Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Atopy

ATOPY Hypersensitivity where tendency to allergy is inherited. [Pg.10]

As noted earlier, routes other than inhalation must also be eonsidered. Thus exposure to a substanee whieh ean be hazardous upon ingestion, absoiption tlirough tlie skin or mueous membranes, or eontaet with skin or mueous membranes needs eontrol to a standard sueh that nearly all the population eould be exposed repeatedly without any adverse health effeet. (Note that this will not neeessarily proteet those who are atopie or with a relevant pre-existing eondition, e.g. dermatitis.)... [Pg.115]

Atopy is the propensity to develop allergic reactions mediated by immunoglobulin E. [Pg.229]

There are few definitive data to substantiate the efficacy of LTRA therapy in refractory asthma, except for patients with aspirin-sensitive asthma. This is a fairly uncommon form of asthma that occurs generally in adults who often have no prior (i.e., childhood) history of asthma or atopy, may have nasal polyposis, and who often are dependent upon oral corticosteroids for control of their asthma. This syndrome is not specific to aspirin but is provoked by any inhibitors of the cycloxygenase-1 (COX-1) pathway. These patients have been shown to have a genetic defect that causes... [Pg.688]

The role of atopy in anaphylaxis has not completely been resolved. On the one hand there is for example no evidence of a higher risk of severe reactions in venom-allergic patients. A recent study by Sturm et al. [38] indicated that patients with high total IgE levels predominantly developed mild to moderate reactions. By contrast, atopy may increase the risk and severity of systemic reactions in beekeepers and their family numbers [39]. On the other hand, atopy and in particular allergic asthma are risk factors for food allergy and therefore are also important risk factors for food-induced anaphylaxis. This is most likely also true for exercise-induced anaphylaxis, but also non-IgE-dependent anaphylaxis induced by NSAIDs or contrast media. [Pg.18]

The role of atopy among drug-induced anaphylaxis depends probably on the elici-tating drug here clearly more data are needed. [Pg.18]

Siroux V. Curt F. Oryszczyn MP, Maccario J, Kauff-mann F Role of gender and hormone-related events on IgE. atopy, and eosinophils in the Epidemiological Study on the Genetics and Environment of Asthma, dO bronchial hyperresponsiveness and atopy. J Allergy Clin Immunol 2004 114 491-498. [Pg.21]

The terms allergy and atopy are in close proximity of our lives in the new millennium since our lifestyles have enormously changed. Encounters with various new molecules in air, water and diet, living in a more polluted world with less exposure to infections, and infectious agents are supposed to be the major causative factors added to the genetic propensity of developing IgE antibodies responsible for symptoms and... [Pg.22]

History. This includes the severity grading of the clinical reaction, the time of administration and onset of symptoms, the concomitant use of other drugs, foods or compounds (latex), previous history of drug allergy, atopy in the personal or family history, other underlying conditions such as mastocytosis or Cl esterase inhibitor deficiency. The actual preparation in its galenic identity should be stored or at least listed. [Pg.197]

Asthma results from a complex interaction of genetic and environmental factors however, the underlying cause is not well understood. There appears to be an inheritable component, as the presence of asthma in a parent is a strong risk factor for the development of asthma in a child. This risk increases when a family history of atopy is also present.13 Approximately 50% of asthma can be attributed to atopy, and atopic asthma is more common in children than adults.3 Furthermore, atopy in childhood asthma is the strongest prognostic factor for continued asthma as an adult.1,3... [Pg.210]

Genetic factors cannot explain the recent rapid rise in asthma prevalence. Asthma appears to require both genetic predisposition and environmental exposure. Many patients with occupational asthma develop the disease late in life upon exposure to specific allergens in the workplace. Environmental influences in utero or in infancy may contribute to the development of asthma. Maternal smoking during pregnancy or exposure to secondhand smoke after birth increases the risk of childhood asthma.3 Adult-onset asthma is not uncommon and may be related to atopy, nasal polyps, aspirin sensitivity, occupational exposure, or a recurrence of childhood asthma. [Pg.210]

Major factors that may contribute to the severity of asthma include allergens typically associated with atopy chemical exposures in occupational environments and exposure to tobacco smoke, irritants, and indoor and outdoor pollution. Other factors include concurrent disease states or medications that may worsen asthma severity. [Pg.211]

Atopy A genetic predisposition to develop type I hypersensitivity reactions against common environmental antigens commonly seen in patients with allergic rhinitis, asthma, and atopic dermatitis. [Pg.1561]

