have also been shown to induce memory problems. One friend of mine was prescribed a statin drug, and he stopped being able to recognize me. After discontinuing this medication, he told me that I looked familiar, but he couldn't even guess at my name or where he knew me from. He waves hello to me from across the street, but doesn't cross it to visit anymore. And that seems to be where the recovery of his memory is stalled. It is with heart-rending sadness that I occasionally see him in passing. I say hello. But if he doesn't notice me waving or hear me shouting, there isn't even an exchange of greetings. He seems happy enough. So perhaps the loss is mostly mine. But I don't imagine that he would willingly have chosen this "new" world of his. Sources: 1. https://en.wikiquote.org/wiki/Dan_Quayle 2. Bredesen DE. Reversal of cognitive decline: a novel therapeutic program. Aging (Albany NY). 2014 Sep;6(9):707-17. 3. Moustafa AA, Chakravarthy S, Phillips JR, Crouse JJ, Gupta A, Frank MJ, Hall JM, Jahanshahi M. Interrelations between cognitive dysfunction and motor symptoms of Parkinson's disease: behavioral and neural studies. Rev Neurosci. 2016 Mar 16. 4. Dey AK, Stamenova V, Turner G, Black SE, Levine B. Pathoconnectomics of cognitive impairment in small vessel disease: A systematic review. Alzheimers Dement. 2016 Feb 25. 5. Gibbons, R. (1889). The Coeliac Affection in Children. Edinburgh Medical Journal. xxxv(iv), 321-330. 6. Ziegler, A., Nødland, M., Tveiten, D. and Reichelt, K.L. (2016) The AD/HD Syndrome as a Group of Biological Disorders. Open Journal of Pediatrics, 6, 22-28. http://dx.doi.org/10.4236/ojped.2016.61005 7. Niederhofer H. Association of attention-deficit/hyperactivity disorder and celiac disease: a brief report. Prim Care Companion CNS Disord. 2011;13(3). pii 8. Niederhofer H, Pittschieler K. A preliminary investigation of ADHD symptoms in persons with celiac disease. J Atten Disord. 2006 Nov;10(2):200-4. 9. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6. 10. Welch E, Ghaderi A, Swenne I. A comparison of clinical characteristics between adolescent males and females with eating disorders. BMC Psychiatry. 2015 Mar 11;15:45. 11. KozÅ‚owska ZE. [Evaluation of mental status of children with malabsorption syndrome after long-term treatment with gluten-free diet (preliminary report)]. Psychiatr Pol. 1991 Mar-Apr;25(2):130-4. Polish. (based on amateur translation) 12. Parisi P, Principessa L, Ferretti A, D'Onofrio D, Del Giudice E, Pacchiarotti C, Villa MP. "EEG abnormalities" may represent a confounding factor in celiac disease: A 4-year follow-up family report. Epilepsy Behav Case Rep. 2014 Mar15;2:40-2. 13. Korkmaz HA, Dizdarer C, Ecevit CO. Hypocalcemic seizure in an adolescent with Down syndrome: a manifestation of unrecognized celiac disease. Turk J Pediatr. 2013 Sep-Oct;55(5):536-8. 14. Devinsky O, Schein A, Najjar S. Epilepsy associated with systemic autoimmune disorders. Epilepsy Curr. 2013 Mar;13(2):62-8. 15. Vincent A, Crino PB. Systemic and neurologic autoimmune disorders associated with seizures or epilepsy. Epilepsia. 2011 May;52 Suppl 3:12-7. 16. Das G, Baglioni P. Coeliac disease: does it always present with gastrointestinal symptoms? QJM. 2010 Dec;103(12):999-1000. 17. Peltola M, Kaukinen K, Dastidar P, Haimila K, Partanen J, Haapala AM, Mäki M, Keränen T, Peltola J. Hippocampal sclerosis in refractory temporal lobe epilepsy is associated with gluten sensitivity. J Neurol Neurosurg Psychiatry. 2009 Jun;80(6):626-30. 18. Currie S, Hadjivassiliou M, Clark MJ, Sanders DS, Wilkinson ID, Griffiths PD, Hoggard N. Should we be 'nervous' about coeliac disease? Brain abnormalities in patients with coeliac disease referred for neurological opinion. J Neurol Neurosurg Psychiatry. 2012 Dec;83(12):1216-21. 19. Ryan AM, Ryan J, Wan-Ahmed M, Hardiman O, Farrell MA, McNamara B, Sweeney BJ. Vacuolar leucoencephalopathy and pulvinar sign in association with coeliac disease. BMJ Case Rep. 2009;2009. pii: bcr08.2008.0650. 