Coeliac Disease: What you need to know (Overcoming Common Problems)

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Refractory celiac disease is rare among adults and is almost never seen in children. Data regarding the true incidence and prevalence of RCD are unreliable, but some have estimated that there might be 20, patients in the USA. However, those estimations are based on incomplete data. In one recent study, 1. Disaccharide intolerance I is a rare inherited metabolic disorder characterized by the deficiency or absence of the enzymes sucrase and isomaltase.

This enzyme complex sucrase-isomaltase assists in the breakdown of certain sugars i. The sucrase-isomaltase enzyme complex is normally found within the tiny, finger-like projections microvilli or brush border lining the small intestine. When this enzyme complex is deficient, nutrients based on ingested sucrose and starch cannot be absorbed properly from the gut. Symptoms of this disorder become evident soon after sucrose or starches are ingested by an affected infant.

Intolerance to starch often disappears within the first few years of life and the symptoms of sucrose intolerance usually improve as the affected child ages. Disaccharide intolerance I is inherited as an autosomal recessive genetic trait. Enteropathy-associated T-cell lymphoma EATL is an aggressive lymphoma of the small intestine that almost always arises in association with celiac disease.

Rarely, the lymphoma may arise in extraintestinal sites. The most common location is the jejunum, and the lymphoma presents as single or multiple tumors or as a diffusely infiltrating intestinal malignancy. EATL typically presents with tumor involvement of the middle or lower thirds of the small intestine leading to obstruction blockage , bleeding, and pain from ulcer formation or perforation puncture. Irritable bowel syndrome IBS , previously known as spastic colon or mucous colitis, is a digestive disorder characterized by abnormal movement motility of the intestines both small and large and altered intestinal sensation visceral hypersensitivity.

Symptoms vary widely and include abdominal pain, bloating, constipation, and diarrhea. IBS is very common; about 50 percent of all patients referred to a gastrointestinal specialist have IBS.

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There is no obvious organic disease present; only the function of the intestines is affected. However, based on the symptoms, this disease can be confused easily with other bowel diseases including celiac disease.

Microscopic colitis collagenous colitis, lymphocytic colitis is not a single disease but comprises two related entities, collagenous colitis and lymphocytic colitis, both characterized by chronic watery diarrhea. Lymphocytic colitis is distinguished primarily by intraepithelial lymphocytic IEL infiltration and collagenous colitis by an abnormal layer of fibrous tissue collagen beneath the surface layer of the intestine. The cause of microscopic colitis is unknown. It typically occurs as a result of chronic pancreatic damage, which may be caused by a variety of conditions including cystic fibrosis in children and young adults , excessive alcohol intake, gallstone disease and medications in older individuals.

It is less frequently but occasionally associated with pancreatic cancer or celiac disease. Pancreatic insufficiency usually presents with symptoms of malabsorption, malnutrition, vitamin deficiencies, and weight loss or inability to gain weight in children and is often associated with steatorrhea fatty, loose, bulky and foul-smelling stools.

Virtually all clinicians studying refractory celiac disease emphasize that the diagnosis is based on eliminating all other possible sources of the symptoms and intestinal injury. One article lists more than 10 conditions that must be considered and eliminated before a convincing diagnosis of refractory celiac disease may be made.

What Are the Treatments for Celiac Disease?

As noted above, examination of the interior wall of the intestine upper and lower by means of an enteroscope or colonoscope as well as obtaining intestinal biopsies to be examined under a microscope is useful, especially to determine if the symptoms are the result of intestinal disorders other than RCD. Capsule endoscopy, which examines the small intestinal lining using a camera mounted on a swallowed pill, may also be useful in evaluating the degree of small intestinal inflammation and injury.

Some specialized centers are able to offer sophisticated examinations of the biopsy materials that in many cases will assist in the diagnosis.

