The use of sulphasalazine as a disease modifying antirheumatic drug
Identifieur interne : 003051 ( Main/Exploration ); précédent : 003050; suivant : 003052The use of sulphasalazine as a disease modifying antirheumatic drug
Auteurs : D. R. Porter ; H. A. CapellSource :
- Bailliere's Clinical Rheumatology [ 0950-3579 ] ; 1990.
English descriptors
- Teeft :
- 5aminosalicylic acid, Acetylator, Acetylator phenotype, Acetylator status, Active disease, Active moiety, Adverse effects, Agranulocytosis, Ankylosing, Ankylosing spondylitis, Antirheumatic, Antirheumatic drug, Aplasia, Arthritis, Blood cells, Bowel, British journal, Capell, Cell aplasia, Clinical parameters, Colitis, Disease modification, Dmards, Dose reduction, Farr, Folate, Gold groups, Hepatic, Hypersensitivity reactions, Inflammatory bowel disease, Intramuscular, Intramuscular gold, Laboratory parameters, Mcconkey, Moiety, Morning stiffness, Open trial, Other trials, Penicillamine, Placebo, Placebo group, Pullar, Radiological progression, Rash, Reactive, Reactive arthritis, Rheumatic, Rheumatic diseases, Rheumatoid, Rheumatoid arthritis, Rheumatology, Sasp, Sasp group, Sasp therapy, Sasp treatment, Scandinavian journal, Significant improvement, Skin rash, Spondylitis, Sulphapyridine, Sulphasalazine, Sulphasalazine therapy, Toxic epidermal necrolysis, Treatment group, Ulcerative, Ulcerative colitis.
Abstract
Summary: SASP is a useful DMARD in RA and is probably useful in early ankylosing spondylitis, psoriatic arthropathy and reactive arthritis. It shares many of the characteristics of other DMARDs such as gold and penicillamine. It produces improvement in clinical and laboratory parameters of disease activity, with a slow onset of action—8–12 weeks elapse before beneficial effect is noted. SASP probably slows radiological progression of RA but definitive proof is difficult to obtain. Although side-effects are common, these are often managed by a reduction in dose, and serious adverse events requiring cessation of therapy are uncommon. Serious side-effects do occur however, and regular monitoring with full blood counts is recommended. The mechanism of action of SASP is unknown and this remains one of the principal areas of research interest.
Url:
DOI: 10.1016/S0950-3579(05)80006-8
Affiliations:
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R." last="Porter">D. R. Porter</name></author><author><name sortKey="Capell, H A" sort="Capell, H A" uniqKey="Capell H" first="H. A." last="Capell">H. A. Capell</name></author></analytic><monogr></monogr><series><title level="j">Bailliere's Clinical Rheumatology</title><title level="j" type="abbrev">BACR</title><idno type="ISSN">0950-3579</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1990">1990</date><biblScope unit="volume">4</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="535">535</biblScope><biblScope unit="page" to="551">551</biblScope></imprint><idno type="ISSN">0950-3579</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0950-3579</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>5aminosalicylic acid</term><term>Acetylator</term><term>Acetylator phenotype</term><term>Acetylator status</term><term>Active disease</term><term>Active moiety</term><term>Adverse effects</term><term>Agranulocytosis</term><term>Ankylosing</term><term>Ankylosing spondylitis</term><term>Antirheumatic</term><term>Antirheumatic drug</term><term>Aplasia</term><term>Arthritis</term><term>Blood cells</term><term>Bowel</term><term>British journal</term><term>Capell</term><term>Cell aplasia</term><term>Clinical parameters</term><term>Colitis</term><term>Disease modification</term><term>Dmards</term><term>Dose reduction</term><term>Farr</term><term>Folate</term><term>Gold groups</term><term>Hepatic</term><term>Hypersensitivity reactions</term><term>Inflammatory bowel disease</term><term>Intramuscular</term><term>Intramuscular gold</term><term>Laboratory parameters</term><term>Mcconkey</term><term>Moiety</term><term>Morning stiffness</term><term>Open trial</term><term>Other trials</term><term>Penicillamine</term><term>Placebo</term><term>Placebo group</term><term>Pullar</term><term>Radiological progression</term><term>Rash</term><term>Reactive</term><term>Reactive arthritis</term><term>Rheumatic</term><term>Rheumatic diseases</term><term>Rheumatoid</term><term>Rheumatoid arthritis</term><term>Rheumatology</term><term>Sasp</term><term>Sasp group</term><term>Sasp therapy</term><term>Sasp treatment</term><term>Scandinavian journal</term><term>Significant improvement</term><term>Skin rash</term><term>Spondylitis</term><term>Sulphapyridine</term><term>Sulphasalazine</term><term>Sulphasalazine therapy</term><term>Toxic epidermal necrolysis</term><term>Treatment group</term><term>Ulcerative</term><term>Ulcerative colitis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: SASP is a useful DMARD in RA and is probably useful in early ankylosing spondylitis, psoriatic arthropathy and reactive arthritis. It shares many of the characteristics of other DMARDs such as gold and penicillamine. It produces improvement in clinical and laboratory parameters of disease activity, with a slow onset of action—8–12 weeks elapse before beneficial effect is noted. SASP probably slows radiological progression of RA but definitive proof is difficult to obtain. Although side-effects are common, these are often managed by a reduction in dose, and serious adverse events requiring cessation of therapy are uncommon. Serious side-effects do occur however, and regular monitoring with full blood counts is recommended. The mechanism of action of SASP is unknown and this remains one of the principal areas of research interest.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Capell, H A" sort="Capell, H A" uniqKey="Capell H" first="H. A." last="Capell">H. A. Capell</name><name sortKey="Porter, D R" sort="Porter, D R" uniqKey="Porter D" first="D. R." last="Porter">D. R. 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