20. Kieslich M, Errázuriz G, Posselt HG, Moeller-Hartmann W, Zanella F, Boehles H. Brain white-matter lesions in celiac disease: a prospective study of 75 diet-treated patients. Pediatrics. 2001 Aug;108(2):E21. 21. Caio G, De Giorgio R, Venturi A, Giancola F, Latorre R, Boschetti E, Serra M, Ruggeri E, Volta U. Clinical and immunological relevance of anti-neuronal antibodies in celiac disease with neurological manifestations. Gastroenterol Hepatol Bed Bench. 2015 Spring;8(2):146-52. 22. Finsterer J, Leutmezer F. Celiac disease with cerebral and peripheral nerve involvement mimicking multiple sclerosis. J Med Life. 2014 Sep 15;7(3):440-4. Epub 2014 Sep 25. 23. McKeon A, Lennon VA, Pittock SJ, Kryzer TJ, Murray J. The neurologic significance of celiac disease biomarkers. Neurology. 2014 Nov 11;83(20):1789-96. 24. Zingone F, Swift GL, Card TR, Sanders DS, Ludvigsson JF, Bai JC. Psychological morbidity of celiac disease: A review of the literature. United European Gastroenterol J. 2015 Apr;3(2):136-45. 25. Carta MG, Conti A, Lecca F, Sancassiani F, Cossu G, Carruxi R, Boccone A, Cadoni M, Pisanu A, Francesca Moro M, Demelia L. The Burden of Depressive and Bipolar Disorders in Celiac Disease. Clin Pract Epidemiol Ment Health. 2015 Dec 31;11:180-5. 26. Catassi C. Gluten Sensitivity. Ann Nutr Metab. 2015;67 Suppl 2:16-26. 27. Lionetti E, Leonardi S, Franzonello C, Mancardi M, Ruggieri M, Catassi C. Gluten Psychosis: Confirmation of a New Clinical Entity. Nutrients. 2015 Jul 8;7(7):5532-9 28. Porcelli B, Verdino V, Bossini L, Terzuoli L, Fagiolini A. Celiac and non-celiac gluten sensitivity: a review on the association with schizophrenia and mood disorders. Auto Immun Highlights. 2014 Oct 16;5(2):55-61. 29. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. 30. Blair A. Wheat-free diet gives food for thought. The Times (UK) June 12, 2004 http://www.timesonline.co.uk/tol/news/uk/article444290.ece 31. Zingone F, Siniscalchi M, Capone P, Tortora R, Andreozzi P, Capone E, Ciacci C. The quality of sleep in patients with coeliac disease. Aliment Pharmacol Ther. 2010 Oct;32(8):1031-6. 32. Brown KJ, Jewells V, Herfarth H, Castillo M. White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. AJNR Am J Neuroradiol. 2010 May;31(5):880-1. 33. Hoggan R. 34. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71. 35. Hadjivassiliou M, Rao DG, Grìnewald RA, Aeschlimann DP, Sarrigiannis PG, Hoggard N, Aeschlimann P, Mooney PD, Sanders DS. Neurological Dysfunction in Coeliac Disease and Non-Coeliac Gluten Sensitivity. Am J Gastroenterol. 2016 Feb 2. 36. Hadjivassiliou M, Duker AP, Sanders DS. Gluten-related neurologic dysfunction. Handb Clin Neurol. 2014;120:607-19. 37. Hadjivassiliou M, Rao DG, Wharton SB, Sanders DS, Grünewald RA, Davies-Jones AG. Sensory ganglionopathy due to gluten sensitivity. Neurology. 2010 Sep 14;75(11):1003-8. 38. Hu WT, Murray JA, Greenaway MC, Parisi JE, Josephs KA. Cognitive impairment and celiac disease. Arch Neurol. 2006 Oct;63(10):1440-6. 39. de la Monte SM. Brain insulin resistance and deficiency as therapeutic targets in Alzheimer's disease. Curr Alzheimer Res. 2012 Jan;9(1):35-66 40. de la Monte SM, Tong M. Brain metabolic dysfunction at the core of Alzheimer's disease. Biochem Pharmacol. 2014 Apr 15;88(4):548-59. 41. de la Monte SM. Type 3 diabetes is sporadic Alzheimer's disease: mini-review. Eur Neuropsychopharmacol. 2014 Dec;24(12):1954-60. 42. Nedergaard M, Goldman SA. Brain Drain. Scientific American. 2016 March; p. 44-49. 43. Stickgold R. Parsing the role of sleep in memory processing. Curr Opin Neurobiol. 2013 Oct;23(5):847-53. 44. Stickgold R. Early to bed: how sleep benefits children's memory. Trends Cogn Sci. 2013 Jun;17(6):261-2 45. Stickgold R, Walker MP. Sleep-dependent memory triage: evolving generalization through selective processing. Nat Neurosci. 2013 Feb;16(2):139-45. 46. Taheri S, Lin L, Austin D, Young T, Mignot E (2004) Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med 1(3): e62. Sleep deprivation raises ghrelin & lowers leptin production.
