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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8400
|
pubmed:dateCreated |
1984-9-25
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pubmed:abstractText |
The syndrome resembling systemic lupus erythematosus (SLE) associated with long-term treatment with hydralazine and isoniazid seems to be due to the drugs themselves rather than their metabolites. This syndrome is associated with deposition of immune complexes; and in the complement system inhibition of C4 is likely to increase deposition of immune complexes. In vitro, hydralazine and isoniazid inhibited 50% of the binding of C4 at 840 mumol/l and 1.05 mmol/l, respectively--ie, within the concentration ranges that have been used in therapy. Acetylated metabolites were not inhibitory at the maximum concentrations tested; and iproniazid, which does not cause SLE, gave 50% inhibition only at a concentration far exceeding that used in therapy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Complement C4,
http://linkedlifedata.com/resource/pubmed/chemical/Hydralazine,
http://linkedlifedata.com/resource/pubmed/chemical/Iproniazid,
http://linkedlifedata.com/resource/pubmed/chemical/Isoniazid,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylhydrazines
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0140-6736
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
25
|
pubmed:volume |
2
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
422-4
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:6147500-Acetylation,
pubmed-meshheading:6147500-Complement C4,
pubmed-meshheading:6147500-Complement Pathway, Classical,
pubmed-meshheading:6147500-Humans,
pubmed-meshheading:6147500-Hydralazine,
pubmed-meshheading:6147500-Iproniazid,
pubmed-meshheading:6147500-Isoniazid,
pubmed-meshheading:6147500-Lupus Erythematosus, Systemic,
pubmed-meshheading:6147500-Phenylhydrazines
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pubmed:year |
1984
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pubmed:articleTitle |
Drugs that induce systemic lupus erythematosus inhibit complement component C4.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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