These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology (AAAAI); the American College of Allergy, Asthma & Immunology (ACAAI); and the Joint Council of Allergy, Asthma and Immunology. The AAAAI and the ACAAI have jointly accepted responsibility for establishing "The Diagnosis and Management of Anaphylaxis Practice Parameter: 2010 Update." This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, or the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion.

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Heat shock protein (HSP) gp96/grp94 contains a signal peptide at the amino terminus and a -KDEL sequence at the carboxy terminus and is a major component of the lumen of the mammalian endoplasmic reticulum (ER). We show, by a number of immunolocalization methods using light and electron microscopy, that a significant proportion of intact gp96 molecules is also expressed on the cell surface. Surface gp96 molecules truly represent surface expression and do not result from adventitious deposition of gp96 released by dead cells on to the live cells in culture. Cell surface expression of gp96 is enhanced by heat shock and exposure to reducing agents. Gp96 molecules are not released from plasma membranes by repeated salt washes, and gp96 is not an integral membrane protein. Our observations suggest that gp96 and perhaps other HSPs are anchored to the cell surface as part of larger molecular complexes, which also transport them to the cell surface.o 1996 Wiley-Liss, Inc.

Background A large percentage of patients with aspirin exacerbated respiratory disease (AERD) report the development of alcohol-induced respiratory reactions, but the true prevalence of respiratory reactions caused by alcoholic beverages in these patients was not known. Objective We sought to evaluate the incidence and characteristics of alcohol-induced respiratory reactions in patients with AERD. Methods A questionnaire designed to assess alcohol-induced respiratory symptoms was administered to patients at Brigham and Women’s Hospital and Scripps Clinic. At least 50 patients were recruited into each of four clinical groups: 1) patients with aspirin challenge-confirmed AERD, 2) aspirin-tolerant asthmatics (ATA), 3) aspirin-tolerant patients with chronic rhinosinusitis (CRS), and 4) healthy controls. Two-tailed Fisher’s exact test with Bonferroni corrections were used to compare the prevalence of respiratory symptoms between AERD and other groups, with P≤0.017 considered significant. Results The prevalence of alcohol-induced upper (rhinorrhea/nasal congestion) respiratory reactions in patients with AERD was 75%, compared to 33% in ATA, 30% in CRS, and 14% in healthy controls (P<0.001 for all comparisons). The prevalence of alcohol-induced lower (wheezing/dyspnea) respiratory reactions in AERD was 51%, compared to 20% in ATA, and 0% in both CRS and healthy controls (P<0.001 for all comparisons). These reactions were generally not specific to one type of alcohol and often occurred after ingestion of only a few sips of alcohol. Conclusion Alcohol ingestion causes respiratory reactions in the majority of patients with AERD and clinicians should be aware that these alcohol-induced reactions are significantly more common in AERD than in aspirin-tolerant controls.