  7. Celiac.com 12/30/2013 - Irritable bowel syndrome (IBS) and fibromyalgia syndrome (FMS) often occur together, and research indicates that many people with IBS plus FMS (IBS/FMS) might actually suffer from undiagnosed celiac disease. To better understand the potential connection between the two, a team of researchers recently conducted an active case finding for celiac disease in two IBS cohorts, one constituted by IBS/FMS subjects and the other by people with isolated IBS. The research team included L. Rodrigo, I. Blanco, J. Bobes, F.J. de Serres. They are affiliated with the department of Gastroenterology at the Central University Hospital of Asturias (HUCA), Celestino Villamil in Oviedo in the Principality of Asturias, Spain. For their study, the team included 104 patients (89.4% females), fulfilling the 1990-ACR criteria for FMS and the Roma III criteria for IBS classification, along with 125 unrelated, age and sex matched IBS non-FMS patients. All patients underwent the following studies: hematological, coagulation and biochemistry test, serological and genetic markers for celiac disease (i.e., tissue-Transglutaminase-2, tTG-2, and major histocompatibility complex HLA-DQ2/DQ8); multiple gastric and duodenal biopsies; FMS tender points (TPs); fibromyalgia impact questionnaire (FIQ), health assessment questionnaire (HAQ), short form health survey (SF-36), and visual analogue scales (VAS) for tiredness and gastrointestinal complaints. Overall results showed that IBS/FMS patients scored much worse values in quality of life and VAS scales than those with isolated IBS (p These seven patients showed substantial improvement in digestion and symptoms once they adopted gluten-free diets. The findings of this screening indicate that a significant percentage of IBS/FMS patients actually have celiac disease. These patients can improve symptoms and possibly prevent long-term celiac-related complications with a strict lifelong gluten-free diet. Source: Arthritis Res Ther. 2013 Nov 27;15(6):R201.
  8. Celiac.com 09/15/2014 - Duodenal intraepithelial lymphocytosis (D-IEL) is an early marker for celiac disease, even though a majority of cases are due to non-celiac disease conditions. Researchers I. Aziz, T. Key, J.G. Goodwin, and D.S. Sanders wanted to identify the predictors of celiac disease in patients presenting with D-IEL. For their study, they reviewed 215 adults with D-IEL who had undergone prospective and systematic evaluation for celiac disease and other recognized associations. They confirmed celiac disease based on presence of HLA-DQ2 and/or DQ8, persistence or progression of D-IEL following a gluten challenge, and an improvement in symptoms with a gluten-free diet. To compare factors in celiac and non-celiac cases, and to determine their sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), the team used binary logistic regression models, adjusted for age and sex. They diagnosed celiac disease in 48 cases (22%) and non-celiac in 167 cases (78%). They found no statistical difference between the celiac and non-celiac group in terms of baseline demographics, anemia, hematinics, or clinical symptoms, such as diarrhea, weight loss, abdominal pain. Compared with their non-celiac counterparts, celiac patients were significantly more likely to have a positive family history of celiac disease (21% vs. 3.6%, OR 6.73; PPV 62.5%, NPV 81%, specificity 96.4%), positive HLA-DQ status (100% vs. 49.1%; PPV 36.4%, NPV 100%, specificity 50.9%), and presence of endomysial antibody (EMA) (48% vs. 0%; PPV 100%, NPV 87%, specificity 100%); all P≤0.001. A total of 29.2% celiac and 83.2% non-celiac cases showed normal tissue transglutaminase antibody (TTG) levels (OR 0.084, P<0.001; PPV 9.2%). Between the groups, there was no difference in the prevalence of TTG levels 1 to 2×upper limit of normal (29.2% celiac vs. 14.4% non-celiac; PPV 33% to 38%). However, TTG levels between 3 and 20×ULN were much more common in the celiac group (33.3% vs. 2.4%, PPV 66.6% to 89%), whereas a TTG>20×ULN was exclusive to celiac disease (8.3%, P<0.001, PPV 100%). For patients with D-IEL, only a positive EMA or TTG greater than 20×ULN at the outset can yield an immediate celiac diagnosis. On their own, factors such as gastrointestinal symptoms, family history, anemia, or other celiac serology results do not reliably distinguish celiac from non-celiac patients. Source: J Clin Gastroenterol. 2014 Jul 10.
