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Autoimmune Disease, Chronic Disease, Genetics, Immunology, Research, Stanford News

Found: Potential new way to predict some multiple-sclerosis patients’ disease course, drug response

Found: Potential new way to predict some multiple-sclerosis patients’ disease course, drug response

I See Nothing“I have multiple sclerosis. Will I become crippled in the future? Or is it going to be the ‘mild’ form? Of the dozen medications out there to treat MS, which one is the best therapy for me?”

Stanford neurologist May Han, MD, who specializes in MS, encounters questions like these from her patients on a daily basis. MS is an autoimmune disease of the brain and spinal cord that causes paralysis, blindness and other disabling symptoms. Over a million people, most of them young adults in the prime of life, suffer from MS worldwide.

While there’s currently no cure for MS, by the end of 2013 there will be 10 FDA-approved MS therapies. The wealth of choices creates a daunting task for physicians: How can they pick the most appropriate therapy for MS patients?

Despite these therapies’ overall efficacy in preventing MS attacks, any one of them can simply fail to work in a particular patient, or cause debilitating and, sometimes, fatal side effects. Right now, physicians lack tools to predict who would respond well to a specific therapy. That’s largely because, Han told me, different patterns of immune mechanisms go awry in different patients:

Despite great strides in MS research over the past 50 years, these differences in immune response from one patient to the next remain poorly understood. As a result, MS still is a disease where the term “only time will tell” perfectly applies. We do not have methods that allow us to predict responses to a selected therapy.

But Han and her colleagues have achieved an important step toward the goal of finding ways to do just that, as reported in a new study in Nature Immunology. Using cutting edge technology to analyze autopsy samples from MS patients, the study authors (including Stanford geneticist Michael Snyder, PhD) identified more than 2,000 proteins that were activated in MS lesions. One of those proteins, sphingosine-1-phosphate receptor 1, was activated only in the MS brain samples, suggesting its importance in MS pathogenesis.

In fact, Gilenya, the first oral medication ever approved for MS, targets that very receptor. Gilenya wards off MS attacks by preventing immune cells from leaving the spleen and lymph nodes. But some patients on the drug, paradoxically, develop worsening MS attacks.

In a mouse version of MS, the authors discovered that certain mutations in the gene coding for the receptor lead to a worsening of MS symptoms. The new findings raise the possibility that these mutations’ presence might contribute to patients’ lack of response to therapy when they’re given drugs such as Gilenya.

Developing a diagnostic test to spot the identified gene mutations might help to predict, for those patients who have them, the course of their disease and response to therapy.

Previously: Two different types of MS, one big step toward personalized medicine, Stanford neuroimmunologist discusses recent advances in MS research and Tool could help predict onset of disability for patients with progressive MS
Photo by garryknight

Autoimmune Disease, Chronic Disease, Genetics, Immunology, Research, Stanford News

Important metabolic defect identified in immune cells of rheumatoid arthritis patients

Important metabolic defect identified in immune cells of rheumatoid arthritis patients

Autoimmunity is a biological betrayal. Your immune system is there to defend you against outsiders (to wit: viral, bacterial, fungal or protozoan pathogens) and to weed out cancer cells before they become tumors. Yet in rheumatoid arthritis, type-1 diabetes and multiple sclerosis, to name a few of the most well known autoimmune diseases, immune soldiers called T cells turn on one or another of your own tissues and launch increasingly vicious aberrant assaults on it.

Nobody’s sure exactly what causes any of these disparate disorders, although combinations of inherited susceptibility and environmental triggers surely loom large as contributors.

In a new study in the Journal of Experimental Medicine, Stanford rheumatologists Connie Weyand, MD, and Jorg Goronzy, MD, and their colleagues have fingered a particular metabolic defect that appears to be specific to rheumatoid arthritis. T cells have an odd job description, which calls for them to mostly sit around and spend their lives loafing but, as soon as they recognize – or get a bit trigger-happy and think they recognize – a foreign intruder, to spring into action, multiplying and morphing as they do.

