BACKGROUND: Despite the frequent use of selective serotonin reuptake inhibitors in patients with coronary heart disease (CHD), their effects on plasma lipid levels have not been systematically investigated. Our objective was to assess the effects of 8 weeks of paroxetine administration on plasma cholesterol and triglyceride levels. METHOD: Blood samples were collected at baseline, after 8 weeks of paroxetine administration, and post-discontinuation in 18 healthy male volunteers. RESULTS: In the 16 of 18 patients whose plasma levels of paroxetine indicated an unequivocal compliance to treatment, paroxetine administration induced an 11.5% increase in low-density lipoprotein cholesterol (LDL-C), which normalized after paroxetine discontinuation. CONCLUSION: The magnitude of the paroxetine-induced increase in LDL-C would lead to a minor increase in CHD risk in a minority of healthy male volunteers without associated CHD risk factors but might increase LDL-C sufficiently to warrant therapeutic intervention in patients with established CHD, based on the National Cholesterol Education Program guidelines.
BACKGROUND: Despite the frequent use of selective serotonin reuptake inhibitors in patients with coronary heart disease (CHD), their effects on plasma lipid levels have not been systematically investigated. Our objective was to assess the effects of 8 weeks of paroxetine administration on plasma cholesterol and triglyceride levels. METHOD: Blood samples were collected at baseline, after 8 weeks of paroxetine administration, and post-discontinuation in 18 healthy male volunteers. RESULTS: In the 16 of 18 patients whose plasma levels of paroxetine indicated an unequivocal compliance to treatment, paroxetine administration induced an 11.5% increase in low-density lipoprotein cholesterol (LDL-C), which normalized after paroxetine discontinuation. CONCLUSION: The magnitude of the paroxetine-induced increase in LDL-C would lead to a minor increase in CHD risk in a minority of healthy male volunteers without associated CHD risk factors but might increase LDL-C sufficiently to warrant therapeutic intervention in patients with established CHD, based on the National Cholesterol Education Program guidelines.
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