[Weekly low-dose methotrexate in rheumatoid arthritis. Review of the literature].
Identifieur interne : 000533 ( PubMed/Corpus ); précédent : 000532; suivant : 000534[Weekly low-dose methotrexate in rheumatoid arthritis. Review of the literature].
Auteurs : P. Manganelli ; W. Troise RiodaSource :
- Minerva medica [ 0026-4806 ] ; 1993.
English descriptors
- KwdEn :
- Arthritis, Rheumatoid (drug therapy), Chemical and Drug Induced Liver Injury, Drug Administration Schedule, Drug Interactions, Hematologic Diseases (chemically induced), Humans, Immune System Diseases (chemically induced), Interleukins, Leukocytes, Mononuclear (drug effects), Lung Diseases (chemically induced), Methotrexate (administration & dosage), Methotrexate (pharmacology), Methotrexate (therapeutic use), Neutrophils (drug effects).
- MESH :
- chemical , administration & dosage : Methotrexate.
- chemical , pharmacology : Methotrexate.
- chemical , therapeutic use : Methotrexate.
- chemical : Interleukins.
- chemically induced : Hematologic Diseases, Immune System Diseases, Lung Diseases.
- drug effects : Leukocytes, Mononuclear, Neutrophils.
- drug therapy : Arthritis, Rheumatoid.
- Chemical and Drug Induced Liver Injury, Drug Administration Schedule, Drug Interactions, Humans.
Abstract
Methotrexate (MTX) is an antifolic drug that in recent years has been largely employed in the treatment of Rheumatoid Arthritis (RA). Both short and long term clinical trials have demonstrated its efficacy and good tolerability. It induces a significant improvement of all clinical variables and a decrease in the erythrocyte sedimentation rate and other acute phase reactants with a steroid sparing effect. The probability of continuing MTX therapy for up to 5 years is 46-55% whereas that of continuing gold, hydroxychloroquine, sulfasalazine or D-penicillamine therapy is less than 20%. MTX is a rapidly acting drug with a clinical response within 4 weeks and a plateau phase after 6 months of therapy. Discontinuation of long-term MTX therapy induces a flare-up of the disease so that patients receiving long-term MTX must continue the drug to maintain clinical benefits. In spite of its clinical efficacy, MTX does not seem to have a significant effect on disease progression as determined radiographically. In this respect, MTX appears to have some superiority when compared to azathioprine, but not when compared to gold salts. MTX has been employed in patients with RA unresponsive to other Disease-Modifying Antirheumatic Drugs (DMARDs), but according to some recent views on the therapeutic strategy of RA, it could be used in early RA as a first choice drug. Toxic effects are the main reason in limiting long-term MTX treatment. Hepatic toxicity is one of the more common side-effects of MTX, but the recognition of its "risk factors" such as alcohol abuse, may reduce it. Acute pneumonitis is one of the more severe complications of MTX therapy and may be life-threatening. In RA patients treated with MTX are also reported complications of immunosuppression, such as Pneumocystis carinii pneumonia whose clinical-radiological picture may be similar to that of acute pneumonitis. The mechanism of action of low-dose weekly MTX in RA is still unclear, but it might be more antiinflammatory than immunosuppressive, as supported by the rapid clinical response. The inhibition of Interleukin-1 activity or other inflammatory cytokines and inflammatory cells may play an important role in the antiinflammatory effect of MTX. MTX effects in RA are not fully understood and further studies are needed to clarify its mechanism of action and its place in the therapeutic strategy of this disease.