Both of those activities take a lot more energy than a T cell in its lazy laid-back-little-loafer lifestyle would have ever dreamed of expending. Nature doth provide, of course, and over the eons our T-cells have evolved (along with other fast-dividing cells) a special metabolic procedure that lets them ramp up their conversion of glucose to energy or to raw materials for making important biomolecules they’ll need in order to work much harder and replicate more rapidly than ordinary cells under ordinary conditions.

Weyand, Goronzy and their team found, in T cells taken from rheumatoid arthritis patients, an apparently intrinsic deficiency in that alternate glucose-conversion operation. As a result, attempts on the part of T cells in the patients’ bodies to cope with environmental insults can cause these cells to burn out and collapse in a fit of exhaustion.

Somewhat paradoxically, it may be the demise of these cellular spent forces that trips off the symptom-generating aspect of rheumatoid arthritis. Weyand suspects that immune tries to counter the chronic loss and growing dearth of relevant T cells by producing ever new batches of them – until, in its haste, it mistakenly produces some that are reactive to joint tissue.

Examination of T cells drawn from patients with another autoimmune disease, lupus, revealed no signs of this defect, which may turn out to be a uniquely predisposing factor for rheumatoid arthritis. (A prematurely aged immune system is one of this disease’s hallmark features.) Because the defect is present long before symptoms develop, it could turn out to be a biomarker for rheumatoid arthritis, giving physicians a leg up on diagnosing people at risk for developing the syndrome.

Previously: Best thing since sliced bread? A (potential) diagnostic for celiac diseaseHow to amp up an aging immune response and Age-related drop in immune responsiveness may be reversible

Ask Stanford Med, Autoimmune Disease, Pediatrics

Stanford pediatric gastroenterologist responds to your questions on celiac disease

Stanford pediatric gastroenterologist responds to your questions on celiac disease

gluten_free_072413In the second part of this month’s installment of Ask Stanford Med, we continue the conversation about pediatric gastrointestinal diseases with KT Park, MD, an instructor in pediatric gastroenterology at Stanford and attending physician for the gastroenterology and hepatology services at Lucile Packard Children’s Hospital. Below Park responds to questions related to celiac disease submitted by readers on the School of Medicine Facebook page and in the comments section on Scope.

Pratik Taur asks: What are treatment options for patients of celiac disease [who don't want a] gluten-free diet?

Unfortunately, the only proven treatment for biopsy-confirmed celiac disease is total gluten avoidance. In fact, research has shown repeatedly that even small amounts of gluten can cause detrimental long-term health consequences, including progressive bone loss. I wish there was a different answer for many patients with true celiac disease (whether they have symptoms or not). For now, a strict gluten-free diet for life is the only treatment option. Below I discuss future treatment options that may become available, but still only considered within research frameworks at this time.

Mylea Charvat asks: With celiac will I ever be able to eat regular pastas and breads again? Is there any research into medication to help those diagnosed with celiac disease digest and tolerate gluten?

I wish there were better news for the here and now. Unfortunately, as you know, a strict gluten-free diet – for now – is the only treatment option for celiac disease. Regular pastas and breads are definitely hard to give up, especially if you really enjoy them. With that said, many laboratories around the world are evaluating different strategies to offer celiac patients more therapeutic options in the future. One hopeful approach is “glutenase therapy” where an enzyme could break down the gluten and render it non-toxic. Other working ideas include: blocking the immune reaction (i.e., auto-antibodies) through an ingestible polymeric resin, “desensitizing” the body’s immune system response to gluten via serial protein-based injections and developing a celiac vaccine. Looking ahead, it is conceivable that celiac patients will one day be able to eat gluten-containing foods, but definitive alternatives to gluten avoidance are not yet ready for general consumer use.

Antonio Ruben Murcia Prieto asks: What about oats for celiac disease?

The topic of oats is very much an evolving discussion among celiac experts. Generally, oats are an excellent source of good nutrients, including vitamins, minerals and antioxidants, and dietary fiber, such as soluble beta-glucans. They are high in protein, and are even thought to help maintain steady insulin levels. The working idea is that the biochemical nature of oats is gluten-free, but the manufacturing process of oats contaminates it with a common cereal protein called prolamins, which are found in wheat, barley and rye containing seeds that celiac patients have to avoid.

