I have EC and am in contact with many other people who do also. We tend to be very sick and stay quite sick for a long period of time, I have never heard of anyone "getting better". Oral Allergy Syndrome is a common underlying cause or trigger, which is when environmental allergies (usually to tree pollen such as birch or alder) cause cells in the GI tract to react leading to GI tract symptoms. This is very hard to figure out on your own. OAS usually causes intense itching and scratchy feeling in your mouth and throat and can feel like anaphylaxis. If you develop an Eosinophilic GI Disease such as EC, exposure to the allergen in the environment can cause you to have GI symptoms such as pain, burning sensation, cramping, and diarrhea. However, many people never figure out if they have allergen triggers or what they are. People with EC commonly also have excess numbers of eosinophils in other parts of the GI tract too. Treatment doesn't tent to help much and we often end up only able to consume 10 or fewer different foods. It's not uncommon for us to not tolerate any foods at all, or only one or two which can't provide enough nutrition or calories, so we end up consuming a medical food replacement called "elemental formula". In severe cases like mine, people end up TPN-dependent. This is when all of a person's nutrition and calories are given intravenously through a central line, which is a semi-permanent IV line placed in your arm or chest, in order to completely bypass the GI tract. Feeding tubes don't generally help people with EC because they don't bypass the colon. Most people on TPN due to EC do not eat at all. It is invasive and considered high risk, but people can do well and live for decades this way. You get used to it. Honestly the relief from the symptoms means it's actually a big improvement in quality of life, even with the complications.
Strong association of mast cells with eosinophilic esophagitis-specific signatures
“Several studies have consistently found increased intraepithelial MCs in EoE biopsies, and positive correlations with some disease markers have also been reported. Our analyses reveal a broad and striking relationship between MCs and most EoE transcriptional signatures, including inflammation, eosinophil recruitment, epithelial remodeling, and fibrosis. Although these findings are strictly correlative, they significantly add to the body of evidence for MC involvement in EoE pathogenesis and suggest these cells may be a key disease driver. Given the limited clinical effect of eosinophil-directed therapies in EoE to date, our data support exploring the clinical benefit of anti-MC agents in EoE.”
Expression of CD25, mast cell markers and T-cell markers in eosinophilic esophagitis
“mast cells were highlighted by CKIT and tryptase in EOE, and not seen in other clinically mimicking cases. There were also significantly higher densities of CD25 and pan-T-cell marker staining in EOE cases. These findings suggest an inflammatory cellular milieu in EOE, beyond just eosinophils, that can be demonstrated by immunohistochemistry”
“Abonia et al. described the presence of a mast-cell-associated transcriptome in EOE, corroborated by a subsequent study that found strong correlation between mast cell-specific protease carboxypeptidase A3 (CPA3) and transcripts of genes involved in fibrosis and epithelial remodeling.”
