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Article: Increased whole blood platelet aggregation in patients with Raynaud's phenomenon with or without systemic sclerosis

TitleIncreased whole blood platelet aggregation in patients with Raynaud's phenomenon with or without systemic sclerosis
Authors
KeywordsPlatelet activation
Vasospastic disease
Issue Date1993
PublisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/03009742.asp
Citation
Scandinavian Journal Of Rheumatology, 1993, v. 22 n. 3, p. 97-101 How to Cite?
AbstractPlatelet activation may have a pathophysiological role in Raynaud's phenomenon (RP). However, previous studies have shown conflicting results. This may be related to patient selection and the choice of platelet function assay. In this study, we have assessed platelet function of 30 patients with severe RP with (n = 14) or without (n = 16) systemic sclerosis (SSc), using a whole blood platelet aggregation (PA) assay. Raynaud's medication or other drugs which may affect PA were stopped at least 2 weeks previously. Spontaneous whole blood PA and that induced by 0.5 μM adenosine diphosphate and 0.6 and 1 μg/ml collagen were significantly increased in both groups of patients when compared with controls. There were no significant differences in PA between the 2 groups of patients. Using a more physiological assay, patients with severe RP, whether or not associated with SSc, were shown to have abnormally increased platelet activity. Hyperactive platelets may further impede blood flow in RP.
Persistent Identifierhttp://hdl.handle.net/10722/161978
ISSN
2023 Impact Factor: 2.2
2023 SCImago Journal Rankings: 0.638
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLau, CSen_US
dc.contributor.authorMclaren, Men_US
dc.contributor.authorSaniabadi, Aen_US
dc.contributor.authorBelch, JJFen_US
dc.date.accessioned2012-09-05T05:16:26Z-
dc.date.available2012-09-05T05:16:26Z-
dc.date.issued1993en_US
dc.identifier.citationScandinavian Journal Of Rheumatology, 1993, v. 22 n. 3, p. 97-101en_US
dc.identifier.issn0300-9742en_US
dc.identifier.urihttp://hdl.handle.net/10722/161978-
dc.description.abstractPlatelet activation may have a pathophysiological role in Raynaud's phenomenon (RP). However, previous studies have shown conflicting results. This may be related to patient selection and the choice of platelet function assay. In this study, we have assessed platelet function of 30 patients with severe RP with (n = 14) or without (n = 16) systemic sclerosis (SSc), using a whole blood platelet aggregation (PA) assay. Raynaud's medication or other drugs which may affect PA were stopped at least 2 weeks previously. Spontaneous whole blood PA and that induced by 0.5 μM adenosine diphosphate and 0.6 and 1 μg/ml collagen were significantly increased in both groups of patients when compared with controls. There were no significant differences in PA between the 2 groups of patients. Using a more physiological assay, patients with severe RP, whether or not associated with SSc, were shown to have abnormally increased platelet activity. Hyperactive platelets may further impede blood flow in RP.en_US
dc.languageengen_US
dc.publisherInforma Healthcare. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/03009742.aspen_US
dc.relation.ispartofScandinavian Journal of Rheumatologyen_US
dc.subjectPlatelet activation-
dc.subjectVasospastic disease-
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshCollagen - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFibrinogen - Analysisen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPlatelet Activationen_US
dc.subject.meshPlatelet Aggregation - Drug Effectsen_US
dc.subject.meshPlatelet Counten_US
dc.subject.meshRaynaud Disease - Physiopathologyen_US
dc.subject.meshScleroderma, Systemic - Complications - Physiopathologyen_US
dc.titleIncreased whole blood platelet aggregation in patients with Raynaud's phenomenon with or without systemic sclerosisen_US
dc.typeArticleen_US
dc.identifier.emailLau, CS:cslau@hku.hken_US
dc.identifier.authorityLau, CS=rp01348en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.3109/03009749309099251-
dc.identifier.pmid8316776-
dc.identifier.scopuseid_2-s2.0-0027276083en_US
dc.identifier.volume22en_US
dc.identifier.issue3en_US
dc.identifier.spage97en_US
dc.identifier.epage101en_US
dc.identifier.isiWOS:A1993LJ69900001-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLau, CS=14035682100en_US
dc.identifier.scopusauthoridMcLaren, M=7005471705en_US
dc.identifier.scopusauthoridSaniabadi, A=18936909200en_US
dc.identifier.scopusauthoridBelch, JJF=7101752870en_US
dc.identifier.issnl0300-9742-

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