One group of investigators analyzed 134 oat grains from various manufacturers in the U.S., Canada, and Europe, and they found that only 25 samples were uncontaminated by prolamins, and the majority of samples tested exceeded the threshold for what would be considered gluten-free. Unfortunately, results from clinical studies have been mixed. Also, even if the cross-contamination problem is resolved, the scientific community seems to agree that some celiac patients may be able to tolerate oats without any health consequences, while a subgroup of celiac patients simply cannot tolerate any oats.

For now, the Celiac Sprue Association says it best with this formal recommendation: “Oat products, grown, processed and packaged to be free of contamination with wheat, barley or rye appear to be suitable for some people with celiac disease, but not ALL people… Oats is not a risk-free choice for those on a gluten-free diet. Since oats are not a risk-free choice for all people with celiac disease, products containing oats do not qualify to use the CSA Recognition Seal.”

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Ask Stanford Med, Autoimmune Disease, Pediatrics

Stanford pediatric gastroenterologist answers your questions on inflammatory bowel diseases

Stanford pediatric gastroenterologist answers your questions on inflammatory bowel diseases

sick_kid_072313While nearly every adult and child experiences stomach issues once in a while, millions suffer from serious autoimmune problems in the intestine, such as celiac disease, and inflammatory bowel disorders, including Crohn’s disease and ulcerative colitis. These chronic digestive diseases, which have no known medical cure, commonly require a lifetime of care for patients.

Ongoing research at Stanford and elsewhere aims to forge new avenues for the diagnosis, therapy and prevention of these diseases. At Stanford, KT Park, MD, an instructor in pediatric gastroenterology, studies the pharmaco-economics of various therapeutic and diagnostic strategies for chronic gastrointestinal diseases, with particular interests in Crohn’s disease, ulcerative colitis, celiac disease and chronic abdominal pain. He is also an attending physician for the gastroenterology and hepatology services at Lucile Packard Children’s Hospital.

For this month’s Ask Stanford Med, we asked Park to answer your questions on advancements in research and treatments for pediatric gastrointestinal diseases. He responds to your questions in a two-part Q&A, first discussing research on fecal microbiota transplantation, the role of diet in treating Crohn’s, and IBD in the developing world.

Migdalia Ramos asks: Why isn’t fecal microbiota transplantation (FMT) seriously researched as a treatment for children with IBD?

You are correct in that the representative literature on fecal microbiota transplantation in IBD is lacking, although one small observational study in children was recently published. The paucity of data doesn’t  mean that scientists and IBD clinicians aren’t thinking about it. As you may know, FMT – after much advocacy by patients, various advocacy groups, and gastroenterology societies such as the American Gastroenterological Association – is now approved by the U.S. Food and Drug Administration for recurrent Clostridium difficile (C. difficile) infections and colitis, subject to ongoing regulatory oversight. Over 14,000 Americans die from C. diff annually. In fact, almost all major FMT literature is in the treatment of recurrent C. difficile colitis, which has over a 90 percent efficacy rate. Despite the success in eradicating C. difficile, FMT cannot be assumed to be safe or effective as a first-line therapy option in IBD, much less IBD in children. A recent systematic review (subscription required) which summarizes what is known and studied regarding FMT and IBD is published in Aliment Pharmacol Therapeutics and available (login required) for free on Medscape.

For now, I offer two additional items to consider. First, in the United States, FMT as per the FDA is considered an investigational new drug. As such, researchers are subject to the same jurisdiction as with any novel pharmacological agent. For clinicians, patient safety has to always take priority. At the moment, I know of one phase I study, which was approved by the FDA for research after two years of rigorous review, evaluating the safety and efficacy of FMT in ulcerative colitis in adults led by researchers at the University of Chicago. Second, despite the seemingly slow beginnings, I think there will be a future for FMT in IBD, but only after experience and applicability have been shown in recalcitrant C. difficile infections. Consider an editorial earlier this year in the New England Journal of Medicine, discussing the history and the future potential of FMT in gastrointestinal diseases. Like you, I’m hoping for and working to support the data needed to establish safety and standardization of FMT for adults and children with IBD in the foreseeable future.