Zimmerman B, Enander I, Zimmerman R, Ahlstedt S. Asthma in children less than 5 years of age eosinophils and serum levels of the eosinophil proteins ECP and EPX in relation to atopy and symptoms. Clin Exp Allergy 1994 24 149-155. [Pg.230]

Palmer LJ, Cookson WOCM. Atopy and asthma. In Genetic Analysis of Multifactorial Diseases (Sham PC, Bishop T,... [Pg.232]

Aim JS, Swartz J, Lilja G, Scheynius A and Pershagen G (1999) Atopy in children of families with an anthroposophic lifestyle . Lancet, 353, 1485-1488. [Pg.38]

Devereux G and Seaton A. 2005. Diet as a risk factor for atopy and asthma. J Allergie Clin Inmunol 115 1109-1117. [Pg.39]

Signs include expiratory wheezing on auscultation, dry hacking cough, or signs of atopy (e.g., allergic rhinitis or eczema). [Pg.920]

JL-4 on IgE. Excessive IL-4 correlates with elevated IgE and risk of atopy. Kishikawa and coworkers [59] demonstrated that administration of IL-12, a potent Thl-promoting cytokine, to Pb-exposed mice restored the balance of Thl (IFN-y) versus Th2 cytokines (IL-6), which reduce corticosterone levels and enhanced host resistance in Listeria-infected mice. This observation links the role of Thl/Th2 balance in host resistance against disease and the potential signihcance of Pb in the disruption of that balance. [Pg.213]

Pre-employment screening of potential workers for risk factors associated with occupational asthma is not viable from a legal/ethical stand or from a practical point of view. Newman-Taylor estimated that seven atopic individuals would have to be denied employment in order to eliminate one case of OA [81]. Since asthma is a complex disease, focus on one risk factor (e.g., atopy) will have little impact on prevention. Investigators have suggested that this can lead to a false sense of control with the opportunity for greater disease [82],... [Pg.585]

Walusiak, J. et al., The risk factors of occupational hypersensitivity in apprentice bakers the predictive value of atopy markers, Int. Arch. Occup. Environ. Health, 75 Suppl, SI 17, 2002. [Pg.586]

Cullinan, P. et al., Allergen exposure, atopy and smoking as determinants of allergy to rats in a cohort of laboratory employees, Eur. Respir. J., 13, 1139, 1999. [Pg.587]

Gautrin, D., Ghezzo, H., and Malo, J.L., Rhinoconjunctivitis, bronchial responsiveness, and atopy as determinants for incident non-work-related asthma symptoms in apprentices exposed to high-molecular-weight allergens, Allergy, 58, 608, 2003. [Pg.587]

Ruiz, R.G., Kemeny, D.M. and Price, J.F., Higherrisk of eczema from maternal atopy than from paternal atopy. Clin. Exp. Allergy, 22, 762, 1992. [Pg.619]


See other pages where Atopy is mentioned: [Pg.436]    [Pg.72]    [Pg.310]    [Pg.229]    [Pg.229]    [Pg.1487]    [Pg.18]    [Pg.22]    [Pg.148]    [Pg.234]    [Pg.40]    [Pg.72]    [Pg.18]    [Pg.47]    [Pg.30]    [Pg.544]    [Pg.578]    [Pg.581]    [Pg.586]    [Pg.610]    [Pg.624]    [Pg.383]   
See also in sourсe #XX -- [ Pg.210 ]

See also in sourсe #XX -- [ Pg.152 , Pg.169 , Pg.217 ]

See also in sourсe #XX -- [ Pg.1863 ]

See also in sourсe #XX -- [ Pg.92 , Pg.327 , Pg.488 , Pg.492 , Pg.496 ]

See also in sourсe #XX -- [ Pg.59 , Pg.310 ]

See also in sourсe #XX -- [ Pg.338 ]

See also in sourсe #XX -- [ Pg.200 ]

See also in sourсe #XX -- [ Pg.10 , Pg.17 , Pg.46 , Pg.51 , Pg.52 , Pg.158 ]

See also in sourсe #XX -- [ Pg.261 , Pg.288 ]

See also in sourсe #XX -- [ Pg.10 , Pg.11 , Pg.356 , Pg.357 ]

See also in sourсe #XX -- [ Pg.125 ]

See also in sourсe #XX -- [ Pg.506 ]




SEARCH



Atopic syndrome atopy

Atopies barrier function

Atopies without dermatitis

Atopy and Antiallergic Therapy

Atopy asthma

Atopy dermatitis

Atopy environmental influences

Atopy sensitization

Atopy susceptibility genes

Food allergy atopy

Occupational atopy

© 2024 chempedia.info