Published Online
on June 23, 2009

A more recent version of this article appeared on August 1, 2009

This Article Full Text (PDF) Data Supplement All Versions of this Article: 2/4/389    most recent CIRCGENETICS.109.853572v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Reuwer, A. Q. Articles by Khaw, K.-T. PubMed Articles by Reuwer, A. Q. Articles by Khaw, K.-T. Related Collections Pathophysiology Risk Factors Developmental biology Acute coronary syndromes Acute myocardial infarction Chronic ischemic heart disease Epidemiology

Original Article

Prolactin Levels and the Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women. A prospective case–control study nested in the Epic–Norfolk cohort.

Anne Q. Reuwer¹; Marcel Th. B. Twickler^1,5; Barbara A. Hutten¹; Frederique W. Molema²; Nicholas J. Wareham³; Geesje M. Dallinga–Thie¹; Roman L. Bogorad⁴; Vincent Goffin⁴; Mijke Smink–Bol²; John J.P. Kastelein¹; S.Matthijs Boekholdt¹ and Kay–Tee Khaw³

¹ Academic Medical Center, Amsterdam, The Netherlands;
² RUN Medical Center, Nijmegen, The Netherlands;
³ University of Cambridge, Cambridge, United Kingdom;
⁴ Université Paris Descartes, Paris, France

⁵ E-mail: t.b.twickler{at}amc.uva.nl

Background—Prolactin is increasingly recognized to play a stimulatory role in the inflammatory response. Since inflammation is considered of crucial importance in the development of atherosclerosis, we aimed to evaluate whether prolactin levels are associated with the occurrence of coronary artery disease (CAD).

Methods and Results—We performed a nested case-control study in the prospective EPIC-Norfolk cohort. Cases were apparently healthy men and women, aged 45-79 years, who developed fatal or non-fatal CAD (n = 882). Controls remained free of CAD (n=1490). Overall, systemic prolactin levels did not differ between cases and controls, and people in the highest prolactin tertile did not have a significantly increased risk of developing future CAD (in men, OR: 1.21; 95%CI 0.92-1.61 and in women OR: 1.12; 95%CI 0.76-1.64). However, in a separate immunohistochemical study, the presence of prolactin receptors could be demonstrated in post mortem human coronary artery plaques (preliminary data).

Conclusions—Elevated systemic prolactin levels do not predict CAD in the general population. However, prolactin receptors were found in human coronary artery plaques. This observation may indicate a role of prolactin within atherosclerotic plaques. More studies are needed to define the possible role of prolactin in atherosclerotic plaque development.

Key Words: atherosclerosis • hormones • inflammation • atherogenesis