What is gluten intolerance?

Quick Answer
A chronic, immune-mediated condition of progressive, itchy skin lesions triggered by the ingestion of gluten.
Expert Answers
enotes eNotes educator| Certified Educator
Causes and Symptoms

Gluten, a protein found in wheat, rye, and barley grains, is a common part of the twenty-first century diet. However, in people who develop gluten intolerance—which most commonly develops between the ages of twenty and forty—gluten triggers a specific immune system response. Gluten intolerance, or gluten sensitivity, comprises celiac disease, which is a gastric reaction, and dermatitis herpetiformis (DH), which is primarily a skin-based reaction. Unlike the majority of food allergies that are mediated by immunoglobulin (Ig) E antibodies, gluten ingestion in patients with DH signals the body to develop an immune response that is mediated by IgA instead. IgA antibodies build up and attack tissue transglutaminase (tTG) and epidermal transglutaminase, enzymes that break down gliadin, a component of wheat gluten. Gliadin, and related substances in rye and barley grains, appears to be the antigen, or trigger, of the immune response that leads to the characteristic symptom of DH—an intensely itchy and progressive skin rash. Indeed, instead of relying on only a dietary challenge for diagnosis of DH, this gluten sensitivity may be diagnosed by immunofluorescence to identify IgA deposits in skin lesions or by screening for the disease-specific presence of a tTG attack.

Symptoms of gluten intolerance in DH begin slowly as small, itchy areas on the skin but progress rapidly to extremely blistered, burning, and itchy lesions that appear in groups, often symmetrically. Affected areas are most often found on the knees, elbows, buttocks, and back. In severe skin disease, prodromal irritation may occur at sites of new lesions. Gastrointestinal discomfort, ranging from stomach pain to oral ulcers, has been reported infrequently along with the primarily dermal symptoms of DH.

Even without gastric symptoms, gastrointestinal biopsies of people with DH reveal abnormal changes to parts of the gastrointestinal wall and IgA deposits in parts of the gastrointestinal wall. Increased tTG reactivity appears proportional to the likelihood of this gastric involvement. Because of this gastric link, some researchers consider DH to be a precursor to the development of celiac disease and related malabsorption problems if the skin condition remains untreated.

Treatment and Therapy

Treatment of DH is twofold. First, symptomatic relief is provided by oral sulfones—dapsone and sulfasalazine—to reduce lesions. Sulfones work by unknown mechanisms, possibly related to enzyme stabilization, and they quickly reduce the severity and number of skin lesions, often within only two days. Dapsone, 150 to 200 milligrams daily, is the first-line agent, and the dose can be reduced to 50 to 100 milligrams daily after severe lesions have healed. Because dapsone in particular is associated with high rates of peripheral neuropathy, at times with sensory loss, sulfasalazine is a secondary sulfone choice. Potential side effects of any sulfone treatment include blood-related problems, such as anemia and decreased leukocyte counts. When an alternative to symptomatic sulfone treatment is required because of such side effects, tetracycline or minocycline may be used successfully but with less dramatic rates of improvement.

Gluten removal from the diet is the only treatment known to induce disease remission, to reduce the IgA accumulation to nearly zero, to heal existing lesions, and to prevent eruption of new lesions. In severe disease occurrences, full improvement of symptoms may take as long as two years; most often, six months of a gluten-free diet will allow a patient to discontinue sulfone treatment without a disease flare. A diet without wheat, rye, or barley must be continued indefinitely for successful disease control, because dermal symptoms return as soon as gluten is reintroduced. Rice, corn, and pure oats are recommended replacement grains. Consultation with a dietician is often suggested to ensure that the gluten-free diet provides adequate nutritional needs and to learn about ways to avoid hidden sources of gluten.

Perspective and Prospects

As early as the 1930s, dentist Weston Price associated greater amounts of processed foods in American diets with increasingly poor oral, digestive, and overall health. During the 1940s and 1950s, Willem Dicke of the Netherlands noted that children with nonspecific health complaints, including gastric pain, experienced improvement during food rations, when most grains were unavailable. Dicke expanded this observation with extensive research, presentations, and publications that pointed to early identification of DH and celiac disease.