  9. Celiac.com 10/24/2012 - Doctors can face challenges when attempting to diagnose celiac disease in patients who have already begun a gluten-free diet, and/or when the results of tests are inconsistent. To better understand this problem, a group of researchers set out to assess the benefits of an in vitro gliadin challenge. The research team included Raffaella Tortora, MD, Ilaria Russo, PhD, Giovanni D. De Palma, MD, Alessandro Luciani, PhD, Antonio Rispo, MD, Fabiana Zingone, MD, Paola Iovino, MD, Pietro Capone, MD and Carolina Ciacci, MD. The study cohort included 57 patients without celiac disease, 166 patients with untreated celiac disease, 55 patients with celiac disease on a gluten-free diet, and 59 patients with challenging diagnosis. The team provided all patients with endoscopy for collection of duodenal samples, which served for the diagnosis of celiac disease and for the in vitro evaluation of the gliadin-induced mucosal expression of seven inflammatory markers: PY99, ICAM-1 (intercellular cell adhesion molecule), HLA-DR, CD3, CD25, CD69, and transglutaminase 2 IgA. Diagnostic work-up for celiac disease included the search of specific serum antibodies. Researchers asked patients in the challenging diagnosis group to stop gluten-free diet to facilitate the search for these antibodies under untreated conditions. They used the area under the receptor-operated curve (ROC) for statistical analyses on accuracy. For patients with and without celiac disease (not including those on a gluten-free diet) HLA-DR offered the best accuracy for diagnosing celiac disease (area under ROC = 0.99). Combining the data from the HLA-DR with data of other markers did not increase test accuracy. The team found similar results in the 39 patients of the difficult diagnosis group undergoing the search celiac disease-speciï¬c antibodies under untreated conditions. In vitro testing of mucosal HLA-DR to gliadin is an accurate tool for the diagnosing celiac disease, and also works in patients who are hard to diagnose. Source: Am J Gastroenterol 2012; 107:111–117; doi:10.1038/ajg.2011.311; published online 27 September 2011
  10. Celiac.com 06/09/2014 - Anemia is extremely common in patients with celiac disease. In some cases, anemia may be the sole manifestation of celiac disease, but there is no good data on rates of celiac disease in Indian patients with nutritional anemia. A research team recently examined rates of celiac disease among nutritional anemia patients at a care center in India. The team included A. Kavimandan, M. Sharma, A.K. Verma, P. Das, P. Mishra, S. Sinha, A. Mohan, V. Sreenivas, S. Datta Gupta, and G.K. Makharia. For their study, the team conducted positive celiac disease screens on adolescent and adult patients presenting with nutritional anemia. They also prospectively screened for celiac disease using IgA anti-tissue transglutaminase antibody (anti-tTG Ab). Subjects with positive antibody screens received upper gastrointestinal endoscopy and duodenal biopsy. In all, the team screened ninety-six patients. Of these patients, 80 had iron deficiency anemia, 11 had megaloblastic anemia, and 5 had dimorphic anemia. Seventy-three patients were receiving hematinics and 36.4 % had received blood transfusions. Nineteen patients had histories of chronic diarrhea persisting for an average of about ten years. Of those, the team found 13 patients with positive IgA anti-tTG Ab screens, 12 of whom agreed to duodenal biopsy. Ten patients showed villous atrophy (Marsh grade 3a in three, 3b in one, and 3c in six), while two patients showed no villous atrophy. In all, ten patients with nutritional anemia, defined as iron deficiency 9, vitamin B12 deficiency 1, were also diagnosed with celiac disease. Multivariate logistic regression showed age, duration of symptoms, and presence of diarrhea to be the main predictors of celiac disease. The team put all patients with celiac disease on gluten-free diet, supplemented with iron and vitamin B. All patients showed significant improvement in hemoglobin concentration. The team recommends celiac disease screening, and appropriate follow-up in all cases of unexplained nutritional anemia. Source: Indian J Gastroenterol. 2014 Mar;33(2):114-8. doi: 10.1007/s12664-013-0366-6. Epub 2013 Sep 1.
