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allergy The diagnosis and management of anaphylaxis: An updated practice parameter.
Lieberman P, Kemp SF, Oppenheimer J, Lang DM, Bernstein IL, Nicklas RA, Anderson JA, Bernstein DI, Bernstein JA, Fink JN, Greenberger PA, Ledford DK, Li J, Sheffer AL, Solensky R, Wolf BL, Blessing-Moore J, Khan DA, Lee RE, Portnoy JM, Schuller DE, Spector SL, Tilles SA.
These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma and Immunology; the American College of Allergy, Asthma and Immunology; and the Joint Council of Allergy, Asthma and Immunology. The American Academy of Allergy, Asthma and Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing "The diagnosis and management of anaphylaxis: an updated practice parameter." 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, and the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion. 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.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15753926&dopt=Abstract allergy medicine
allergy [In Process Citation]
[Article in Croatian]
Janosevic Lj, Janosevic S, Stankovic P, Djukic V, Stosic-Divjak S, Dotlic J, Racic A.
Institut za otorinolaringologiju i maksilofacijalnu hirurgiju Klinickog centra Srbije, Beograd.
Almost one third to one half of all patients in otorhinolaryngologic practice experience some kind of inflammation of the upper respiratory tract out of which allergic mechanisms, either as primary factors or secondary ones, appear in 30-40% of adults and 60-80% of children and adolescents. The objective of this study was to analyse inflammatory conditions of the upper airways on the basis of allergic state of the patient and to establish the classification that will respect the actual immunological alteration level (subclinical allergy, clinical allergy) and spreading (localized allergy, generalized allergy). Inclusion criteria for all sixty nine patients were the diagnosis of chronic upper airway inflammation and their exposition just to ubiquitous allergens. Diagnostic procedure included anamnesis, physical examination and allergic in vivo testing of the skin and nasal mucosa to inhalant allergens. The certain categories of results were established for the skin prick-test (positive, negative, indefinite), specific nasal provocation test (positive, negative, hyperreactive) and nasal symptoms (present, absent). By using a strictly determined combination of results, we were able to define the six groups in our classification: nasal clinical allergy (30% of patients), non-nasal clinical allergy (19% of patients), localized nasal allergy (11% of patients), latent allergy (3% of patient), nonspecific nasal hyperreactivity (12% of patient) and non-allergic inflammation (25% of patients). Our classification takes into consideration the modern knowledge in the field of allergology and may bring an additional quality in respect to selection of therapy options, long-term follow-up of allergy status evolution in the individual person as well as intragroup and intergroup analysis of parameters important to evaluate the effects of antiallergic prevention or therapy.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15756793&dopt=Abstract allergy medicine
allergy [Latex allergy--Part II]
[Article in Polish]
Chelminska M.
Klinika Alergologii Katedry Pneumonologii i Alergologii Akademii Medycznej w Gdansku.
Diagnosis of latex allergy consists of four methods: anamnesis, skin tests, laboratory examinations and specific allergen challenge. Anamnesis is the source of information on the symptoms and reactions of IgE-dependend allergy, different accompanying factors and atopy diseases. The recognition of latex allergy is possible with positive SPT and/or sIgE (latex). Specific allergen challenge is performed in situation with positive anamnesis, negative SPT and negative sIgE (latex). Latex allergy treatment is not defferent than other allergic diseases. Specific immunotherapy is new methods in these cases. Because of absence of standardized latex allergens, this method is still on experimental issue. The inconsistent results do not allow the recomendation of immunotherapy in everyday practice. The most important profilactic activity in case of latex allergy is to reduce the exposition to latex among the medical staff and the patients.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15757281&dopt=Abstract allergy medicine
allergy Cytokines, allergy, and asthma.
Ngoc LP, Gold DR, Tzianabos AO, Weiss ST, Celedon JC.
aChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA bPediatric Pulmonary Medicine, Massachusetts General Hospital for Children and Harvard Medical School, Boston, MA, USA cDepartment of Medicine, Harvard Medical School, Boston, MA, USA dDivision of Pulmonary/Critical Care Medicine, Beth Israel Deaconess Med. Ctr, Boston, MA, USA.
PURPOSE OF REVIEW: This review examines recent articles on the relationship of cytokines to allergy and asthma with particular emphasis on immune mechanisms involved in disease development in early life. RECENT FINDINGS: It was previously proposed that reduced microbial exposure in early life is responsible for a shift of the Th1/Th2 balance in the immune system towards the proallergenic Th2 response. This Th1/Th2 imbalance results in the clinical expression of allergy and/or asthma. In recent years, accumulating data from mice and humans have identified Th2 cytokines [interleukin (IL)-4, IL-13, and IL-5] as major contributors to allergy and asthma. Interestingly, the Th1 cytokine interferon-gamma has recently been shown to act concurrently with Th2 cytokines in maintaining the chronic inflammatory response in allergic diseases, particularly in asthmatic airways. Most recently, evidence suggests that suppression of T-regulatory cells may contribute to the underlying immune mechanisms involved in allergy and asthma. SUMMARY: An enhanced Th2 immune response and the elaboration of cytokines such as IL-4, IL-13, and IL-5 contribute to the induction of allergy and asthma. Interferon-gamma, a Th1 cytokine, acts in conjunction with Th2 (IL-4, IL-13, and IL-5) in maintaining chronic allergic inflammation. The mechanisms leading to an enhanced Th2 response are still controversial. Th2-dominated immune responses may result from immune suppression of T-regulatory cells as well as Th1 cells. Understanding early-life immune mechanisms responsible for atopic diseases, specifically how cytokines of T-regulatory cells act to balance the Th1 and Th2 immune response, continues to be a fruitful area of research.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15764907&dopt=Abstract allergy medicine
allergy Intestinal worms and human allergy.
