Thromb Haemost 2001; 86(02): 550-556
DOI: 10.1055/s-0037-1616085
Review Article
Schattauer GmbH

Different Effects of Oral and Transdermal Hormone Replacement Therapies on Factor IX, APC Resistance, t-PA, PAI and C-reactive Protein

A Cross-sectional Population Survey
Gordon D. O. Lowe
1   From the University Department of Medicine, Glasgow Royal Infirmary, Department of General Practice, University of Glasgow
,
Mark N. Upton
1   From the University Department of Medicine, Glasgow Royal Infirmary, Department of General Practice, University of Glasgow
,
Ann Rumley
1   From the University Department of Medicine, Glasgow Royal Infirmary, Department of General Practice, University of Glasgow
,
Alex McConnachie
1   From the University Department of Medicine, Glasgow Royal Infirmary, Department of General Practice, University of Glasgow
,
Denis St. J. O’Reilly
2   Institute of Biochemistry, Glasgow Royal Infirmary, Glasgow, UK
,
Graham C. M. Watt
1   From the University Department of Medicine, Glasgow Royal Infirmary, Department of General Practice, University of Glasgow
› Author Affiliations
Further Information

Publication History

Received 24 December 1999

Accepted after resubmission 15 February 2001

Publication Date:
12 December 2017 (online)

Summary

The effects of hormone replacement therapy (HRT) on thrombosis risk, thrombotic variables, and the inflammatory marker C-reactive protein (CRP) may vary by route of administration (oral versus transdermal). We studied the relationships of 14 thrombotic variables (previously related to cardiovascular risk) and CRP to menopausal status and to use of HRT subtypes in a cross-sectional study of 975 women aged 40-59 years. Our study confirmed previously-reported associations between thrombotic variables and menopausal status. Oral HRT use was associated with increased plasma levels of Factor IX, activated protein C (APC) resistance, and CRP; and with decreased levels of tissue plasminogen activator (t-PA) antigen and plasminogen activator inhibitor (PAI) activity. Factor VII levels were higher in women taking unopposed oral oestrogen HRT. The foregoing associations were not observed in users of transdermal HRT; hence they may be consequences of the “first-pass” effect of oral oestrogens on hepatic protein synthesis. We conclude that different effects of oral and transdermal HRT on thrombotic and inflammatory variables may be relevant to their relative thrombotic risk; and suggest that this hypothesis should be tested in prospective, randomised studies.

 
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