  11. Celiac.com 04/01/2013 - There haven't been many studies that evaluate the usefulness of capsule endoscopy in equivocal celiac disease. A team of researchers recently set out to conduct an evaluation of capsule endoscopy in adult celiac disease, and to assess its potential role in equivocal cases of celiac disease compared with patients with biopsy-proven and serology-proven celiac disease who have persisting symptoms. The research team included M. Kurien, K.E. Evans, I. Aziz, R. Sidhu, K. Drew, T.L. Rogers, M.E. McAlindon, and D.S.Sanders. They are affiliated with the Department of Gastroenterology at Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Foundation Trust in Sheffield, South Yorkshire, United Kingdom. To determine the use of capsule endoscopy in patients with equivocal celiac disease, compared to patients with biopsy-proven and serology-proven celiac disease who have ongoing symptoms. To do this, the team conduced a prospective cohort study of 62 patients with equivocal celiac disease and 69 patients with non-responsive celiac disease. They measured outcome according to the diagnostic yield of capsule endoscopy in equivocal cases and accuracy of mucosal abnormality detection in patients with non-responsive celiac disease. They found that the 62 cases of equivocal celiac disease could be divided into two subgroups: group A, with 32 cases of antibody-negative villous atrophy, and group B with 30 cases of Marsh 1-2 changes. In group A, using capsule endoscopy, the team was able to diagnose celiac disease or Crohn's disease in 9 of 32 patients (28%), compared with just 2 of the 30 patients in group B (7%; P = .044). In patients with persistent celiac disease symptoms, the team made significant capsule endoscopy findings in 8 of 69 patients (12%), including 2 cases of enteropathy-associated lymphoma, 4 cases of type 1 refractory celiac disease, 1 polypoidal mass histologically confirmed to be a fibroepithelial polyp, and 1 case of ulcerative jejunitis. This outcome was significantly lower than the diagnostic yield of capsule endoscopy in antibody-negative villous atrophy (P = .048). It is important to remember that this study was restricted to a single clinic. That said, this is the first time that researchers have used capsule endoscopy to systematically evaluate equivocal celiac disease. Because the diagnostic rates for capsule endoscopy in patients with antibody-negative villous atrophy are better than that of capsule endoscopy in patients with celiac disease with persisting symptoms, the researchers are encouraging the use of capsule endoscopy in equivocal cases, especially in cases where patients antibody-negative villous atrophy. Source: Gastrointest Endosc. 2013 Feb;77(2):227-32. doi: 10.1016/j.gie.2012.09.031.
  12. Celiac.com 06/04/2012 - Non-responsive celiac disease is very much what it sounds like: celiac disease where symptoms seem to resist treatment and continue even in the face of a gluten-free diet. A team of researchers recently set out to look for the most likely causes of persistent symptoms in celiac disease patients on a gluten-free diet. The research team included David H. Dewar, Suzanne C. Donnelly, Simon D. McLaughlin, Matthew W. Johnson, H. Julia Ellis, and Paul J. Ciclitira. They are variously affiliated with King's College London, Division of Diabetes and Nutritional Sciences, Department of Gastroenterology, and The Rayne Institute at St. Thomas' Hospital in London. Their goal for the study was to investigate all patients referred to our center with non-responsive celiac disease (NRCD), to establish a cause for their continued symptoms. For their study, the research team assessed all non-responsive celiac disease who were referred to their gastroenterology center over an 18-mo period. They then established the etiology of ongoing symptoms for these patients. For all patients, the team established a thorough case history and conducted a complete examination with routine blood work including tissue transglutaminase antibody measurement. Additionally, each patient was examined by a specialist gastroenterology dietician to try to spot any gaps in their diets, or any hidden sources of gluten consumption. When possible, the team conducted a follow-up small intestinal biopsy, and compared the results against the biopsies from the referring hospital. Patients with persistent symptoms received colonoscopy, lactulose hydrogen breath testing, pancreolauryl testing and a computed tomography scan of the abdomen. The team monitored patient progress over a minimum of two year period. Overall, the team looked at 112 patients with non-responsive celiac disease. They determined that twelve of those did not actually have celiac disease. Of the remaining 100 patients, nearly half, 45%, were not adequately following a strict gluten-free diet. Of these, 24 (53%) were found to be accidentally consuming gluten, while 21 (47%) admitted to not faithfully following a gluten-free diet. Microscopic colitis was found in 12% and small bowel bacterial overgrowth in 9%. Refractory celiac disease was found in 9%. Three of these were diagnosed with intestinal lymphoma. After 2 years, 78 patients remained well, eight had continuing symptoms, and four had died. In most cases of non-responsive celiac disease, the team found a reversible cause can be found in 90%. In the vast number of those cases, continued consumption of gluten was the main cause. The team is proposing the use of an algorithm for further investigation of the matter. Source: World J Gastroenterol. 2012 Mar 28;18(12):1348-56.
