In 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.”
FS asks: Is it possible for compromised tight junctions caused by celiac/gluten sensitivity to turn into ulcerations, and over time, into stenoses in the small bowl? Or do MRI-identified stenoses in the small bowl, coupled with chronic anemia, indicate a definitive Crohn’s diagnosis?
Celiac disease and Crohn’s disease can occur together, although very rare to have both. In either disease, diagnostic confirmation has to come from endoscopy-obtained intestinal and colonic specimens (reviewed by an experienced GI pathologist). MRIs, imaging tests and laboratory results cannot confirm Crohn’s disease or celiac disease. So, it is important to obtain the full screening work-up and ensure that a board-certified gastroenterologist is overseeing the various points of care.
I will comment briefly on the tight junctions, which are microscopic “bridges” joining one cell to another to form an impermeable barrier. Compromised tight junction in Crohn’s disease have been documented and studied. Although the root cause of this phenomenon is not known, one working hypothesis is that uncontrolled IBD upregulates inflammatory cytokines (molecules such as TNF-α), which disrupt the original intestinal impermeability. Lastly, even though severe unmanaged celiac disease have reportedly caused duodenal (first portion of the small intestine) stenosis, classical MRI-identified stenoses along the intestinal tract are more often the result of a stricturing-type of moderate-to-severe Crohn’s disease. In other words, Crohn’s – not celiac – is more likely to cause intestinal narrowing.
Kumar Thurimella asks: I’m a current MD/PhD applicant with an interest in gastrointestinal disease. In your opinion, how much of a role do the microbes in our gut play (our gut microbiome) as opposed to a genetic predisposition we may carry in our own genome with respect to IBD/celiac disease?
You bring up one of the most interesting and yet difficult questions in “IBD-ology.” Surveying the published literature on this topic as a whole, we know that the development of IBD is an intricate interplay between genetics, environmental triggers, and the unique gut microbiome. At this time, it is difficult to place a precise estimate on how much the gut microbiome plays in the development of IBD.
Personally, my ongoing scavenging through the literature leads me to hypothesize that a significant proportion of our lifetime IBD risk is indeed affected by the ecology of our gut bacteria. For example, take one very recent report published in Nature. The investigators show that innate lymphoid cells are actively involved in regulating CD4+ T-regulatory cells – the very cells that help control how our body’s immune system distinguishes between host (self) bacteria versus pathogenic bacteria in the gut.
In sum, what we know is that our body’s inflammatory response to the commensal or symbiotic bacteria in our intestinal tract is regulated by complex molecular mechanisms of checks-and-balances. We also know that genetics is most definitely involved, via multiple pathways such as innate immunity, adaptive immunity and epithelial function. Yet, understanding how precisely our unique gut microbiome – dynamically tailored from birth to what we eat today for lunch – affects the genetic predisposition for IBD is undoubtedly one of the most active and exciting frontiers in gastroenterology research.
Previously: Stanford pediatric gastroenterologist answers your questions on inflammatory bowel diseases, Ask Stanford Med: Pediatric gastroenterologist taking questions on inflammatory bowel diseases, Chat with Stanford pediatric gastroenterologist on celiac disease research archived on Storify, Spreading awareness of inflammatory bowel disease, one bathroom stall at a time and Getting to know – and thanking – the faces of Crohn’s disease
Photo by Memphis CVB