PubMed: 8247309
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pubmed:8247309Le document en format XML
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Troise Rioda</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1993">1993</date><idno type="RBID">pubmed:8247309</idno><idno type="pmid">8247309</idno><idno type="wicri:Area/PubMed/Corpus">000533</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000533</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">[Weekly low-dose methotrexate in rheumatoid arthritis. Review of the literature].</title><author><name sortKey="Manganelli, P" sort="Manganelli, P" uniqKey="Manganelli P" first="P" last="Manganelli">P. Manganelli</name><affiliation><nlm:affiliation>USL 4 di Parma II Divisione Medica e Reumatologia, Università degli Studi di Parma.</nlm:affiliation></affiliation></author><author><name sortKey="Troise Rioda, W" sort="Troise Rioda, W" uniqKey="Troise Rioda W" first="W" last="Troise Rioda">W. Troise Rioda</name></author></analytic><series><title level="j">Minerva medica</title><idno type="ISSN">0026-4806</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Arthritis, Rheumatoid (drug therapy)</term><term>Chemical and Drug Induced Liver Injury</term><term>Drug Administration Schedule</term><term>Drug Interactions</term><term>Hematologic Diseases (chemically induced)</term><term>Humans</term><term>Immune System Diseases (chemically induced)</term><term>Interleukins</term><term>Leukocytes, Mononuclear (drug effects)</term><term>Lung Diseases (chemically induced)</term><term>Methotrexate (administration & dosage)</term><term>Methotrexate (pharmacology)</term><term>Methotrexate (therapeutic use)</term><term>Neutrophils (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Methotrexate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Methotrexate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Methotrexate</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Interleukins</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Hematologic Diseases</term><term>Immune System Diseases</term><term>Lung Diseases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Leukocytes, Mononuclear</term><term>Neutrophils</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Arthritis, Rheumatoid</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Chemical and Drug Induced Liver Injury</term><term>Drug Administration Schedule</term><term>Drug Interactions</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Methotrexate (MTX) is an antifolic drug that in recent years has been largely employed in the treatment of Rheumatoid Arthritis (RA). Both short and long term clinical trials have demonstrated its efficacy and good tolerability. It induces a significant improvement of all clinical variables and a decrease in the erythrocyte sedimentation rate and other acute phase reactants with a steroid sparing effect. The probability of continuing MTX therapy for up to 5 years is 46-55% whereas that of continuing gold, hydroxychloroquine, sulfasalazine or D-penicillamine therapy is less than 20%. MTX is a rapidly acting drug with a clinical response within 4 weeks and a plateau phase after 6 months of therapy. Discontinuation of long-term MTX therapy induces a flare-up of the disease so that patients receiving long-term MTX must continue the drug to maintain clinical benefits. In spite of its clinical efficacy, MTX does not seem to have a significant effect on disease progression as determined radiographically. In this respect, MTX appears to have some superiority when compared to azathioprine, but not when compared to gold salts. MTX has been employed in patients with RA unresponsive to other Disease-Modifying Antirheumatic Drugs (DMARDs), but according to some recent views on the therapeutic strategy of RA, it could be used in early RA as a first choice drug. Toxic effects are the main reason in limiting long-term MTX treatment. Hepatic toxicity is one of the more common side-effects of MTX, but the recognition of its "risk factors" such as alcohol abuse, may reduce it. Acute pneumonitis is one of the more severe complications of MTX therapy and may be life-threatening. In RA patients treated with MTX are also reported complications of immunosuppression, such as Pneumocystis carinii pneumonia whose clinical-radiological picture may be similar to that of acute pneumonitis. The mechanism of action of low-dose weekly MTX in RA is still unclear, but it might be more antiinflammatory than immunosuppressive, as supported by the rapid clinical response. The inhibition of Interleukin-1 activity or other inflammatory cytokines and inflammatory cells may play an important role in the antiinflammatory effect of MTX. MTX effects in RA are not fully understood and further studies are needed to clarify its mechanism of action and its place in the therapeutic strategy of this disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8247309</PMID><DateCompleted><Year>1994</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>23</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0026-4806</ISSN><JournalIssue CitedMedium="Print"><Volume>84</Volume><Issue>10</Issue><PubDate><Year>1993</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Minerva medica</Title><ISOAbbreviation>Minerva Med.