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Depression and the use of antidepressants are each associated with an increased risk of venous thromboembolism (VTE), according to a review and meta-analysis published in Annals of Medicine.
The research also showed that each of the various classes of antidepressant medications is associated with an increased risk of VTE.
The researchers noted that this study does not prove cause and effect, and further studies are needed to determine what is driving the observed increase in VTE risk.
Some previous studies have indicated that depression and antidepressant use might be associated with an increased risk of VTE, but other studies have shown no evidence of associations.
Therefore, Setor Kunutsor, MD, PhD, of the University of Bristol in Bristol, UK, and his colleagues conducted a systematic review and meta-analysis of observational studies evaluating the associations of depression and antidepressant use with VTE risk.
The researchers looked at 8 observational studies with data on 960,113 non-overlapping participants. There were 9027 cases of VTE in this population.
To determine the association between depression and VTE, the researchers conducted a pooled analysis of 3 studies comparing patients with depression and without. These studies included 865,878 participants and 4676 cases of VTE.
The relative risk (RR) for VTE was 1.31 (95% CI, 1.13-1.53) among patients with depression.
The researchers also conducted a pooled analysis of 6 studies comparing antidepressant users to non-users. These studies included 828,327 participants and 8273 cases of VTE.
The RR for VTE was 1.27 (95% CI, 1.06-1.51) among patients taking antidepressants.
In addition, individual antidepressants were associated with an increased risk of VTE. This includes:
- Tricyclic antidepressants—RR=1.16 (95% CI, 1.06-1.27)
- Selective serotonin reuptake inhibitors—RR=1.12 (95% CI, 1.02-1.23)
- “Other” antidepressants*—RR=1.59 (95% CI, 1.21-2.09).
The researchers said these data show that antidepressant use and depression are each associated with an increased risk of VTE, and these results add to accumulating evidence that a relationship exists between depression, antidepressant use, and VTE.
“These findings are very useful to me as both a clinician and a researcher,” Dr Kunutsor said. “It gives me the information I need, especially when prescribing antidepressant medications to my patients.”
Still, Dr Kunutsor and his colleagues conceded that more research is needed to determine if the observed associations are causal and if depression, antidepressant use, or both drive the increased risk of VTE.
To so this, studies would need to isolate depression from antidepressant medications. For example, researchers could assess if non-depressed individuals who use antidepressants for other conditions have an increased risk of VTE.
*The “other” antidepressants include monoamine oxidase inhibitors, triazolopyridine, serotonin norepinephrine reuptake inhibitors, and norepinephrine dopamine reuptake inhibitors.
Depression and the use of antidepressants are each associated with an increased risk of venous thromboembolism (VTE), according to a review and meta-analysis published in Annals of Medicine.
The research also showed that each of the various classes of antidepressant medications is associated with an increased risk of VTE.
The researchers noted that this study does not prove cause and effect, and further studies are needed to determine what is driving the observed increase in VTE risk.
Some previous studies have indicated that depression and antidepressant use might be associated with an increased risk of VTE, but other studies have shown no evidence of associations.
Therefore, Setor Kunutsor, MD, PhD, of the University of Bristol in Bristol, UK, and his colleagues conducted a systematic review and meta-analysis of observational studies evaluating the associations of depression and antidepressant use with VTE risk.
The researchers looked at 8 observational studies with data on 960,113 non-overlapping participants. There were 9027 cases of VTE in this population.
To determine the association between depression and VTE, the researchers conducted a pooled analysis of 3 studies comparing patients with depression and without. These studies included 865,878 participants and 4676 cases of VTE.
The relative risk (RR) for VTE was 1.31 (95% CI, 1.13-1.53) among patients with depression.
The researchers also conducted a pooled analysis of 6 studies comparing antidepressant users to non-users. These studies included 828,327 participants and 8273 cases of VTE.
The RR for VTE was 1.27 (95% CI, 1.06-1.51) among patients taking antidepressants.
In addition, individual antidepressants were associated with an increased risk of VTE. This includes:
- Tricyclic antidepressants—RR=1.16 (95% CI, 1.06-1.27)
- Selective serotonin reuptake inhibitors—RR=1.12 (95% CI, 1.02-1.23)
- “Other” antidepressants*—RR=1.59 (95% CI, 1.21-2.09).
The researchers said these data show that antidepressant use and depression are each associated with an increased risk of VTE, and these results add to accumulating evidence that a relationship exists between depression, antidepressant use, and VTE.
“These findings are very useful to me as both a clinician and a researcher,” Dr Kunutsor said. “It gives me the information I need, especially when prescribing antidepressant medications to my patients.”
Still, Dr Kunutsor and his colleagues conceded that more research is needed to determine if the observed associations are causal and if depression, antidepressant use, or both drive the increased risk of VTE.
To so this, studies would need to isolate depression from antidepressant medications. For example, researchers could assess if non-depressed individuals who use antidepressants for other conditions have an increased risk of VTE.
*The “other” antidepressants include monoamine oxidase inhibitors, triazolopyridine, serotonin norepinephrine reuptake inhibitors, and norepinephrine dopamine reuptake inhibitors.
Depression and the use of antidepressants are each associated with an increased risk of venous thromboembolism (VTE), according to a review and meta-analysis published in Annals of Medicine.
The research also showed that each of the various classes of antidepressant medications is associated with an increased risk of VTE.
The researchers noted that this study does not prove cause and effect, and further studies are needed to determine what is driving the observed increase in VTE risk.
Some previous studies have indicated that depression and antidepressant use might be associated with an increased risk of VTE, but other studies have shown no evidence of associations.
Therefore, Setor Kunutsor, MD, PhD, of the University of Bristol in Bristol, UK, and his colleagues conducted a systematic review and meta-analysis of observational studies evaluating the associations of depression and antidepressant use with VTE risk.
The researchers looked at 8 observational studies with data on 960,113 non-overlapping participants. There were 9027 cases of VTE in this population.
To determine the association between depression and VTE, the researchers conducted a pooled analysis of 3 studies comparing patients with depression and without. These studies included 865,878 participants and 4676 cases of VTE.
The relative risk (RR) for VTE was 1.31 (95% CI, 1.13-1.53) among patients with depression.
The researchers also conducted a pooled analysis of 6 studies comparing antidepressant users to non-users. These studies included 828,327 participants and 8273 cases of VTE.
The RR for VTE was 1.27 (95% CI, 1.06-1.51) among patients taking antidepressants.
In addition, individual antidepressants were associated with an increased risk of VTE. This includes:
- Tricyclic antidepressants—RR=1.16 (95% CI, 1.06-1.27)
- Selective serotonin reuptake inhibitors—RR=1.12 (95% CI, 1.02-1.23)
- “Other” antidepressants*—RR=1.59 (95% CI, 1.21-2.09).
The researchers said these data show that antidepressant use and depression are each associated with an increased risk of VTE, and these results add to accumulating evidence that a relationship exists between depression, antidepressant use, and VTE.
“These findings are very useful to me as both a clinician and a researcher,” Dr Kunutsor said. “It gives me the information I need, especially when prescribing antidepressant medications to my patients.”
Still, Dr Kunutsor and his colleagues conceded that more research is needed to determine if the observed associations are causal and if depression, antidepressant use, or both drive the increased risk of VTE.
To so this, studies would need to isolate depression from antidepressant medications. For example, researchers could assess if non-depressed individuals who use antidepressants for other conditions have an increased risk of VTE.
*The “other” antidepressants include monoamine oxidase inhibitors, triazolopyridine, serotonin norepinephrine reuptake inhibitors, and norepinephrine dopamine reuptake inhibitors.