Cooper PJ.
Laboratorio de Investigaciones, Hospital Pedro Vicente Maldonado, Pichincha Province, Ecuador.
SUMMARY The immunoepidemiological interactions between intestinal worm (or geohelminth) infections and allergy are of great interest to parasitologists, immunologists, and allergists because of the close similarities between the human immune response to geohelminth parasites and environmental allergens. Allergic diseases appear to be most rare in populations living in the rural tropics with high rates of infection with geohelminth parasites, and this has led to suggestions that the relationship between geohelminth infections and allergy may be causal. Allergic sensitization and disease results from a complex interaction between environmental exposures and genetic background, and the numerous epidemiological studies that have investigated the relationship between allergy and geohelminth infections have provided conflicting findings. The strongest epidemiological evidence for a causal association is provided by intervention studies that demonstrate evidence for an effect of anthelmintic treatment on atopy or asthma risk. There is evidence also for an inverse relationship between geohelminth infection and either atopy or asthma symptoms from cross-sectional studies that have been conducted in areas of high infection prevalence. Chronic geohelminth infections could affect allergy risk by modulation of the immune response to environmental allergens, and an area of great research activity at present is the investigation of the role of regulatory T cells in modulating host inflammatory responses. However, a causal association between geohelminth infections and allergy remains to be proven, and prospective and intervention studies are required that investigate the development of allergy in early life at a time when humans are first exposed to geohelminth parasites and their antigens.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15771681&dopt=Abstract allergy medicine
allergy Prevalence of latex allergy in the community at age 7 years.
Roberts G, Lack G, Northstone K, Golding J; the ALSPAC Study Team.
Paediatric Allergy, Asthma and Immunology, Imperial College at St Mary's, London, UK.
Summary Background Latex allergy has been highlighted as a problem in children during the last decade based on a number of case series of children with particular problems such as spina bifida. The actual prevalence of latex allergy in the general United Kingdom population is unclear. Objective To estimate the prevalence of childhood latex allergy in the general population. Methods The Avon Longitudinal Study of Parents and Children is a geographically based cohort that has been prospectively followed since birth. The children were invited for skin prick testing at 7 years of age. Results Four subjects out of 1877 tested were sensitized to latex. None had a history of clinical reactions to latex. Conclusion This study suggests that the prevalence of latex sensitization and clinical latex allergy in the general childhood population are very low, 0.2% (95% confidence interval 0.1-0.6%) and 0.0% (0-0.2%), respectively.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15784106&dopt=Abstract allergy medicine
allergy Putative regulatory T cells are impaired in cord blood from neonates with hereditary allergy risk.
Haddeland U, Karstensen AB, Farkas L, Bo KO, Pirhonen J, Karlsson M, Kvavik W, Brandtzaeg P, Nakstad B.
Laboratory for Immunohistochemistry and Immunopathology (LIIPAT), Institute of Pathology, University of Oslo, Rikshospitalet University Hospital, Oslo, Norway.
Haddeland U, Karstensen AB, Farkas L, Bo KO, Pirhonen J, Karlsson M, Kvavik W, Brandtzaeg P, Nakstad B. Putative regulatory T cells are impaired in cord blood from neonates with hereditary allergy risk. Pediatr Allergy Immunol 2005. (c) 2005 Blackwell MunksgaardThe hygiene hypothesis implies that the increasing prevalence of allergy in 'westernized' countries is explained by reduced bacterial exposure in early life, but the underlying mechanism remains elusive. We therefore wanted to study the effect of bacterial lipopolysaccharide (LPS) on the generation of regulatory T (T(R)) cells in neonates, and to analyze differences between neonates with allergy risk because of a family history of atopy (FH(+)) and controls without such hereditary risk (FH(-)). Cord blood mononuclear cells from the FH(+) and FH(-) groups were stimulated with beta-lactoglobulin in the presence of LPS. T-cell phenotypes suggestive of T(R) cells [CD25(+), CD25(high) and integrin (CD103(+))], and the intracellular proliferation antigen Ki-67 were quantified by flow cytometry. Release of the immunosuppressive cytokine transforming growth factor beta1 (TGF-beta1) from its inactive complex was determined by enzyme-linked immunosorbent assay. The analyses revealed the generation of T-cell phenotypes suggestive of T(R) cells including a CD25(high) T-cell subset which was inversely related to T-cell proliferation (r = -0.54, p < 0.05) and to activation-induced release of TGF-beta1 (r = -0.80, p < 0.001). The CD25(high) T-cell subset tended to be impaired in the FH(+) group (% of CD3(+) T cells: FH(+), 5.1% vs. FH(-), 12.6%), and notably, the FH(+) group showed a significantly reduced capacity for generation of both CD25(+) (FH(+), 16.2% vs. FH(-), 34.9%; p < 0.01) and T cells (FH(+), 2.1% vs. FH(-), 3.9%; p < 0.05). Our findings suggested that early-life exposure to a dietary antigen in the presence of LPS might modulate the immune system by generating T(R) cells. This capacity was impaired in neonates with hereditary allergy risk, but clinical follow-up will be required to determine a possible effect on allergy emergence.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15787866&dopt=Abstract allergy medicine
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