  13. Celiac.com 06/15/2012 - Diagnosing celiac disease can be challenging for doctors if a patient has already started a gluten-free diet, and/or when test results are inconsistent. A research team set out to evaluate the in vitro gliadin challenge in such patients. Researchers included Raffaella Tortora MD; Ilaria Russo PhD; Giovanni D De Palma MD; Alessandro Luciani PhD; Antonio Rispo MD; Fabiana Zingone MD; Paola Iovino MD; Pietro Capone MD; and Carolina Ciacci MD They are variously affiliated with the Department of Clinical and Experimental Medicine at Federico II University of Naples in Naples, Italy; the Department of Surgery, Endoscopy Unit at Federico II University of Naples in Naples, Italy; the Institute of Pediatrics at the University of Foggia in Foggia, Italy; and the University of Salerno, School of Medicine, Gastroenterology at Campus di Baronissi in Salerno, Italy. For their study, the team included 57 patients without celiac disease (negative controls), 166 patients with untreated celiac disease and 55 patients with celiac disease following a gluten-free diet (positive controls), and 59 patients with difficult diagnosis. The team conducted duodenal biopsies on all patients which provided the data for diagnosing the celiac disease and for the in vitro evaluation of the gliadin-induced mucosal expression of seven inflammatory markers: PY99, ICAM-1 (intercellular cell adhesion molecule), HLA-DR, CD3, CD25, CD69, and transglutaminase 2 IgA. As part of their diagnostic work-up for celiac disease, the team included a test for specific serum antibodies. The team asked patients in the difficult diagnosis group to discontinue their gluten-free diets to that they could test for antibodies under untreated conditions. To maintain statistical accuracy, the team used the area under the receptor-operated curve (ROC) to analyze the results. They found that HLA-DR was most accurate in diagnosing celiac disease on negative controls and positive controls, excluding patients on a gluten-free diet (area under ROC=0.99). Test accuracy did not increase by combining HLA-DR data with data of other markers. The results were similar in the 39 patients of the difficult diagnosis group who underwent the test for celiac disease-specific antibodies under untreated conditions. Finally, the results showed that in vitro response of mucosal HLA-DR to gliadin is an accurate tool for diagnosing celiac disease, including in patients with difficult diagnosis. Source: The American Journal of Gastroenterology. 2012;107(1):111-117.
  14. Celiac.com 06/14/2010 - Enteropathy associated T-cell lymphoma (EATL) is a rare type of for which there are currently no standardized diagnostic or treatment protocols. A team of researchers recently evaluated enteropathy-associated T-cell lymphoma and compared standard therapies with a novel regimen including autologous stem cell transplantation The research team included Michal Sieniawski, Nithia Angamuthu, Kathryn Boyd, Richard Chasty, John Davies, Peter Forsyth, Fergus Jack, Simon Lyons, Philip Mounter, Paul Revell, Stephen J. Proctor, and Anne L. Lennard. The team describe EATL in a population-based setting and evaluates a new treatment with aggressive chemotherapy and autologous stem cell transplantation (ASCT). In 1979, the Scotland and Newcastle Lymphoma Group began to collect data on all patients newly diagnosed with lymphoma in the Northern Region of England and Scotland. The research team reviewed the records of patients diagnosed with EATL from 1994 and 1998. 54 patients had features of EATL. The overall annual rate was 0.14/100,000. Doctors treated 35 patients with systemic chemotherapy (mainly anthracycline-based chemotherapy) and with surgery. They treated 19 patients with surgery alone. Patients showed a median progression-free survival (PFS) of 3.4 months and overall survival (OS) of 7.1 months. Starting in 1998 patients eligible for intensive treatment received the novel regimen IVE/MTX (ifosfamide, vincristine, etoposide/methotrexate)–ASCT, with a total 26 patients included. PFS and OS at the five year mark were 52% and 60%, respectively, a substantial improvement over the historical group treated with anthracycline-based chemotherapy (P .01 and P .003, respectively). In contrast to the poor outcomes when treated with conventional therapies, the IVE/MTX-ASCT regimen offers acceptable toxicity and significantly improved outcome for cases of EATL. Researchers are affiliated variously with the Department of Haematological Sciences, Newcastle University, Newcastle upon Tyne; the Department of Haematology, Craigavon Area Hospital, Portadown; the Department of Haematology, University Hospital of North Staffordshire, Stoke on Trent; the Department of Haematology, Western General Hospital, Edinburgh; the Department of Haematology, Raigmore Hospital, Inverness; the Department of Haematology, Harbour Hospital, Poole; the Department of Haematology, Sunderland Royal Hospital, Sunderland; the Department of Haematology, University Hospital of North Tees, Stockton on Tees; and the Department of Haematology, Staffordshire General Hospital, Stafford, United Kingdom Source: Blood, 6 May 2010, Vol. 115, No. 18, pp. 3664-3670. DOI 10.1182/blood-2009-07-231324.