</ISOAbbreviation></Journal><ArticleTitle>[Weekly low-dose methotrexate in rheumatoid arthritis. Review of the literature].</ArticleTitle><Pagination><MedlinePgn>541-52</MedlinePgn></Pagination><Abstract><AbstractText>Methotrexate (MTX) is an antifolic drug that in recent years has been largely employed in the treatment of Rheumatoid Arthritis (RA). Both short and long term clinical trials have demonstrated its efficacy and good tolerability. It induces a significant improvement of all clinical variables and a decrease in the erythrocyte sedimentation rate and other acute phase reactants with a steroid sparing effect. The probability of continuing MTX therapy for up to 5 years is 46-55% whereas that of continuing gold, hydroxychloroquine, sulfasalazine or D-penicillamine therapy is less than 20%. MTX is a rapidly acting drug with a clinical response within 4 weeks and a plateau phase after 6 months of therapy. Discontinuation of long-term MTX therapy induces a flare-up of the disease so that patients receiving long-term MTX must continue the drug to maintain clinical benefits. In spite of its clinical efficacy, MTX does not seem to have a significant effect on disease progression as determined radiographically. In this respect, MTX appears to have some superiority when compared to azathioprine, but not when compared to gold salts. MTX has been employed in patients with RA unresponsive to other Disease-Modifying Antirheumatic Drugs (DMARDs), but according to some recent views on the therapeutic strategy of RA, it could be used in early RA as a first choice drug. Toxic effects are the main reason in limiting long-term MTX treatment. Hepatic toxicity is one of the more common side-effects of MTX, but the recognition of its "risk factors" such as alcohol abuse, may reduce it. Acute pneumonitis is one of the more severe complications of MTX therapy and may be life-threatening. In RA patients treated with MTX are also reported complications of immunosuppression, such as Pneumocystis carinii pneumonia whose clinical-radiological picture may be similar to that of acute pneumonitis. The mechanism of action of low-dose weekly MTX in RA is still unclear, but it might be more antiinflammatory than immunosuppressive, as supported by the rapid clinical response. The inhibition of Interleukin-1 activity or other inflammatory cytokines and inflammatory cells may play an important role in the antiinflammatory effect of MTX. MTX effects in RA are not fully understood and further studies are needed to clarify its mechanism of action and its place in the therapeutic strategy of this disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Manganelli</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>USL 4 di Parma II Divisione Medica e Reumatologia, Università degli Studi di Parma.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Troise Rioda</LastName><ForeName>W</ForeName><Initials>W</Initials></Author></AuthorList><Language>ita</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><VernacularTitle>Il methotrexate a basse dosi settimanali nell'artrite reumatoide. Rassegna della letteratura.</VernacularTitle></Article><MedlineJournalInfo><Country>Italy</Country><MedlineTA>Minerva Med</MedlineTA><NlmUniqueID>0400732</NlmUniqueID><ISSNLinking>0026-4806</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007378">Interleukins</NameOfSubstance></Chemical><Chemical><RegistryNumber>YL5FZ2Y5U1</RegistryNumber><NameOfSubstance UI="D008727">Methotrexate</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001172" MajorTopicYN="N">Arthritis, Rheumatoid</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056486" MajorTopicYN="N">Chemical and Drug Induced Liver Injury</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004334" MajorTopicYN="N">Drug Administration Schedule</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004347" MajorTopicYN="N">Drug Interactions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006402" MajorTopicYN="N">Hematologic Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007154" MajorTopicYN="N">Immune System Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007378" MajorTopicYN="N">Interleukins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007963" MajorTopicYN="N">Leukocytes, Mononuclear</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008171" MajorTopicYN="N">Lung Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008727" MajorTopicYN="N">Methotrexate</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009504" MajorTopicYN="N">Neutrophils</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>102</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1993</Year><Month>10</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1993</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1993</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8247309</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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