Epidemiology of Celiac Disease

Celiac disease is one of the most common, chronic genetic gastrointestinal conditions affecting just under 1% of Caucasian individuals. Whilst it was initially recognized in Northern Europeans, celiac disease will affect Caucasians wherever they live. It can affect people of mixed ethnic background. It is apparently rare in Southeast Asia and sub-Saharan Africa. While celiac disease was once considered primarily a childhood disease, in many geographic locations, celiac disease is more commonly diagnosed in adulthood. The median age in one study in the US was 50 years of age. Even in childhood, the age at diagnosis is now increased from early infancy to later in childhood or adolescence. The spectrum of disease has also changed with an increasing proportion of patients being diagnosed with mono-symptomatic or less severe celiac disease. Many of these patients would not have been diagnosed in the past, but their symptoms described as functional disorders. It is not uncommon to diagnose celiac disease in those of advanced age. Patients in their 80s may be diagnosed for the first time with celiac disease, some of these having symptoms that persist for many years prior to diagnosis. The delay time to diagnosis may be anywhere between 8 and 11 years from the time of first clinical presentation to the actual diagnosis being made.

Diagnosed celiac disease appears to be more common in women than men. However, in those individuals who are identified by population-based screening, the prevalence of the disease appears to be equal between genders. The explanation for this is unclear, however, presentation of disease may be more common in women because of the nutritional challenges posed by pregnancy and menstruation, especially when producing iron deficiency anemia. The predisposition of women to autoimmune disease may also increase the likelihood of the occurrence of symptomatic celiac disease.

The sister condition of celiac disease is dermatitis herpetiformis, which is the skin manifestation of gluten-sensitive enteropathy. It is an extremely itchy immunobullous disease that affects the extensor surfaces of elbows, knees, buttocks, the hairline, and the torso and is much less common than celiac disease. Probably the ratio between the two in geographic areas where both have been estimated is approximately 10:1. However, in countries where there has traditionally been less celiac disease awareness, such as North America, the ratio may be closer to 3:1.

The incidence of celiac disease and the prevalence of celiac disease have been estimated in a number of geographic locations. These have shown incidence estimates of approximately between 1 and 9 cases per 100 000 person years and prevalence rates of anywhere from 1 in 2000 to 1 in 300. The latter high estimate is based on geographic locations where there have been active case findings such as Tampere in Finland. The lower rates are the prevalence based on clinically diagnosed cases. However, these measures may greatly underestimate the true prevalence of celiac disease in the community. Two specific lines of research would suggest this. One is a systematic follow-up of birth cohorts for the occurrence of celiac disease by using serologic screening. In one geographic location in Denver, Colorado, almost 1% of children became persistently seropositive for markers for celiac disease by 7 years of age. This cumulative prevalence is remarkably similar to population-based studies in both Europe and North America that suggest prevalence in an adult general population of approximately 1 in 133. The estimates of the prevalence of celiac disease in most Caucasian studies have been remarkably similar, varying from 1 in 300 to 1 in 87.

Gluten challenge

Gut permeabilization

Environmental insults

Th1 adaptive response to gliadin and an autoreactive response to tTG

Gluten challenge

Gut permeabilization

Environmental insults

innate response ^^^

Release of tTG2 Minor tissue damage

Figure 2 Maelstrom of celiac disease. An initial perturbation of the mucosal immune system would activate the innate immune response, increase epithelial permeability, and inflame the mucosal environment, resulting in overexpression of MHC class II molecules and the presentation of gliadin peptides to CD4+ T cells. tTG produced by fibroblasts in the damaged lining would deamidate gliadin peptides and amplify the CD4+ T cell response to gliadin. The released tTG would subsequently be targeted by the humoral immune response as an autoantigen, further advancing the mucosal immune system down a spiraling pathway towards self-destruction and villous atrophy.

All the studies so far have been carried out in predominantly Caucasian populations. No studies have been carried out that have incorporated substantial numbers of African-Americans, nor have systematic studies been carried out in sub-Saharan Africa. Areas of North Africa are at least as commonly affected as Europe. Individuals from Southeast Asia very rarely develop celiac disease.

The major effect of these screening studies has been to illustrate the wide spectrum of disease that incorporates celiac disease. Many individuals are completely asymptomatic. Others may be severely ill, presenting at an early age. It is possible that some individuals who have developed celiac disease may have no symptoms whatsoever despite the presence of demonstrable serologic and histopathologi-cal changes of celiac disease.

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