Linked Life Data

6103258

Source:http://linkedlifedata.com/resource/pubmed/id/6103258

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8174
pubmed:dateCreated
1980-7-12
pubmed:abstractText
Animal work suggests that with certain doses of aspirin the antithrombotic effect exerted via the inhibition of the proaggregatory platelet thromboxane A2 (TXA2) may be neutralised by the concomitant vascular reduction of the antiaggregatory prostacyclin (PGI2). Such a situation might result not only in therapeutic ineffectiveness but also in a thrombotic tendency. A patient with a bleeding disorder characterised by a mildly prolonged bleeding time and defective platelet-release reaction due to a congenital deficiency of cyclo-oxygenase provided an opportunity for studying this problem. Her platelets did not aggregate with arachidonic acid, but they did so with a synthetic endoperoxide analogue. Thrombin added to her platelet-rich plasma and whole blood did not generate thromboxane B2 (TXB2). Washed platelets, when incubated with 14C-arachidonic acid, did not produce the cyclo-oxygenase metabolites. A biopsy specimen of her vein did not generate PGI2, as measured both by platelet-aggregation inhibition and radioimmunoassay of 6-keto-PGF1 alpha. Clinically, the patient had a mild bleeding tendency but no thrombotic problems. The findings suggest that in man aspirin therapy, even at doses which inhibit PGI2 formation, would only impair haemostasis mildly without producing a thrombotic tendency.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0140-6736
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
898-901
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Congenital deficiency of thromboxane and prostacyclin.
pubmed:publicationType
Journal Article, Case Reports