Steroid resistance in asthma: Our current understanding
Identifieur interne : 002F21 ( Main/Merge ); précédent : 002F20; suivant : 002F22Steroid resistance in asthma: Our current understanding
Auteurs : Alan K. Kamada ; Donald Y. M. Leung [États-Unis] ; Stanley J. Szefler [États-Unis]Source :
- Pediatric Pulmonology [ 8755-6863 ] ; 1992-11.
English descriptors
- Teeft :
- Abnormality, Adequate trial, Allergy, Allergy clin imrnunol, Allergy clin lmmunol, Alternative therapies, American lung association, Asthma, Asthmatic, Binding affinity, Bronchial asthma, Bronchoalveolar lavage fluid, Chronic asthma, Clin, Corrigan, Cutaneous vasoconstrictor response, Cyclosporin, Cytokine production, Data support, Early stage, Further inhibition, Glucocorticoid, Glucocorticoid burst therapy, Glucocorticoid receptor, Glucocorticoid receptor characteristics, Glucocorticoid therapy, Kamada, Lymphocyte, Lymphocyte cultures, Monocyte, Mononuclear cells, Open bars, Open circles, Other triggers, Peripheral blood, Prednisolone, Prednisone therapy, Psychosocial factors, Rapid elimination, Receptor, Receptor number, Resistant group, Respiratory medicine, Severe asthma, Significant difference, Solid circles, Steroid, Steroid resistance, Steroidresistant asthmatics, Systemic glucocorticoid therapy, Thymidine uptake, Tsai frew, Tumor necrosis factor.
Abstract
While much information has recently been obtained regarding the features of steroid‐resistant asthma, it continues to be a dilemma for practitioners, and investigation into its mechanisms will remain an important part of asthma research. Until a clear marker defining steroid‐resistant asthmatics is found, the principle first put forth by Carmichael and colleagues6 should be adhered to: that is, asthmatics resistant to glucocorticoid therapy need to be identified at an early stage so that unnecessary and perhaps harmful therapy can be discontinued. A 10 day course of high‐dose (≥30 mg/day) systemic glucocorticoid therapy, as suggested by Kamada and colleagues,11 may constitute an adequate trial and may sufficiently identify asthmatics who may require alternative treatments. A more rational approach to the selection of alternative asthma treatments will be gained when the mechanisms of steroid resistance are identified. © 1992 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/ppul.1950140307
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Kamada</name><affiliation><wicri:noCountry code="subField">Medicine</wicri:noCountry></affiliation></author><author><name sortKey="Leung, Donald Y M" sort="Leung, Donald Y M" uniqKey="Leung D" first="Donald Y. M." last="Leung">Donald Y. M. Leung</name><affiliation></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Colorado</region></placeName><wicri:cityArea>Departments of Pediatrics, University of Colorado Health Sciences Center, Denver</wicri:cityArea></affiliation></author><author><name sortKey="Szefler, Stanley J" sort="Szefler, Stanley J" uniqKey="Szefler S" first="Stanley J." last="Szefler">Stanley J. 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Until a clear marker defining steroid‐resistant asthmatics is found, the principle first put forth by Carmichael and colleagues6 should be adhered to: that is, asthmatics resistant to glucocorticoid therapy need to be identified at an early stage so that unnecessary and perhaps harmful therapy can be discontinued. A 10 day course of high‐dose (≥30 mg/day) systemic glucocorticoid therapy, as suggested by Kamada and colleagues,11 may constitute an adequate trial and may sufficiently identify asthmatics who may require alternative treatments. A more rational approach to the selection of alternative asthma treatments will be gained when the mechanisms of steroid resistance are identified. © 1992 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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