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A randomized placebo‐controlled study of the effect of low dose aspirin on platelet reactivity and serum thromboxane B 2 production in non‐pregnant women, in normal pregnancy, and in gestational hypertension
Author(s) -
LOUDEN K. A.,
PIPKIN FIONA BROUGHTON,
SYMONDS E. M.,
TUOHY P.,
O'CALLAGHAN C.,
HEPTINSTALL S.,
FOX SUSAN,
MITCHELL J. R. A.
Publication year - 1992
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.1992.tb13751.x
Subject(s) - aspirin , medicine , placebo , thromboxane b2 , pregnancy , gestation , preeclampsia , platelet , thromboxane , randomized controlled trial , endocrinology , biology , pathology , alternative medicine , genetics
Objective To investigate the effect of 60 mg aspirin daily on platelet reactivity and prostaglandin production in various groups of patients. Similar regimens, which are thought to act through inhibition of platelet thromboxane production, are currently undergoing clinical assessment for the prevention of pre‐eclampsia and intrauterine growth retardation. Design A prospective randomized placebo controlled study. Setting University Hospital, Nottingham. Subjects 12 non‐pregnant female volunteers, 18 normal primigravidae before 16 weeks gestation and 16 pregnant women admitted with gestational hypertension (GH) at a mean gestation of 38 weeks. Interventions In the non‐pregnant women blood samples were taken before and after a 10‐day course of 60 mg aspirin daily. The primigravidae had blood samples taken at 16 weeks and then they were randomized to receive either 60 mg aspirin daily or a matched placebo. Further blood samples were obtained at 28, 32 and 36 weeks. Main outcome measures Changes in platelet reactivity and release reaction, and serum thromboxane production, were estimated in whole blood. Results 60 mg aspirin daily significantly inhibited cyclo‐oxygenase dependent platelet aggregation, release reaction and serum thromboxane production in non‐pregnant and pregnant women, and in women with GH ( P <0.01 ). When adrenaline was used as the aggregating agent, the cyclo‐oxygenase pathway was recruited in the increased reactivity seen in the third trimester of normal pregnancy, and was sensitive to inhibition by low dose aspirin. Conclusion Low dose aspirin would appear to be an appropriate agent for the inhibition of platelet reactivity associated with hypertensive pregnancy.