Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients.
Identifieur interne : 003A34 ( Main/Exploration ); précédent : 003A33; suivant : 003A35Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients.
Auteurs : A. Szczeklik ; R J Gryglewski ; G. Czerniawska-MysikSource :
- British Medical Journal [ 0007-1447 ] ; 1975-01-11.
English descriptors
- Teeft :
- Adverse reactions, Angioneurotic oedema, Antiinflammatory drugs, Arachidonic acid, Aspirin, Aspirin hypersensitivity, Aspirinsensitive patients, Asthma, Asthma attacks, Asthmatic, Asthmatic attacks, Asthmatic patients, Benzydamine, Biosynthesis, Clinical immunology, Dos, Enzymic activity, Flufenamic, Flufenamic acid, Indomethacin, Inhibitory action, Internal medicine, Mefenamic, Mefenamic acid, Mmol phosphate buffer, Nasal polyps, Paracetamol, Peak expiratory flow, Phenylbutazone, Prostaglandin, Prostaglandin biosynthesis, Rhinorrhoea, Salicylamide, Therapeutic doses, Untoward reactions.
Abstract
Eleven patients with asthma and aspirin hypersensitivity have been challenged with eight non-steroidal anti-inflammatory drugs. Each drug was given by mouth in at least three different doses and the patients' symptoms and peak expiratory flow (PEF) rates were observed over a three-hour period. Indomethacin 5 mg caused bronchoconstriction in all patients. Therapeutic doses of mefenamic or flufenamic acid caused bronchoconstriction in most patients. Phenylbutazone 200-400 mg induced a moderate fall in PEF. There were no reactions to therapeutic doses of salicylamide, paracetamol, benzydamine, and chloroquine. Microsomal prostaglandin synthetase, activity was inhibited by aspirin, indomethacin, mefenamic acid, flufenamic acid, and phenylbutazone. The other four drugs had no inhibitory effect. We suggest that precipitation of attacks in asthmatic patients hypersensitive to certain anti-inflammatory drugs is related to drug's ability to inhibit prostaglandin biosynthesis.
Url:
DOI: 10.1136/bmj.1.5949.67
Affiliations:
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Le document en format XML
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Szczeklik</name></author><author><name sortKey="Gryglewski, R J" sort="Gryglewski, R J" uniqKey="Gryglewski R" first="R J" last="Gryglewski">R J Gryglewski</name></author><author><name sortKey="Czerniawska Mysik, G" sort="Czerniawska Mysik, G" uniqKey="Czerniawska Mysik G" first="G" last="Czerniawska-Mysik">G. Czerniawska-Mysik</name></author></analytic><monogr></monogr><series><title level="j">British Medical Journal</title><title level="j" type="abbrev">Br Med J</title><idno type="ISSN">0007-1447</idno><idno type="eISSN">1468-5833</idno><imprint><publisher>British Medical Journal Publishing Group</publisher><date type="published" when="1975-01-11">1975-01-11</date><biblScope unit="volume">1</biblScope><biblScope unit="issue">5949</biblScope><biblScope unit="page" from="67">67</biblScope></imprint><idno type="ISSN">0007-1447</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0007-1447</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adverse reactions</term><term>Angioneurotic oedema</term><term>Antiinflammatory drugs</term><term>Arachidonic acid</term><term>Aspirin</term><term>Aspirin hypersensitivity</term><term>Aspirinsensitive patients</term><term>Asthma</term><term>Asthma attacks</term><term>Asthmatic</term><term>Asthmatic attacks</term><term>Asthmatic patients</term><term>Benzydamine</term><term>Biosynthesis</term><term>Clinical immunology</term><term>Dos</term><term>Enzymic activity</term><term>Flufenamic</term><term>Flufenamic acid</term><term>Indomethacin</term><term>Inhibitory action</term><term>Internal medicine</term><term>Mefenamic</term><term>Mefenamic acid</term><term>Mmol phosphate buffer</term><term>Nasal polyps</term><term>Paracetamol</term><term>Peak expiratory flow</term><term>Phenylbutazone</term><term>Prostaglandin</term><term>Prostaglandin biosynthesis</term><term>Rhinorrhoea</term><term>Salicylamide</term><term>Therapeutic doses</term><term>Untoward reactions</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Eleven patients with asthma and aspirin hypersensitivity have been challenged with eight non-steroidal anti-inflammatory drugs. Each drug was given by mouth in at least three different doses and the patients' symptoms and peak expiratory flow (PEF) rates were observed over a three-hour period. Indomethacin 5 mg caused bronchoconstriction in all patients. Therapeutic doses of mefenamic or flufenamic acid caused bronchoconstriction in most patients. Phenylbutazone 200-400 mg induced a moderate fall in PEF. There were no reactions to therapeutic doses of salicylamide, paracetamol, benzydamine, and chloroquine. Microsomal prostaglandin synthetase, activity was inhibited by aspirin, indomethacin, mefenamic acid, flufenamic acid, and phenylbutazone. The other four drugs had no inhibitory effect. We suggest that precipitation of attacks in asthmatic patients hypersensitive to certain anti-inflammatory drugs is related to drug's ability to inhibit prostaglandin biosynthesis.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Czerniawska Mysik, G" sort="Czerniawska Mysik, G" uniqKey="Czerniawska Mysik G" first="G" last="Czerniawska-Mysik">G. Czerniawska-Mysik</name><name sortKey="Gryglewski, R J" sort="Gryglewski, R J" uniqKey="Gryglewski R" first="R J" last="Gryglewski">R J Gryglewski</name><name sortKey="Szczeklik, A" sort="Szczeklik, A" uniqKey="Szczeklik A" first="A" last="Szczeklik">A. Szczeklik</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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