EC Smit asks: Why isn’t diet part of the treatment plan for Crohn’s disease when people who have excluded known gastrointestinal irritants, such as gluten and carrageenan, have found relief and remission?

Let me first try to address your concerns and questions with a concession. Interventional dietary alternatives in the treatment of IBD are often underemphasized. Knowing this, our Stanford group is longitudinally recording and making some headway in characterizing how specific and modified carbohydrate diets have impacted health for patients with Crohn’s disease. We’re still in the early phases of our prospective study, but we hope to gain more momentum.

With that said, I understand your perspective. Presently, the medical community in the United States can place more focus on pharmacological therapies than nutritional ones. I think this tendency may have to do with two important considerations. First, although Crohn’s disease is a gastrointestinal disease, it is in essence an autoimmune problem. Conventional and experiential wisdom tells us that controlling immune dysregulation requires immune-modulating agents, such as drugs that can help the body stop attacking its own cells or block the biological response that causes inflammation. And historically, we have found success with this established framework – as most Crohn’s patients achieve sustained remission following an evidence-based treatment plan. Despite the potential severity of the initial disease presentation, most patients return to living life without a noticeable difference in their overall quality-of-life.

Second, patient tolerance and continued adherence to the type of diet programs shown to be potentially effective in Crohn’s disease are difficult, to say the least. As you may know, the Specific Carbohydrate Diet (SCD) is one purported dietary intervention for Crohn’s disease. Although substantially more efficacy data are needed, we know that the SCD dietary plan is a very restrictive low carbohydrate diet, which is difficult to maintain strict adherence for patients, especially among children and adolescents. Similarly, elemental or polymeric diets, which have been reported to be helpful in active Crohn’s disease, are also difficult to perpetuate on a day-to-day basis for long-term disease management. For clinicians, we have to do our part in informing patients of all the alternatives while helping patients and their family to optimize daily quality-of-life.

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Autoimmune Disease, Chronic Disease, Genetics, Immunology, Research, Stanford News

Night of the living dead gene: Pseudogene wakes up, puts chill on inflammation

Night of the living dead gene: Pseudogene wakes up, puts chill on inflammation

night of the living deadBecause proteins do the vast bulk of visible work inside every living cell, scientific efforts to understand the workings of the genome (the sum of all the DNA in all the chromosomes of each of our cells) have traditionally focused on genes – the recipes for proteins.

But only one-fiftieth of the vast stretches of DNA that constitute our chromosomes consists of protein-coding genes. The rest of it was long looked at as little more than a junkyard composed of vast expanses of genetic gibberish.

There’s been a sea-change in scientific perceptions of “junk DNA.” In recent years the applicable metaphor has been less a junkyard than a graveyard, littered with broken skeletons of, for example, viruses and other creepy-crawlies that had curled up in the genome and gone to sleep forever.

Scattered among that detritus are a large number of pseudogenes. These are DNA sequences that closely resemble genes but don’t code for proteins. There are more than 11,000 in the human genome – that’s about one for every two bona fide protein-coding genes. Scientists figure pseudogenes are extra copies of working genes that were accidentally inserted into the genome during divisions of our ancient ancestors’ germ cells. Redundant but harmless, these DNA doppelgangers were permitted by evolution to come along for the ride. Over the intervening eons, pseudogenes have gradually piled up, mutated and decayed to the point where, it’s thought, they no longer do anything at all.

It turns out that although they don’t generate proteins, pseudogenes can generate RNA, which intrigues Stanford molecular biologist Howard Chang, MD, PhD. RNA is best known as the intermediate material in classic protein production. Gene-reading machines in cells produce RNA copies, or “transcripts,” of protein-coding genes. These RNA transcripts leave the cell nucleus and head for the cytoplasm, where they transmit genes’ instructions to protein-making machines situated there.

