Kerri S Rawson1, David Dixon1, Roberto Civitelli2, Tim R Peterson3,4,5,6, Benoit H Mulsant7,8, Charles F Reynolds9,10,11, Eric J Lenze1. 1. Department of Psychiatry, School of Medicine, Washington University, St. Louis, Missouri. 2. Department of Pathology, School of Medicine, Washington University, St. Louis, Missouri. 3. Department of Internal Medicine, School of Medicine, Washington University, St. Louis, Missouri. 4. Division of Bone and Mineral Diseases, School of Medicine, Washington University, St. Louis, Missouri. 5. Department of Genetics, School of Medicine, Washington University, St. Louis, Missouri. 6. Institute of Public Health, School of Medicine, Washington University, St. Louis, Missouri. 7. Centre for Addiction and Mental Health, Toronto, Ontario, Canada. 8. Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. 9. Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania. 10. Department of Behavioral and Community Health Sciences, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania. 11. Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania.
Abstract
OBJECTIVES: Epidemiologic data suggest older adults receiving serotonergic antidepressants may have accelerated bone loss. We examined bone turnover marker changes and patient-level variables associated with these changes in older adults receiving protocolized antidepressant treatment. DESIGN: Open-label, protocolized treatment study. SETTING: Medical centers in Pittsburgh, St Louis, and Toronto. PARTICIPANTS: Older adults with major depression (N = 168). MEASUREMENTS: Serum levels of the bone resorption marker C-terminal cross-linking telopeptide of type 1 collagen (CTX) and the bone formation marker procollagen type 1 N propeptide (P1NP) were assayed before and after 12 weeks of treatment with venlafaxine. Whether CTX and P1NP changes were associated with depression remission and duration of depression and genetic polymorphisms in the serotonin transporter (5HTTLPR) and 1B receptor (HTR1B) were also examined. RESULTS: CTX increased and P1NP decreased during venlafaxine treatment, a profile consistent with accelerated bone loss. Two individual-level clinical variables were correlated with bone turnover; participants whose depression did not go into remission had higher CTX levels, and those with chronic depression had lower P1NP levels. HTR1B genotype predicted P1NP change, whereas 5HTTLPR genotype was unrelated to either biomarker. CONCLUSION: Bone turnover markers change with antidepressant treatment in a pattern that suggests accelerated bone loss, although the clinical significance of these changes is unclear. These data are preliminary and argue for a larger, controlled study to confirm whether antidepressants are harmful to bone metabolism and whether certain individuals might be at increased risk.
OBJECTIVES: Epidemiologic data suggest older adults receiving serotonergic antidepressants may have accelerated bone loss. We examined bone turnover marker changes and patient-level variables associated with these changes in older adults receiving protocolized antidepressant treatment. DESIGN: Open-label, protocolized treatment study. SETTING: Medical centers in Pittsburgh, St Louis, and Toronto. PARTICIPANTS: Older adults with major depression (N = 168). MEASUREMENTS: Serum levels of the bone resorption marker C-terminal cross-linking telopeptide of type 1 collagen (CTX) and the bone formation marker procollagen type 1 N propeptide (P1NP) were assayed before and after 12 weeks of treatment with venlafaxine. Whether CTX and P1NP changes were associated with depression remission and duration of depression and genetic polymorphisms in the serotonin transporter (5HTTLPR) and 1B receptor (HTR1B) were also examined. RESULTS:CTX increased and P1NP decreased during venlafaxine treatment, a profile consistent with accelerated bone loss. Two individual-level clinical variables were correlated with bone turnover; participants whose depression did not go into remission had higher CTX levels, and those with chronic depression had lower P1NP levels. HTR1B genotype predicted P1NP change, whereas 5HTTLPR genotype was unrelated to either biomarker. CONCLUSION: Bone turnover markers change with antidepressant treatment in a pattern that suggests accelerated bone loss, although the clinical significance of these changes is unclear. These data are preliminary and argue for a larger, controlled study to confirm whether antidepressants are harmful to bone metabolism and whether certain individuals might be at increased risk.
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