Atopy patch testing has been used in some cases for the potential identification of delayed, non-IgE (cell-mediated) reactions. Diagnostic criteria
The diagnosis of eosinophilic esophagitis requires all of the following:

Symptoms related to esophageal dysfunction. Eosinophil-predominant inflammation on esophageal biopsy, characteristically consisting of a peak value of ≥15 eosinophils per high power field (HPF). Exclusion of other causes that may be responsible for symptoms and esophageal eosinophilia. Treatment
The goal of EoE treatment is to control the symptoms by decreasing the number of eosinophils in the esophagus and, subsequently, reducing the esophageal inflammation. Management consists of dietary, pharmacological, and endoscopic treatment. Dietary management
Dietary treatment can be effective, as there does appear to be a role of allergy in the development of EOE. Allergy testing is not particularly effective in predicting which foods are driving the disease process. If no specific allergenic food or agent is present, a trial of the six food elimination diet (SFED) can be pursued. Various approaches have been tried, where either six food groups (cows milk, wheat, egg, soy, nuts and fish/seafood), four groups (animal milk, gluten-containing cereals, egg, legumes) or two groups (animal milk and gluten-containing cereals) are excluded for a period of time, usually six weeks. A "top down" (starting with six foods, then reintroducing) approach may be very restrictive. Four- or even two-group exclusion diets may be less difficult to follow and reduce the need for many endoscopies if the response to the limited restriction is good.Alternative options to SFED includes the elemental diet, which is an amino acid based diet.
Pleural thickening is an increase in the bulkiness of one or both of the pulmonary pleurae. Causes
Pleural plaques
Pleural plaques are patchy collections of hyalinized collagen in the parietal pleura. They have a holly leaf appearance on X-ray. They are indicators of asbestos exposure, and the most common asbestos-induced lesion. They usually appear after 20 years or more of exposure and never degenerate into mesothelioma. They appear as fibrous plaques on the parietal pleura, usually on both sides, and at the posterior and inferior part of the chest wall as well as the diaphragm. See also
Pleural disease


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