Chang and other researchers (including 1989 Nobel Prize winner Tom Cech, PhD, of Colorado University, and 2006 Nobelist Andy Fire, PhD, of Stanford) have rocked the field by showing that RNA does much more than just help make proteins.

In a study just published in eLife, Chang and his colleagues have identified a pseudogene that, aroused by an intracellular alarm responsible for fanning inflammation’s fires, generates a “long, noncoding RNA” (a species of RNA whose discovery Chang  pioneered and I wrote about at length in this Stanford Medicine article) that shuts off the alarm – a classic case of what engineers and biologists call negative feedback. As Chang told me when I interviewed him for my news release on this study:

Inflammation tells your body something is wrong… But after it does its job of alerting immune cells to a viral or bacterial infection or spurring them to remove debris from a wound site, it has to get turned off before it causes harm to healthy tissue.

That’s what the cell-soothing pseudogene does. Chang’s team has named it Lethe, after the stream in Greek mythology that makes the deceased who cross it forget their pasts.

Previously: New job description for RNA, oldest professional biomolecule, Master regulator for skin development identified by Stanford researchers and The RNA insurrection: Genes’ “humble servant” rules from behind the scenes
Photo by techno.donm

Autoimmune Disease, Immunology, Nutrition, Research, Stanford News

Best thing since sliced bread? A (potential) new diagnostic for celiac disease

Best thing since sliced bread? A (potential) new diagnostic for celiac disease

sliced breadSomething approaching 1 percent of people of European ancestry have celiac disease: an autoimmune intolerance to gluten, a protein found in wheat, barley and rye. That’s roughly 3 million people in the United States, only 5 to 10 percent of whom have actually been diagnosed.

As in other autoimmune disorders such as type-1 diabetes, rheumatoid arthritis and multiple sclerosis, celiac disease is marked by an immune attack on the body’s own cells (in this case, cells lining the small intestine) as if they were invading viral or bacterial pathogens. The way to avoid this condition’s discomforting, often debilitating and potentially devastating effects is to stay away from all foods that contain gluten – a major sacrifice for most, at least until the food industry began pushing gluten-free foods in earnest not too long ago.

An estimated 1.6 million Americans follow a gluten-free diet without an established diagnosis of celiac disease. Though many folks swear by that Spartan regimen, it’s safe to say that at least some of them are deriving no benefit from the sacrifice. (Let me be clear: If you tell me that since going gluten-free you’re symptom-free, I’ll take your word for it.)

Available tests for diagnosing celiac disease rely on measuring blood levels of circulating antibodies to gluten, or biopsying the intestine. But anyone who has been on a gluten-free diet long enough will test completely normal. Even if these individuals do have celiac disease, the tests won’t show it unless they kick-start their autoimmunity by continuously eating gluten-containing foods for two to four weeks – enough time for a new round of intestinal tissue damage to occur – before being tested. That’s a lot to ask of them.

Now, a team led by Stanford immunologist Mark Davis, PhD, has laid the groundwork for a way to diagnose celiac disease in a much shorter time – six days – and with a much-reduced gluten intake. In a new study published in Proceedings of the National Academy of Sciences, Davis and his colleagues asked volunteers who had previously been definitively diagnosed with celiac disease and had been on gluten-free diets for at least a month to eat  four slices of white bread per day for three days in a row. Then, using extremely sophisticated techniques pioneered in Davis’s lab, the investigators analyzed several classes of circulating immune cells from volunteers’ blood samples. These analyses were able to detect gluten-focused, gut-ward bound immune cells in the blood by Day 6 -much sooner than telltale antibodies would appear, and a whole lot less invasive than a gut biopsy.

“This might be a very easy diagnostic to use for celiac disease, and more accurate than any out there now,” Davis, the director of Stanford’s Institute for Immunity, Transplantation and Infection, told me, expressing special gratitude for “these heroic volunteers, who cheerfully agreed to eat bread and experience discomfort to advance the science of their disease.”

