Eosinophilic Gastroenteritis

An Update

Alfredo J Lucendo; Angel Arias

Disclosures

Expert Rev Gastroenterol Hepatol. 2012;6(5):591-601. 

In This Article

Epidemiology of EGE

Until few decades ago, EGID was not of particular interest to gastroenterologists. However, the wide recognition of eosinophilic esophagitis (EoE), the most frequent manifestation of this family of disorders that currently represents the most common cause of dysphagia and food impaction in young males and the second most common cause of chronic esophageal disturbance after gastroesophageal reflux disease,[6] has increase the awareness and diagnosis of new cases of EGID. The disorder begins with a constellation of symptoms that depend on topography and the intensity of the inflammatory response, eventually leading to endoscopic evaluation of these patients.

This rise in the prevalence of EGID and immunoallergic diseases in general has occurred in parallel with a decrease in infectious diseases, a coincidence that has been explained through the hygienic hypothesis.[7] This hypothesis asserts that reduced exposure to microorganisms during childhood can modify the patterns of gut microflota, leading to a change in the fine tuning of Th1, Th2 and T-regulatory responses. This gives rise to an imbalance of the immune system and a predisposition for developing allergic and autoimmune disorders triggered by altered or missing innate immune cell activation. In fact, the influence of Th2 cells, which are important in the development of responses mediated by IgE, usually fades after the first 2 years of life in nonallergic individuals. This is possibly due to a secondary stimulation of Th1 responses after bacterial infections,[8] a phenomenon which is limited in over-hygienic environments. Environmental exposure thus seems to be an important risk factor as genetic predisposition for developing EGID. For example, one US study recently demonstrated that the increased prevalence of EoE parallels that of bronchial asthma in common geographical areas, being higher in urban as compared with rural settings,[9,10] as well as in cold climate zones compared with tropical and arid areas.[11]

Except for EoE, available data about the epidemiology of EGID in general and EGE in particular are limited. Due to its low prevalence, most of accumulated knowledge on EGE comes from individual case reports and short case series. Because these methods lack systematization, it is impossible to establish well-based conclusions or even a consensus with regard to diagnostic criteria: the density of eosinophilic infiltration or its precise location in the layers of the wall of the digestive tract vary widely from one study to the other. Since a certain eosinophil count can form part of the normal histology of the stomach and small bowel walls, and because this can vary between different geographical areas,[8] a commonly accepted diagnostic criteria for EGE has not yet been defined. Still, an increase in the prevalence of EGE could have existed in several settings during the last years. In fact, the number of studies on EGE referenced in PubMed in the last decade has doubled since the 1980s representing almost 40% of the overall available scientific information on the disease.

Reported cases of EGE show no predominance of individuals of any gender or race. Although it can affect all ages, the majority of cases occur in adults in the third to the fifth decades of life,[12–15] with pediatric series also being described.[16,17] While no accurate epidemiological estimations for EGE exist to date, an incidence of approximately one case per 100,000 inhabitants has been traditionally proposed.[3,14] However, these figures have been recently updated after an American electronic survey which estimated an overall prevalence of 28 per 100,000 EGE or colitis.[10] Most patients are diagnosed during an endoscopic examination for a variety of symptoms, usually abdominal pain or diarrhea. An internet database has been set up recently in order to register cases and further clarify many of the unknowns of the disease.[18]

Finally, it must be taken into account that a better awareness of EGID (and of EGE in particular) by clinicians and pathologists forms the cornerstone of accurate diagnosis of the disorder, which may subsequently contribute to the rise in its epidemiology, especially in different parts of Europe.

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