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Paroxetine-induced increase in LDL cholesterol levelsDepartment of Psychiatry, University of Alberta, Edmonton, Alberta, Canada jean-michel.lemelledo{at}ualberta.ca
Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada
Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada
Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada
Department of Psychiatry, University of Ottawa, Ottawa, Ontario, Canada
Anxiety Disorders Clinic, McMaster University Medical Centre, Department of Psychiatry and Behavioural Neurociences, McMaster University, Hamilton, Ontario, Canada
Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada
Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada Abstract Paroxetine is widely prescribed because it has the indication for multiple psychiatric disorders. Our objective was to assess the effect of short-term administration of paroxetine on low-density lipoprotein cholesterol (LDL-C) levels in both healthy controls (HCs) and in patients with panic disorder (PD). Blood samples for measurement of LDL-C were collected atbaseline, after 8 weeks of paroxetine administration and post-discontinuation in 24 male HCs and nine male patients suffering from PD, for a total of 33 subjects. Paroxetine treatment, both in HCs and PD patients, induced a mean 9% increase per subject in LDL-C that normalized post-discontinuation, suggesting causality. The National Cholesterol Education Program (NCEP) guidelines suggest that this paroxetine-induced increase in LDL-C is clinically significant but would not warrant therapeutic intervention in this population selected to be at low cardiovascular risk. However, the increase in LDL-C levels raised above the threshold of 2.7 mmol/L (100 mg/dL) in 36% of our low-risk subjects. The LDL-C increase in this subgroup would be associated with a minor increase in coronary heart disease (CHD) risk. A similar 9% paroxetine-induced increase in LDL-C observed in the large number of psychiatric patients suffering from comorbid established CHD would be detrimental from a cardiovascular perspective and would oppose the new NCEP therapeutic goals of decreasing LDL-C levels by 30–40% in high and moderately high-risk patients. It is possible that longer treatment duration and use of higher doses of paroxetine would lead to a greater increase in LDL-C.
Key Words: coronary heart disease low-density lipoprotein cholesterol paroxetine selective serotonin reuptake inhibitors
This version was published on September
1, 2009 Journal of Psychopharmacology, Vol. 23, No. 7,
826-830 (2009) |
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