In the second half of the twentieth century, more research evolved to identify biopsy results and immune responses in patients with skin lesions as similar to those in patients with gastric symptoms of celiac disease; the term “nonceliac gluten sensitivity” (NCGS) was coined to identify patients whose skin and mild gastric symptoms improved despite negative test results for celiac disease, and the differentiation of DH and celiac disease began. However, since the diagnosis of NCGS is based mainly on having symptoms similar to celiac disease but testing negative for it, the diagnosis remains somewhat controversial in the medical community. Some clinicians contest the role that gluten plays in the disorder. One 2013 Australian study found no significant difference between reactions to a gluten-free diet and a placebo in patients with presumptive NCGS, but other studies have found improvement in symptoms with the gluten-free diet.

As research about the abnormal immune system response to gluten continues, potential links to other autoimmune disorders, such as autoimmune thyroid disease, multiple sclerosis, and irritable bowel syndrome, have been identified. Additionally, researchers are trying to determine how closely linked celiac disease and DH may be and whether lack of disease control in either gluten sensitivity may lead to progressive gastric disease, malabsorption, and even lymphoma.

Awareness of gluten sensitivity increased greatly in the twentieth century and into the twenty-first, which has made identification of gluten-free foods simpler. Still, gluten is a common filler ingredient and may be hidden in foods such as gravy, beer, or soy sauce; medications such as vitamin supplements; and even makeup such as lip balm. As with many chronic conditions, patient education is key to reducing symptoms and improving quality of life.

Researchers at the Mayo Clinic indicated that cases of celiac disease rose considerable in the first decade of the twenty-first century, plateauing in 2004; experts believe that this is largely due to greater awareness of the disease and better diagnostic tools rather than an actual increase in prevalence. However, the prevalence of NCGS is harder to pin down, as it is a newer diagnosis that is not as well understood. A 2015 review found that studies have estimated the rate at anything from 0.5 percent to 13 percent of the population. A 2013 Swedish report stated that infants, beginning at four months, can bolster their defenses against celiac disease by consuming small doses of grain-based foods in tandem with breastfeeding.

Bibliography

Boettcher, E., and S. E. Crowe. "Dietary Proteins and Functional Gastrointestinal Disorders." American Journal of Gastroenterology 108.5 (2013): 728–36. Print.

Czaja-Bulsa, Grazyna. "Non Coeliac Gluten Sensitivity—A New Disease with Gluten Intolerance." Clinical Nutrition 34.2 (2015): 189–94. Print.

Feldman, M., L. S. Friedman, and L. J. Brandt. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Maryland Heights: Saunders, 2010. Print.

Gluten Intolerance Group of North America. GIG Newsletter Education Bulletin: Dermatitis Herpetiformis. Auburn: Author, 2009. Print.

Habif, T. P. “Vesicular and Bullous Diseases.” Clinical Dermatology. 5th ed. Rockville: Mosby, 2009. Print.

Humbert, P., F. Pelletier, and B. Dreno, et al. “Gluten Intolerance and Skin Diseases.” European Journal of Dermatology 16.1 (2006): 4–11. Print.

Ivarsson A. "Prevalence of Childhood Celiac Disease and Changes in Infant Feeding." Pediatrics 131.3 (2013): 687–94. Print.

Love, H. W. “Dermatitis Herpetiformis and a Gluten-Free Diet.” American Family Physician 67.3 (2003): 470. Print.

"Middle-Class Children More Likely to Be Diagnosed with Gluten Intolerance." Telegraph [London] 23 Jan. 2015: 4. Print.

Molina-Infante, J., S. Santolaria, D. S. Sanders, and F. Fernández-Bañares. "Systematic Review: Noncoeliac Gluten Sensitivity." Alimentary Pharmacology & Therapeutics, 41.9 (2015): 807–20. Print.

Sampson, H. A., and A. W. Burks. “Adverse Reactions to Food: Non-IgE-Mediated Food Hypersensitivity.” Middleton’s Allergy: Principles and Practice. Ed. N. F. Adkinson et al. 7th ed. Rockville: Mosby, 2008. Print.

Turchin, I., and B. Barankin. “Dermatitis Herpetiformis and Gluten-Free Diet.” Dermatology Online Journal 11.1 (2005). Print.

Wangen, Stephen. Healthier Without Wheat: A New Understanding of Wheat Allergies, Celiac Disease, and Non-Celiac Gluten Intolerance. Seattle: Innate Health, 2009. Print.