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These studies emphasize the presence of abnormal populations of T lymphocytes in the tissue indicating a diagnosis of the more aggressive Type II RCD. Other imaging studies barium X-ray, CT scan, capsule enteroscopy and MRE may be undertaken, especially if there is concern for the presence of a lymphoma. Several therapies for RCD have been tried in uncontrolled tests with inconclusive results. Among the therapies tested in this way are: elemental diet an elemental diet is a liquid diet consisting of nutrients that require no digestion, including amino acids, carbohydrates, vitamins, minerals, and triglycerides ; and total parental nutrition TPN that is defined as nutrition maintained entirely by intravenous injection or by some other nongastrointestinal route.

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Steroid therapy is a mainstay of treatment but its beneficial effect is short-lived in patients of lymphoma. Treatment involving other immunosuppressive drugs such as azathioprine, cyclosporine, enteric-coated budesonide, 5-aminosalicylic acid 5-ASA , or inflixamab has been used with a limited number of patients. More recently chemotherapy with cladribine with or without autologous stem cell transplantation has also been reported to be useful. Information on current clinical trials is posted on the Internet at www.

All studies receiving U.

For information about clinical trials sponsored by private sources, contact: www. Celiac Disease and Refractory Celiac Disease. Feldman, Friedman, and Brandt, editors. W B Saunders Co. McGraw-Hill Companies. New York, NY; Textbook for Gastroenterology. Philadelphia, PA; ; Mechanisms and management of refractory celiac disease. Nat Rev Gastroenterol Hepatol. Epub Sep 8. It found that 1 of every Americans had celiac disease.

This was pretty much in line with the most recent European numbers. How was it possible that a disease so well-identified in some places had been practically invisible in the U. Intuitively, the vast majority of the symptoms are gastrointestinal: chronic diarrhea, weight loss, failure to thrive. You can have joint pain, a skin rash. You can change your behavior because inflammation spills into the brain. You can have infertility. Over the last couple decades, the diagnosis and treatment of celiac disease in the U.

He, like Fasano, is a gastroenterologist. Lebwohl and other researchers have looked all over the world for clues that could explain why celiac disease is triggered in one person and not another. But celiac disease is present in Asia. In virtually every country in the world, celiac disease has been identified. For example, in India we know that the necessary gene is similarly present in the north and the south of the country.

The going explanation — and I think this is a plausible explanation — is that there is a lot more gluten consumption in the north. This is a very ancient population that was displaced from their normal position because of the civil war in Northern Africa. That led to very high mortality because of malnutrition, famine, no food available. Unicef and the W.

Celiac Disease and Anxiety

The answer was wheat. The population there for 4, years — whose diet was based mainly on camel milk, camel meat, fruits and vegetables — for the first time in their history, were introduced to gluten. DUBNER: Was it the sudden influx of that diet that triggered it or was it a case of selection among the population just the way that natural selection works over time? Was it related to that? There were people there were much more susceptible.

Remember, once upon a time there was high mortality of celiac disease. Benjamin Lebwohl again:. But there was one. This was an epidemic that primarily affected the youngest children, so infants and children under two years of age. It typically caused what we call the classical form of celiac disease: babies with diarrhea, failing to grow, etc.

Then in the mids, just as rapid as the rise was a rapid fall. The working hypothesis was that it had to do with how those infants were being fed.

Rates of breastfeeding were not very high and in general were not overlapping with the first introduction of gluten into the diet. Moreover, infant formula had very high quantities of gluten, which is very different from today. When more overlap with breastfeeding was encouraged and when gluten was minimized from the infant formula, that coincided with the end of the epidemic. LEBWOHL: There was a study that compared rates of celiac disease in two regions very close to each other geographically but very different socioeconomically.

These two regions were in Finland and right across the border with Russia in a region called the Russian Karelia. The genetic makeup of those two populations was similar. They both had rates of the celiac disease genes that were comparable. But when screened, celiac disease was present in about one in in Finland and about one in in the Russian Karelia, right across the border. The researchers suspected that income had something to do with it. One theory: lower-income people had more exposure to certain bacteria that somehow protect them from celiac disease.

For instance, the bacteria H.

Pylori , known to cause ulcers, seems to cut the risk of celiac disease in half. Emma Morgenstern is a producer on our show. I came to terms with it fairly quickly because I had to. Mazal tov.