Although the conception of celiac disease has expanded, some fallacies about its clinical characteristics and management remain, according to an invited presentation by Ciaran P. Kelly, MD, at the American College of Gastroenterology 2019 Annual Meeting, published in the American Journal of Gastroenterology.
Fallacy #1 – Celiac Disease Occurs Mainly in Europeans and Those of European Descent
Throughout the majority of the twentieth century, celiac disease was generally associated with Europeans and those of European descent. However, worldwide epidemiologic data is now available showing that celiac disease is remarkably ubiquitous. Overall, the global pooled seroprevalence of celiac disease is 1.4% (95% CI, 1.1%–1.7%), and the prevalence of biopsy-confirmed celiac disease is 0.7% (95% CI, 0.5%–0.9%).
In the United States, a study found that the ethnic group with the highest prevalence of villous atrophy, which is suggestive of celiac disease, is not of European origin but from Punjab (3.08% vs 1.8% overall in North America).
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Fallacy #2 – Individuals With Celiac Disease Are Not Obese
According to the authors, “In the western world, it is estimated that between 15 and 31% of individuals with celiac disease are overweight at the time of the diagnosis and 6.8-13% are obese.”
In a cohort of 679 adults with celiac disease who were followed for a mean of 39.5 months, one-third had a high body mass index (BMI) at diagnosis (21% overweight and 12% obese). The investigators observed that BMI increased significantly on a gluten-free diet (GFD) (mean 24.0-24.6 kg/m2; P <.001), and 22% of those with a normal or high BMI at diagnosis increased their BMI substantially (by >2 points). Conversely, others have reported that BMI may decrease on a GFD for some overweight or obese individuals.
Fallacy #3 – Serum TTG-IGA Tests Are Not Useful to Diagnose or Exclude Celiac Disease in Patients With Low Serum IGA
Among those who are immunoglobulin A (IgA) deficient, tissue transglutaminase (TTG) immunoglobulin G (IgG) and anti-endomysial (EMA) IgG appear to have a similar sensitivity and specificity to TTG IgA-based tests in those who are IgA sufficient. In an evaluation of 1,000 consecutive patients screened for celiac disease, TTG IgA was determined to be highly sensitive (100%) for celiac disease in those with partial IgA deficiency. In children, similar findings have been reported.
Fallacy #4 – All Individuals With Celiac Disease Respond to a GFD
A GFD is an imperfect treatment for celiac disease. Many individuals with celiac disease simply do not respond to this type of diet. Despite adhering to an apparently strict GFD, greater than 15% of adults have persistent or frequent symptoms of celiac disease.
Although gluten ingestion is the most common cause of nonresponsive celiac disease (NRCD), it is not the only cause. Some other causes of NRCD need very different management approaches, such as microscopic colitis, other food intolerances, small intestinal bacterial overgrowth, and irritable bowel syndrome (IBS).
Fallacy #5 – The GFD is Mainly Used to Treat Celiac Disease
In 2012, it was estimated that at least 2 million people were following a GFD in the United States, but only 300,000 (15%) actually had celiac disease. The researchers report that an increasing proportion of individuals adopt a gluten-free or gluten-reduced diet for various reasons. These reasons include relief of gastrointestinal or extraintestinal symptoms due to having nonceliac gluten sensitivity (NCGS) or IBS. On the other hand, others are known to avoid gluten as part of social trends.
Fallacy #6 – A Clinical Response to a GFD Indicates a Diagnosis of Celiac Disease
Self-treatment with a GFD prior to medical consultation is increasingly common due to the increased awareness of GFD. This diet is widely used by individuals without celiac disease. In addition to celiac disease, NCGS and IBS may also respond to a GFD.
The authors note that, “Differentiating between celiac disease and other conditions is clinically important because only celiac disease requires a lifelong strict GFD, carries risk for significant health complications, and is associated with a risk of disease in children and other relatives.” Genotyping of the HLADQ2 and DQ8 haplotypes may be of use when there is diagnostic uncertainty. With regard to the 40% of the population who are HLADQ2 and/or DQ8 carriers, a prolonged gluten challenge remains the clinical tool of choice to confirm or rule out celiac disease.
Fallacy #7 – The GFD Has Solved the Problem of Celiac Disease
GFD is considered an imperfect therapy, and the treatment burden is high. Among patients at the Beth Israel Deaconess Medical Center, following a GFD for treatment of celiac disease was reportedly more burdensome than treatments for type 1 diabetes, IBS, inflammatory bowel disease (IBD), and congestive heart failure. The authors report that, “Those with end-stage renal disease on hemodialysis were the only group to report a higher treatment burden than those with celiac disease.”
A strict GFD is difficult to maintain. The following groups are known to particularly struggle with a GFD: the elderly, the illiterate, those with mental or psychological impairment, and those with limited financial resources.
Fallacy #8 – An “Almost” Gluten-Free Diet is Adequate
Adherence to a strict 100% GFD is very challenging. The researchers note that patients often ask if a less strict diet is adequate.
In a double-blind microchallenge study, patients with biopsy confirmed celiac disease who had normal duodenal villous architecture after being on a strict GFD for 2 years or longer were randomly assigned to receive 10 mg gluten, 50 mg gluten, or a cornstarch placebo daily for 3 months in conjunction with their usual strict GFD. At baseline, villous height crypt depth ratio (Vh:Cd) was determined to be similar in all 3 groups. However, compared with the placebo group, there was a significant decrease in Vh:Cd in the 50-mg group after 3 months. The investigators found that 19/39 study participants (including 2 in the 50-mg group) had an increase/improvement in their Vh:Cd over the course of the trial.
In a study among children that compared the effects of a daily intake of 100 mg and 500 mg of gluten, both groups had a worsening of the Vh:Cd and frequencies of intraepithelial lymphocytes, with the exception of 1 child in the 100 mg group, who had a slight improvement of the Vh:Cd ratio.
The researchers assert that individual responses to gluten exposure can be highly variable. Nevertheless, a chronic gluten exposure of at least 50 mg for more than a month will likely cause intestinal damage.
Fallacy #9 – Most Patients With Known Celiac Disease Follow a GFD
Even among highly motivated patients, eliminating all dietary gluten may be difficult to achieve. These difficulties have been acknowledged for years, as the definition of “gluten-free” is not definitive and allows 20 parts per million of gluten in foods.
In England, a survey of adults diagnosed with celiac disease found that 40% reported intentional gluten exposure within the past 6 months, and an additional 30% reported unintentional gluten exposure during the same time period.
Fallacy #10 – A GFD is Sufficient Therapy for Celiac Disease
All current guidelines for the management of celiac disease recommend lifelong compliance with a strict GFD. However, this treatment has an incomplete efficacy. Surveys suggest that the majority of patients with celiac disease would be interested in a medical therapy, but no medications have yet to be approved for disease treatment. Thus, there are many opportunities for novel, non-dietary treatments.
Disclosure: Some study authors declared affiliations with the industry. Please see the original reference for a full list of authors’ disclosures.
Disclosure: This research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. Please see the original reference for a full list of disclosures.
Reference
Silvester JA, Therrien A, Kelly CP. Celiac disease: fallacies and facts. Am J Gastroenterol. Published online June 1, 2021. doi:10.14309/ajg.0000000000001218
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