  15. Celiac.com 05/04/2010 - A team of clinicians recently set out to assess the effectiveness of treating collagenous sprue with a combination of gluten-free diet and steroids. The team was made up of Alberto Rubio-Tapia, Nicholas J. Talley, Suryakanth R. Gurudu, Tsung-Teh Wu, and Joseph A. Murray. They are affiliated variously with the Division of Gastroenterology and Hepatology of the Mayo Clinics in Scottsdale, Arizona, Jacksonville, Florida, and Rochester, Minnesota, and the Division of Anatomic Pathology in Rochester Mayo Clinic. Deposits of subepithelial collagen that form a distinctive band in the small bowel are one of the clinical hallmarks of collagenous sprue. For the study, the team evaluated clinical characteristics, treatments, and outcomes of patients with collagenous sprue. The team looked at medical records for thirty patients with collagenous sprue from the Mayo Clinics from Scottsdale, Jacksonville, and Rochester, for the periods covering 1993 and 2009. 21 of the patients were female (70%), ranging in age from 53–91 years. The majority of patients suffered from severe diarrhea and weight loss. However, collagenous spore is commonly associated with collagen deposits or chronic inflammation in other parts of the gastrointestinal tract, as well as other immune-mediated disorders. 16 patients (53%) were hospitalized to treat dehydration, while 21 patients (70%) suffered from associated immune-mediated diseases, the most common of which was celiac disease. Other common associated diseases included microscopic colitis, hypothyroidism, and autoimmune enteropathy. Subjects showed subepithelial layers of collagen deposits in the small bowel ranging from 20 –56.5μm, and averaging 29 μm thickness. Eight patients showed subepithelial collagen deposits in the colon or stomach. 24 patients (80%) showed a positive clinical response to treatment with a combination of a gluten-free diet and immunosuppressive drugs. Nine patients showed confirmed histologic improvement, while five patients experienced complete remission. Of two patients who died, one succumbed to complications from collagenous sprue, while one died of another illness. Most patients with collagenous sprue show a positive clinical response to a combination of gluten-free diet and steroids. Source: Clinical Gastroenterology and Hepatology 2010;8:344–349. doi:10.1016/j.cgh.2009.12.023
  16. Celiac.com 12/12/2004 - A new study that was presented on November 1, 2004 by Julian Abrams, MD, and colleagues from Columbia University Medical Center in New York City at the American College of Gastroenterology (ACG) 69th Annual Scientific Meeting indicates that using only antibody to tissue transglutaminase (tTG) to diagnose celiac disease will likely result in missed diagnoses—and the accuracy of the tTG results depends on which lab conducts the test. Many clinical studies during the past few years have indicated that tTG testing is as accurate as endomyosial antibody (EMA), which has caused many labs to use tTG rather than EMA, and even the recent National Institutes of Health Consensus Conference on Celiac Disease advocated the use of tTG over EMA. In the study the researchers evaluated the effectiveness of tTG in a general referral practice medical setting by reviewing 137 patients who had duodenal biopsy and tTG testing for celiac disease, out of which 117 were biopsy confirmed. Serum from these individuals was sent to four different commercial laboratories for analysis, and the results from these labs were compared. The average tTG sensitivity overall was 71% with a specificity of 67%. In patients with total villous atrophy sensitivity was as high as 92%, and in those with only partial villous atrophy it was as low as 38%. One of the four laboratories tested samples from 48 of the patients and their sensitivity was only 51%, while the specificity was 100%. According to these results it appears that tTG testing—at least outside of the clinical study setting—may not be accurate, and its accuracy depends heavily on which lab is used. Unfortunately the researchers did not reveal the names of the commercial laboratories used in their study, but we hope they will do so when the study is published.
