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As a chronic inflammatory disease with eosinophilic infiltrate of the esophagus, eosinophilic esophagitis (EoE) causes a variety of gastrointestinal (GI) clinical manifestations. None of the symptoms, endoscopic features, or biopsy findings is pathognomonic of the disease, even with high degrees of esophageal eosinophilia. The pathogenesis has been explored by several studies, yet it still far from being completely understood. Evidence supports a role of allergen-driven Th2 lymphocyte mechanism, though not in every patient. This article addresses the disease's clinical manifestations, endoscopic findings, diagnosis, and differential diagnoses. In addition to the current diagnostic criteria, we summarize some recently emerging procedures that promise of enhancing more precise diagnosis and institution of early appropriate management, with consequent better quality of life and reduction of complications.

Food allergy is mostly a childhood disease that differs from the adult-onset allergy in several aspects, including the prevalence, commonly offending foods, symptomatology, and prognosis. The prevalence is much overestimated by the public, but it probably affects up to 6% of children. In some cases, the diagnosis might be clearly evident, but in most cases an expert evaluation may be needed that usually includes verification by challenge testing. Currently, the management of food allergy is avoidance of the offending foods together with the availability of pharmacologic agents for symptomatic treatment, including self-administered epinephrine. The latter is of utmost importance in highly allergic subjects because accidental trivial exposure is not uncommon. Recent studies promise immunomodulatory agents that might be of potential use for prophylaxis. One such agent is anti-immunoglobulin E, which might be available in the near future.

Though not widely recognized, food hypersensitivity by inhalation can cause major morbidity in affected individuals. The exposure is usually more obvious and often substantial in occupational environments but frequently occurs in non-occupational settings, such as homes, schools, restaurants, grocery stores, and commercial flights. The exposure can be trivial, as in mere smelling or being in the vicinity of the food. The clinical manifestations can vary from a benign respiratory or cutaneous reaction to a systemic one that can be life-threatening. In addition to strict avoidance, such highly-sensitive subjects should carry self-injectable epinephrine and wear MedicAlert® identification. Asthma is a strong predisposing factor and should be well-controlled. It is of great significance that food inhalation can cause de novo sensitization.

BackgroundSkin testing (ST) is the most common screening method for allergy evaluation. Measurement of serum specific IgE is also commonly used, but less so by allergists than by other practitioners. The sensitivity and specificity of these testing methods may vary by type of causative allergen and type of allergic manifestation. We compared ST reactivity with serum specific IgE antibodies to common indoor allergens in patients with respiratory allergies.Methods118 patients (3 mo-58 yr, mean 12 yr) with allergic rhinitis and/or bronchial asthma had percutaneous skin testing (PST) supplemented by intradermal testing (ID) with those allergens suspected by history but showed negative PST. The sera were tested blindly for specific IgE antibodies by the radioallergosorbent test (Phadebas RAST). The allergens wereD. farinae(118), cockroach (60), cat epithelium (90), and dog epidermal (90). Test results were scored 0–4; ST ≥ 2 + and RAST ≥ 1 + were considered positive.ResultsThe two tests were in agreement (i.e., either both positive or both negative) in 52.2% (dog epidermal) to 62.2% (cat epithelium). When RAST was positive, ST was positive in 80% (dog epidermal) to 100% (cockroach mix). When ST was positive, RAST was positive in 16.3% (dog epidermal) to 50.0%(D. farinae). When RAST was negative, ST was positive in 48.5% (cat epithelium) to 69.6% (D. farinae). When ST was negative, RAST was positive in 0% (cockroach) to 5.6% (cat epithelium). The scores of ST and RAST showed weak to moderate correlation (r = 0.24 to 0.54). Regardless of history of symptoms on exposure, ST was superior to RAST in detecting sensitization to cat epithelium and dog epidermal.ConclusionFor all four indoor allergens tested, ST was more sensitive than RAST. When both tests were positive, their scores showed poor correlation. Sensitizations to cat epithelium and dog epidermal are common, even in subjects who claimed no direct exposure.

Summary: Using radioimmunoassay techniques, we measured IgE and IgD levels in paired colostrum and plasma samples obtained within 4 days postpartum. In colostrum, IgE was detected in concentrations of 0.5–6 IU/ml in 16 out of 39 samples (41%) and < 0.5 IU/ml in the remainder, whereas IgD was detected in all samples in concentrations of 2–2000 μg/dl. Only a moderate correlation was found between colostral and plasma levels of both IgE (r = + 0.60) and IgD (r = +0.74). The correlation coefficient between IgE and IgD in plasma was 0.23, whereas in colostrum it was only 0.05. The colostrum:plasma ratio of IgE varied strikingly from that of IgD; tbe ratio of IgD was 0.1–22.2 times that of IgE. The findings argue against passive transfer of IgE and IgD from the circulation to milk and suggest possible local mammary production of either or both of these two immunoglobulins. Speculation: In some patients, local production of IgE and/or IgD probably occurs in the mammary gland. One may hypothesize that previous antigenic exposure at other mucosal surfaces may not only determine the IgA antibody content of milk but also may influence the specificity of antibodies belonging to other immunoglobulin classes that appear in human milk. Whether the IgE and IgD antibodies in breast milk have similar specificities for antigens as the IgA antibodies in milk remains an interesting but unanswered question.

141 serial blood samples were obtained from 19 patients (14-40 yr) with HA+IM including 9 from whom pre-illness samples were available. All specimens were simultaneously studied immunologically, and most were studied hematologically and serologically. IgE was determined by a paper disc solid phase radioimmunoassay, and IgM by single radial immunodiffusion.