Previously: Chat with Stanford pediatric gastroenterologist on celiac disease research archived on Storify, Deja vu: Adults’ immune systems “remember” microscopic monsters they’ve never seen before, Living the gluten-free life, From frustration to foundation: Embracing a diagnosis of celiac disease and Gluten: The “new diet villain”?
Photo by treehouse1977

Ask Stanford Med, Autoimmune Disease, Chronic Disease, Pediatrics, Stanford News

Ask Stanford Med: Pediatric gastroenterologist taking questions on inflammatory bowel diseases

Ask Stanford Med: Pediatric gastroenterologist taking questions on inflammatory bowel diseases

sick_kid_070813Millions of Americans suffer from inflammatory bowel disorders, including Crohn’s disease and ulcerative colitis, and autoimmune problems in the intestine, such as celiac disease. These conditions occur when the body’s immune system wrongly attacks part of the gastrointestinal tract, and symptoms can often be aggravated by a person’s dietary choices, turning food into more of a nuisance than nourishment.

There is no known medical cure for these chronic digestive diseases, and patients commonly require a lifetime of care. At Stanford, KT Park, MD, an instructor in pediatric gastroenterology, conducts research comparing the pharmaco-economics of various therapeutic and diagnostic strategies for chronic gastrointestinal diseases, with particular interests in Crohn’s disease, ulcerative colitis, celiac disease and chronic abdominal pain. He is also an attending physician for the gastroenterology and hepatology services at Lucile Packard Children’s Hospital.

Earlier this year, Park and colleagues published findings (subscription required) showing that screening adolescents who are either symptomatic or at high-risk for celiac disease is more cost-effective than universal screening. He recently participated in a Twitter chat about the research and discussed topics related to celiac disease and his latest study.

In an effort to continue the Twitter conversation, and expand it to the broader topic of inflammatory bowel diseases, we’ve asked Park to respond to your questions on treating pediatric gastrointestinal diseases. You can submit a question by either sending a tweet that includes the hashtag #AskSUMed or posting it in the comments section below. We’ll collect questions until Wednesday (July 17) at 5 PM Pacific Time.

When submitting questions, please abide by the following ground rules:

  • Stay on topic
  • Be respectful to the person answering your questions
  • Be respectful to one another in submitting questions
  • Do not monopolize the conversation or post the same question repeatedly
  • Kindly ignore disrespectful or off topic comments
  • Know that Twitter handles and/or names may be used in the responses

Park will respond to a selection of the questions submitted, but not all of them, in a future entry on Scope.

Finally – and you may have already guessed this – an answer to any question submitted as part of this feature is meant to offer medical information, not medical advice. These answers are not a basis for any action or inaction, and they’re also not meant to replace the evaluation and determination of your doctor, who will address your specific medical needs and can make a diagnosis and give you the appropriate care.

Previously: Chat with Stanford pediatric gastroenterologist on celiac disease research archived on Storify, Living the gluten-free life, Spreading awareness of inflammatory bowel disease, one bathroom stall at a time, Getting to know – and thanking – the faces of Crohn’s disease, From frustration to foundation: Embracing a diagnosis of celiac disease and Gluten: The “new diet villain?”
Photo by Lance Nishihira

Autoimmune Disease, Clinical Trials, Immunology, Research, Stanford News

Can a series of DNA vaccine shots halt type-1 diabetes progression?

Can a series of DNA vaccine shots halt type-1 diabetes progression?

A new kind of so-called ‘reverse’ vaccine built to dial down the autoimmune reaction that causes type-1 diabetes is showing promise, a study of 80 patients given once-weekly injections of the vaccine for 12 weeks reveals.

Results of an early-stage clinical trial of the vaccine, just reported in Science Translational Medicine, suggest that the vaccine may be able to slow or, at best, halt the destruction of the insulin-secreting pancreatic beta cells that are targeted by an errant immune system.

When I interviewed Stanford neuroimmunologist Larry Steinman, MD, for our news release on the trial, he told me:

We’re very excited by these results, which suggest that the immunologist’s dream of shutting down just a single subset of dysfunctional immune cells without wrecking the whole immune system may be attainable… This vaccine is a new concept. It’s shutting off a specific immune response, rather than turning on specific immune responses as conventional vaccines for, say, influenza or polio aim to do.

