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We tested the effects of four eosinophil granule cationic proteins: major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO), and eosinophil-derived neurotoxin (EDN), on guinea pig tracheal epithelium in vitro. Examination by inverted microscopy revealed that MBP, both the form stabilized by alkylation of sulfhydryl groups as well as the native form of the molecule, ECP, EPO by itself, as well as EPO + H2O2 + halide, but not EDN, cause dose-related damage to the tracheal epithelium. The lowest concentrations of MBP and ECP causing damage were 10 and 100 micrograms/ml, respectively. In contrast, EDN, although biochemically similar to ECP, did not damage the tracheal epithelium in concentrations of up to 200 micrograms/ml. MBP caused exfoliation, as well as bleb formation and ciliostasis. EPO in the presence of the H2O2-producing enzyme glucose oxidase (GO), Cl-, 0.11 M, and iodide caused ciliostasis, bleb formation, and exfoliation of epithelial cells at concentrations as low as 1 U/ml (3.9 micrograms/ml). EPO + GO in the presence of Cl-, 0.11 M, alone or with Cl- and l-, 10(-4) M, or Cl- and Br-, 5 x 10(-5) M, were all toxic to epithelium. Surprisingly, EPO by itself caused partial ciliostasis, bleb formation, and exfoliation of epithelial cells in a dose-related manner at concentrations as low as 10 to 30 U/ml (39 to 121 micrograms/ml). These results confirm prior observations showing the toxicity of MBP to tracheal epithelium and indicate that ECP and EPO alone, as well as EPO + GO + halide, cause damage. Thus, several eosinophil granule proteins are able to damage respiratory epithelium.

Background We aimed to test the hypothesis that 3-D volume-based scoring of computed tomographic (CT) images of the paranasal sinuses was superior to Lund-Mackay CT scoring of disease severity in chronic rhinosinusitis (CRS). We determined correlation between changes in CT scores (using each scoring system) with changes in other measures of disease severity (symptoms, endoscopic scoring, and quality of life) in patients with CRS treated with triamcinolone. Methods The study group comprised 48 adult subjects with CRS. Baseline symptoms and quality of life were assessed. Endoscopy and CT scans were performed. Patients received a single systemic dose of intramuscular triamcinolone and were reevaluated 1 month later. Strengths of the correlations between changes in CT scores and changes in CRS signs and symptoms and quality of life were determined. Results We observed some variability in degree of improvement for the different symptom, endoscopic, and quality-of-life parameters after treatment. Improvement of parameters was significantly correlated with improvement in CT disease score using both CT scoring methods. However, volumetric CT scoring had greater correlation with these parameters than Lund-Mackay scoring. Conclusion Volumetric scoring exhibited higher degree of correlation than Lund-Mackay scoring when comparing improvement in CT score with improvement in score for symptoms, endoscopic exam, and quality of life in this group of patients who received beneficial medical treatment for CRS.

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Angioedema is a constellation of syndromes that present a great challenge to the clinician. The term "angioedema" describes the localized, transient, episodic edema of the deeper layers of the skin or of the mucosa of the gastrointestinal tract. Although angioedema may affect any part of the body, the skin and gastrointestinal tract are involved most commonly by far. Episodic abdominal pain arising from angioedema affecting any intra-abdominal organ may occur without skin angioedema; therefore, angioedema must be included in the differential diagnosis of intermittent, unexplained abdominal pain. Angioedema is caused by extravasation of plasma in the affected areas, which at times is accompanied by nonspecific, minimal cellular infiltrate. The most commonly identified causes of angioedema are medications, allergens, and physical agents, but most angioedema is idiopathic. Rare forms of angioedema associated with either hereditary or acquired faulty activation of the complement and kallikrein-kinin systems have been extensively described. Taking a comprehensive personal and family history, performing a physical examination, and compulsively monitoring the response to therapy are the most rewarding and cost-effective diagnostic and treatment tools. Diligent and knowledgeable follow-up by the attending physician spares patients costly and unnecessary tests as well as harmful treatment. The most effective treatment depends on the identification of the causative mechanism and--especially when the mechanism is not identified--on the clinician's knowledge and experience with innovative therapeutic regimens.

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