SEX...

...actually has almost nothing to due with Eosinophilic esophagitis (EE). In fact, study results show there is a highly conserved EE transcript profile between patients of different sex, age, and allergic status. (1)

Esophagitis describes any inflammation of the esophagus and is most commonly caused by acid reflux. In this case esophageal epithelium is damaged by acid, leaked from the stomach, because it lacks the protective mucosa of gastric epithelium. DAMP’s initiate local inflammation via innate immunity.

In EE there is an abnormal infiltration of eosinophils in the epithelium of the esophagus. Because of the involvement of eosinophils in allergy and because many EE patients suffer from other allergic diseases it is believed that EE is caused by allergy (Type I immunopathology), but at this time the specific allergen is unknown. This being said there are also atopic cases in which EE patients are nonallergic. The major symptom associated with EE is dysphagia (difficulty swallowing). Narrowing of the esophagus is caused by cellular inflammation and an expansion of the basal layer due to inflammatory damage. During endoscopy and barium swallow, rings or furrows may be present in the esophagus. Proper diagnosis requires biopsy to visualize the presence of eosinophils, which are not seen in other cases of esophagitis.

Dr. Marc Rothenberg's laboratory has described several genes with pathological importance in EE. Most notable is the up regulation of eotaxin-3, which is a chemoattractant for eosinophils and mast cells. A SNP in eotaxin-3 has also been correlated with disease susceptibility and CCR3 (eotaxin-3 receptor) knockout mice show resistance to experimentally induced EE. (1)

Sometimes EE can be treated with dietary modification but if the allergen is not found, medical therapy and mechanical dilation of the esophagus are needed. Drug therapies include swallowed corticosteroids, anti-IL-5 (mepolizumab), and antihistamines. The effectiveness of these drugs among patients suggests a few things regarding disease pathology. Immediate hypersensitivity to an allergen can be controlled by antihistamine, leading one to believe there is an allergic element to EE. IL-5 stimulates the growth of eosinophils. A Th2 association may be possible as anti-IL-5 inhibits said chemical message. Patients that do not respond to antihistamines but show improvement when treated with steroids imply a possible late-phase reaction. Maybe this is due to chronic exposure to an allergen, which no longer stimulates mast cells but is causing Th2-mediated cellular infiltration.

Maybe you shouldn’t go eat worms?

1. Blanchard C, Wang N, Stringer KF, Mishra A, Fulkerson PC, Abonia JP, Jameson SC, Kirby C, Konikoff MR, Collins MH, Cohen MB, Akers R, Hogan SP, Assa'ad AH, Putnam PE, Aronow BJ, Rothenberg ME (February 2006). "Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis". J. Clin. Invest. 116 (2): 536–47. doi:10.1172/JCI26679. PMC 1359059. PMID 16453027.
2. http://en.wikipedia.org/wiki/Eosinophilic_esophagitis#cite_ref-pmid16453027_4-0
3. http://www.medicinenet.com/eosinophilic_esophagitis/article.htm