Recently, I was asked to write a blog about gluten and gluten enteropathy. It has taken a lot longer than expected. Why is that? Well, it’s a subject about which much has been written, and the available research is voluminous. It has been studied extensively with the hope of finding a simple, reliable, serologic way of diagnosing the disease and to find the genetic component that can lead to a reversible, permanent cure. Serologic (blood) tests exist, yes, but doctors still rely heavily on the results of biopsies of the small intestinal lining to confirm the diagnosis.
You probably know someone who is “gluten sensitive.” They say if they eat gluten-containing foods* they get diarrhea, bloating, abdominal pain, and generally don’t feel good. They consistently have symptoms after eating these foods, so the only way to prevent problems is to avoid them. They learn through trial and error what not to eat.
Gluten Enteropathy (GE) is also called Celiac disease and in Europe, Coeliac Disease. Sufferers are born with a genetic intolerance to gluten, a “storage protein” found in wheat grains. The purpose of gluten, normally, is to improve the texture of, and add moisture to, certain foods. It also improves the “flavor of processed foods.” Barley, rye, wheat, and oats contain gluten which is “highly resistant to gastric, pancreatic, and intestinal protein digestion.” Patients learn through ingestion of gluten that it triggers the many symptoms they experience.
GE is seen more often in women than men (2:1 or 3:1 ratio), and it can occur at any age. But it has peaks of occurrence in the first two years of life (after weaning from breast milk) and in the second and third decades. In some cases the problem is present in a patient, but it can has yet to become clinically apparent. However, it always eventually becomes obvious. The majority of GE patients are of European ancestry.
Symptoms range from negligible to severe with diarrhea, abdominal distension, loss of appetite and abdominal pain being most common. The average Western diet contains from 5-20 gm of gluten, and dietary gluten intake consistently causes symptoms. Children with GE ultimately don’t grow or gain weight (failure to thrive) normally, while adults have chronic diarrhea, weight loss, and a sickly appearance (asthenia). In severe cases, hospitalization for weight loss and malnutrition is often necessary.
Non-intestinal problems also develop in long-standing or more serious cases. Iron deficiency anemia, osteoporosis, osteopenia, and B-12 and folic acid deficiencies occur in adults. Children, on the other hand, have short stature, dental problems, mouth sores, headaches, low sperm count, and delayed onset of menstrual periods, absence of menstrual flow, recurrent miscarriages, and early menopause. Calcium, vitamin D, and electrolyte (sodium, potassium) imbalances can occur.
Once suspicion of GE is determined, the “gold standard diagnostic criterion” is biopsy of the duodenum or other portion of the small intestine. Tissue sampling shows classic changes in the villi of the intestinal lining that are diagnostic for GE. Villi are the finger-like projections found in the lining that absorb digested food. In GE, the villi are flattened, thinned out, or completely absent, and as such, digested food cannot be absorbed and symptoms result. The base of the villi swells and becomes inflamed making the small intestinal lining resistant to absorbing food material.
Serologic (blood) tests are also done to test for antibodies that attack the intestinal lining. Positive celiac-specific serologic tests help to confirm the diagnosis. One reference referred to the diagnosis being made by the “4-out-of-5 rule.” The five criteria are:
- Typical symptoms
- Positive antibody test
- HLA-DQ2 or H-DQ8 test positive
- Intestinal damage on biopsy
- Response to gluten-free diet
If four of these five criteria are present, the patient has gluten enteropathy.
Complications of long term GE are osteoporosis due to poor absorption of calcium and vitamin D, intestinal lymphoma, and adenocarcinoma of the small intestine, very rare disorders.
The “cornerstone” of treatment, and the only effective treatment, for GE is avoidance of dietary gluten—ie. wheat, rye, barley, oats, and cereals and other foods that contain them. Nutritional counseling is a must as is strict adherence to a gluten-free diet. “Forty percent of patients don’t do well without gluten and desire alternative treatment.” Larazotide acetate blocks gluten from being absorbed in the small intestine, and patients who take it are able to better tolerate small amounts of gluten in their diet. The drug also seems to help regenerate the intestinal lining.
Biopsy-proven gluten enteropathy is not a common disorder. It’s “prevalence in North America is 0.5%,” meaning 0.5% of the population of North America has GE. Those are the patients who have had biopsies. Millions of others, however, have clinical disease based on improvement of symptoms with a gluten-free diet. They have not had a biopsy, but very likely do have GE. I can’t recall having having more than 2 or 3 patients with GE. They were all managed and treated by the gastroenterologists who had performed their small bowel biopsy. All were doing well because they were adherent to the diet. None had complications. GE is one of those disorders that is thought to be something else before it is proven to be GE. That situation can exist for years until a doctor tuned in to the patient’s symptoms, suspects GE enough to do a small bowel biopsy. A biopsy-proven diagnosis is iron clad. Once you’re diagnosed with GE, it does not “get better” or “go away.” Diet adherence for life is required. Unless advances in genetics occur, a “cure” for GE is very unlikely.
* FOODS THAT CONTAIN GLUTEN
BREADS: rolls, buns, bagels, tortillas, croissants, cornbread
BAKED GOODS: cake, cookies, pie, doughnuts, muffins, waffles, pancakes
PASTA: spaghetti, lasagna, fettuccine, macaroni
CEREALS: breakfast cereals, granola
CRACKERS: pretzels, goldfish, chips, graham crackers
FLOUR:
GRAVY:
SALAD DRESSING, SAUCES:
SNACKS, CHIPS, DIPS, FROZEN MEALS:
NOODLES:
CROUTONS:
References: Singh P, Arora A, et al. Global Prevalence of Celiac Disease: Systematic Review and Meta-Analysis Clin Gastro Hepatology 2018;16:823-836.
Biesiekierski JR What is Gluten? J Gastroenterol Hepatology 2017 Mar;32 suppl 1:78-81.
Ciclitira PJ, Ellis HJ, Lundin KEA Gluten-free Diet—What is toxic? Best Pract Res Clin Gastroenterol 2005 Jun;19(3):359-371.
Dunne MR, Byrne G, Chirdo FG, Feighery C. Coeliac Disease Pathogenesis: The Uncertainties of a Well-known Immune Mediated Disorder. Frontiers in Immunology 2020 July 8;11(1374):1-12.
Cao G, et al. Celiac Disease: a comprehensive current review. BMC Medicine 2019;17:142.
Catassi C, Verdu EF, Bai JC, Lionetti E. Coeliac Disease Lancet 2022 Jun 25;399(10344):2413-
2426.
Foods that contain Gluten celiac.org