  17. V. Kumar,* M. Jarzabek-Chorzelska, J. Sulej, Krystyna Karnewska,** T. Farrell,* and S. Jablonska *IMMCO Diagnostics, Inc., Buffalo, New York 14228; Departments of Microbiology and Dermatology, State University of New York at Buffalo, Buffalo, New York 14214; and Department of Dermatology, Warsaw School of Medicine, Warsaw, Poland; ** Department of Gastroenterology and Pediatrics, Selesian School of Medicine, Warsaw, Poland Clinical Diagnostic Immunology 9:1295-1300, 2002. Celiac.com 12/31/2002 - Background: Immunoglobulin A (IgA) deficiency is 10-15 times more common in patients with Celiac Disease (celiac disease) than in normal subjects. Serological tests have become the preferred methods of detecting both symptomatic and asymptomatic patients with celiac disease. However, commercially available serological methods are limited in that they detect only the IgA isotype of antibodies (with the exception of IgG gliadin assays); hence, IgA deficient celiac disease patients may yield false negative serology. Methods: Fifteen celiac disease and ten non-celiac disease IgA deficient pediatric cases were examined for IgA and IgG antibodies to endomysium, gliadin and tissue transglutaminase. Results: Twenty five specimens with IgA deficiency were examined. Fifteen were celiac disease cases and ten were non-celiac disease cases. All fifteen IgA deficient celiac disease cases were positive for endomysium antibodies of the IgG isotype and for IgG gliadin antibodies. All but one of the IgA deficient celiac disease cases were also positive for IgG tissue transglutaminase antibodies. None of the non-celiac disease IgA deficient cases were positive for any of the antibody markers. All the specimens examined were also negative for IgA specific antibodies to endomysium, gliadin, and tissue transglutaminase. Conclusions: IgG specific antibody tests for endomysium, gliadin and tissue transglutaminase are useful for the identification of IgA deficient celiac disease patients. IgG antibody tests along with tests routinely being used in clinical laboratories can reliably detect all active celiac disease patients. In addition, the levels of these celiac disease-specific IgG antibodies could be used to monitor patient dietary compliance.
  18. The following was sent to me from Rio de Janeiro by Dr. José Cesar da Fonseca Junqueira. If you have any questions you can e-mail him at: cjunqueira@ax.apc.org.br Rio de Janeiro - 05/27/96 - Celiac Disease. A Comparative study of two periods. Junqueira JC, Calçado AC, Percope S. 1996 Federal University of Rio de Janeiro Martagão Gesteira - Institute of Pediatrics. The aim of this study was to compare cases of celiac disease diagnosed in outpatients with malabsortion cases. The study was conducted at the Pediatric Gastroenterology Service of the Pediatric Institute Martagão Gesteira at the Federal University of Rio de Janeiro Brazil. It was done in two phases: from 1975 -1984 and from 1985 - 1994 (group 1, N=31 and group 2, N=21). Patients were selected based on the results of jejunal biopsy (group IV) and the favorable reaction to a gluten free diet. Data from the first interview (age, sex, nutritional status and prevalent symptoms) were analyzed. The number of biopsies and the level of compliance with the diet were also observed. The data collected was processed in a computer using EPI INFO 6.03 (January 1996)as software. The frequency of celiac disease over the studied years was compared with international data. There were no significant differences between the two groups in our study. However, the cases free of gastroenterological symptoms (atypical celiac disease) were not observed. The average age difference between the groups (group um X=24,39 months; group 2 X=32,03) was not statistically significant. A bigger study must be carried out to prove this theory. The analysis of nutritional status of the groups reveals the existence of severely undernourished patients. The number of biopsies and the level of compliance with diet were similar in the two groups. The decrease in the number of cases as well the increase in the age of patients were observed in group 2. These phenomena were probably due to a delayed exposure to gluten and to the expansion of the period of breast feeding. Other causes should be analyzed in a bigger research program. The conclusion of this study shows that there has been no change in the clinical features of the disease and points to the need for serological screening so that the entire spectrum of the disease can be established. Both groups had malabsorption and were very under-nourished (over 45%). One patient was diagnosed as having Diabetes Mellitus several years after and an other one is under investigation for poliarthrites. Serological investigation is not available in our country. The final conclusion is that we must have such serological screening to know the real spectrum of the disease. Adult celiac disease is not diagnosed in our country, mainly because the adult doctors do not know the full spectrum of celiac disease. Ill be presenting this work as a thesis at the University on May 29, 1996.
×