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Atopy asthma

Cysteinyl leukotiiene receptor G300S Atopy/asthma association Gain of function (167,287-292) n s... [Pg.165]

Rare reports of T immu-noglobuhn E levels/atopy Asthma... [Pg.166]

A history of atopy (asthma, hay fever or eczema) or of allergy to any injected substance is frequently seen in patients reacting to anaesthetic drugs and this association can be confirmed statistically. In most of these cases there is probably a raised IgE level, but this is not an essential feature in patients having true hyper-sensitivity reactions. Repeated exposure to... [Pg.278]

Anaphylaxis, atopy, asthma. Mediated by IgE. Autoimmune haemolytic anaemia, Goodpasture s syndrome, thrombocytopaenia. Mediated by IgM or IgG and complement. [Pg.243]

Atopy/asthma association Tristan da Cunha population Gain of function [10,385-390]... [Pg.198]

Noguchi E, Shibasaki M, Arinami T, et al No association between atopy/asthma and the ILeSOVal polymorphism of IL- 4 receptor. Am J Respir Crit Care Med 1999 160 342-345. (Ill)... [Pg.32]

Musaliri S, van Meeibeeck J, Musango L, Brusselle G, Joos G, Seminega B (2011) Prevalence of atopy, asthma and COPD in an urban and a rural area of tm African country. Respir Med 105 1596-1605... [Pg.62]

It has to be distinguished between mucosal atopy (asthma, hay fever) and atopic skin diathesis (ASD) regarding the risk of developing OCD. Nowadays, there is sufficient evidence that mucosal atopy, without skin manifestations, is not associated with increased risk of ICD (Rystedt 1985 Diepgen and Fartasch 1993, Diepgen et al. 1993, Majoie et al. 1996). [Pg.11]

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]

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]

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]

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

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]

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]

Von Hertzen LC, Haahtela T Asthma and atopy - the price of affluence Allergy 2004 59 124-137. [Pg.121]

Palmer LJ, Celedon JC, Weiss ST, Wang B, Fang Z, Xu X Ascaris lumbricoides infection is associated with increased risk of childhood asthma and atopy in rural China. Am J Respir Crit Care Med 2002 165 1489-1493. [Pg.121]

El Biaze M, Boniface S, Koscher V, Mamessier E, Dupuy P, Milhe F, et al T cell activation, from atopy to asthma more a paradox than a paradigm. Allergy 2003 58 844-853. [Pg.172]

The IgE-mediated food allergy is one of the main atopie diseases. Its symptoms, espeeially among ehildren, are not disease-eharaeteristie. GI symptoms observed after an ingestion of partieular food are eommonly thought to be the result of previously diagnosed respiratory or skin disorders, thus food allergy may remain misdiagnosed if it eoexists with asthma or atopie eezema/dermatitis. [Pg.119]

Matricardi, P.M., et al. (2000). Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma, epidemiological study, B.M.J., 320, 412-417. [Pg.124]

The subject of possible relation of the acute byssinotic response in a cotton mill to asthma in general and to atopy is one on which there appears to be relatively little information. [Pg.217]

Certain Investigators, however, have expressed interest in the matter recently. The possibility that a history of asthma may increase the probability of an acute byssinotic reaction to cotton dust is suggested by a paper by Hamilton et al. ( ). The senior author of this paper had had asthma as a child. Promptly after exposure to the air in a dusty part of a cotton mill he exhibited pronounced shortness of breath with tightness in the chest and accompanying major temporary decreases in FEVi and arterial oxygen tension. The episode is described as "byssinosis". The authors remark It is unlikely that many textile workers with an initial response to cotton dust such as the one described here would remain working in dusty areas." Although the authors state that "It is not possible from the present study to conclude that a prior history of atopy confers sensitivity to cotton dust", the present writers were left with the impression that the authors suspect that such may be the case. [Pg.218]

Jones et al. (49) also point to a possible connection between atopy and risk of byssinosis. Most but not all persons with extrinsic asthma exhibit atopy (50). From observations on 255 workers in four cottonseed crushing mills, Jones et al. (49) conclude that "Atopy and exposure to dust were found to have significant interaction large mean declines in FEVi and FEF25-75 occurred only in the workers exposed to 1 inter dust who were also atopic." They also state "These findings point to atopy as a risk factor in the bronchoconstrictor response to cotton dust aerosol, and, by inference, a risk in byssinosis. [Pg.218]

There is therefore a need to investigate atopy, particularly as that variable may interact with dust exposure, in cotton textile mills." The reader is left with the thought that perhaps "reactors" who exhibit symptoms of acute byssinosis in a cotton mill might be in some sense people who are not obvious asthmatics but who, however, have some minimal or borderline type of asthma or other mildly increased bronchial sensitivity. Merchant et al. (51) tested workshift declines in FEVi workers exposed to cotton dust. In their summary they state "The patterns of FEVi response over a week suggest that there are distinct individual patterns of response not dependent upon previous cotton dust exposure."... [Pg.218]

Fig. 8.2 Alignment of the protein structure of the cysteinyl leukotriene 1 (CysLTj) and 2 (CysLT ) receptors in relation to rhodopsin. The amino acids conserved between these family A receptors are shown. The consensus is greater than 50%. These data formed the basis of the model predicting the CysLTj and CysLT transmembrane domains (helices 1-7), the four [3-sheets, and the putative cysteinyl leukotiiene-binding domain. The amino acid variants that are associated with atopy or asthma, the G300S CysLTj variant, and the M201V CysLT variant are each boxed and noted with arrows... Fig. 8.2 Alignment of the protein structure of the cysteinyl leukotriene 1 (CysLTj) and 2 (CysLT ) receptors in relation to rhodopsin. The amino acids conserved between these family A receptors are shown. The consensus is greater than 50%. These data formed the basis of the model predicting the CysLTj and CysLT transmembrane domains (helices 1-7), the four [3-sheets, and the putative cysteinyl leukotiiene-binding domain. The amino acid variants that are associated with atopy or asthma, the G300S CysLTj variant, and the M201V CysLT variant are each boxed and noted with arrows...

See other pages where Atopy asthma is mentioned: [Pg.366]    [Pg.414]    [Pg.366]    [Pg.414]    [Pg.436]    [Pg.310]    [Pg.148]    [Pg.544]    [Pg.578]    [Pg.581]    [Pg.383]    [Pg.192]    [Pg.114]    [Pg.129]    [Pg.181]    [Pg.192]    [Pg.124]    [Pg.145]   
See also in sourсe #XX -- [ Pg.31 ]




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