Although there’s still a very, very long way to go before this novel therapy sees widespread use, it’s already exceptional in several ways.

When we hear the word “vaccine,” we ordinarily think of a shot people get to fire up their immune systems so that infectious organisms will be thwarted in their never-ending efforts to invade us all. Many of us also know a vaccine is typically composed of proteins – or bits of them, or groups of them – purified or derived from the particular pathogen that vaccine targets. These proteinaceous particles serve as “mug shots” that, presented properly to the immune system’s patrolling bloodhound cells, puts them in a snarling mood and greatly amps up both the speed and the volume of the immune response.

But the new vaccine a) is given after, not before, a person  gets sick; b) targets not an invading pathogen but a disorder of internal origin; c) is intended to diminish, not enhance, the immune response; and d) is made not of proteins or components or combinations of them, but of DNA containing the gene that codes for a protein (in this case, a protein called proinsulin, which is the precursor to insulin).

That’s a lot of exceptions. Here’s just one more: Steinman is a world authority on multiple sclerosis, but his name isn’t usually associated with type 1 diabetes. Nor are those of rheumatologists P.J. Utz, MD, and Bill Robinson, MD. However, all three physicians are laser-focused on autoimmune disorders, for which type 1 diabetes – almost certainly caused by an inappropriate aggressive immune response aimed at the only cells in the body that make insulin – is a poster child.

Previously: Black hat in Alzeimer’s, white hat in multiple sclerosis?, Stanford neuroimmunologist discusses recent advancements in MS research and New thinking about osteoarthritis, older people’s nemesis
Photo by planetc1

Autoimmune Disease, Nutrition, Pediatrics, Research

Chat with Stanford pediatric gastroenterologist on celiac disease research archived on Storify

Chat with Stanford pediatric gastroenterologist on celiac disease research archived on Storify

Yesterday, Stanford pediatric gastroenterologist KT Park, MD, took questions about topics related to celiac disease and his latest research on screening for the condition as part of a Twitter chat hosted by the American Gastroenterological Association (AGA). Those who were unable to participate in the chat can review the conversation on the AGA Storify page.

Park started out the conversation with a number of interesting statistics about celiac disease and the gluten-free movement, including that celiac disease affects about 3 million Americans and that an estimated 1.4 million more are undiagnosed. He also noted that undiagnosed celiac disease is a public health concern because 70 percent of untreated patients have reduced bone mineral density, increasing osteoporosis risk.

As the conversation continued, Park discussed a recently published study (subscription required) he co-authored comparing the methods of screening adolescents who are either symptomatic or at high-risk for celiac disease to universal screening. The goal of the study was to determine if one approach proved better at preventing bone loss and non-traumatic hip and vertebral fractures in celiac patients. Park and colleagues’ findings showed screening only those at risk was more cost effective in preventing bone loss and fractures among patients with undiagnosed or subclinical disease. He also talked about gluten sensitivity and the growing popularity of the gluten-free diet. It’s worth taking a moment to read.

Previously: Join Stanford pediatric gastroenterologist for Twitter chat on celiac disease research, Living the gluten-free life, From frustration to foundation: Embracing a diagnosis of celiac disease and Gluten: The “new diet villain?”

Autoimmune Disease, Nutrition, Pediatrics, Research, Stanford News

Chatting about celiac disease: Stanford expert answering questions this afternoon

Chatting about celiac disease: Stanford expert answering questions this afternoon

Know someone who has celiac disease? Thinking of going gluten-free? As a reminder, Stanford pediatric gastroenterologist KT Park, MD, is taking questions on these topics and his latest research in a Twitter chat today at noon Pacific time. Park’s chat is being hosted by the American Gastroenterological Association and can be followed by using the hashtag #CeliacChat.

Previously: Join Stanford pediatric gastroenterologist for Twitter chat on celiac disease research, A discussion on going gluten-free, From frustration to foundation: Embracing a diagnosis of celiac disease, Gluten: The “new diet villain?” and A call for a new way to classify gluten-related disorders

Stanford Medicine Resources: