Switching Antidepressant Class Does Not Improve Response or Remission in Treatment-Resistant Depression

Souery, Daniel; Serretti, Alessandro; Calati, Raffaella; Oswald, Pierre; Massat, Isabelle; Konstantinidis, Anastasios; Linotte, Sylvie; Bollen, Joseph; Demyttenaere, Koen; Kasper, Siegfried; Lecrubier, Y.; Montgomery, Stuart; Zohar, Joseph; Mendlewicz, Julien

doi:10.1097/jcp.0b013e3182228619

Cited by 95 publications

(54 citation statements)

References 19 publications

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“…This important revision is in line with the most recent data, showing no advantage in favour of switching to a different class of antidepressant (Bschor & Baethge, 2010;Papakostas et al, 2008;Ruhé et al, 2006;Rush et al, 2006;Souery et al, 2011aSouery et al, , 2011b. This important revision is in line with the most recent data, showing no advantage in favour of switching to a different class of antidepressant (Bschor & Baethge, 2010;Papakostas et al, 2008;Ruhé et al, 2006;Rush et al, 2006;Souery et al, 2011aSouery et al, , 2011b.…”

Section: Definition Of Trd In Clinical Trialssupporting

confidence: 82%

Definitions and Predictors of Treatment‐resistant Depression

Souery¹,

Pitchot

Kasper

et al. 2013

Treatment‐resistant Depression

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Section: Definition Of Trd In Clinical Trialssupporting

confidence: 82%

Definitions and Predictors of Treatment‐resistant Depression

Souery¹,

Pitchot

Kasper

et al. 2013

Treatment‐resistant Depression

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“…Guidelines of scientific associations for the treatment of patients with MDD recommend that, when remission is not achieved with an AD after 6 to 8 weeks of treatment at adequate dose, this should be changed [10]. However, controversy remains and there are no conclusive data as to which is the best alternative available [19,47,48]. …”

Section: Discussionmentioning

confidence: 99%

Assessment of pharmacological strategies for management of major depressive disorder and their costs after an inadequate response to first-line antidepressant treatment in primary care

et al. 2012

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BackgroundThe aim of the study was to determine the most common treatment strategies and their costs for patients with an inadequate response to first-line antidepressant treatment (AD) in primary care.MethodA retrospective cohort study of medical records from six primary care centers was conducted. Adults with a major depressive disorder diagnosis, at least 8 weeks of AD treatment after the first prescription, and patient monitoring for 12 months were analyzed. Healthcare (direct cost) and non-healthcare costs (indirect costs; work productivity losses) were described.ResultsA total of 2,260 patients were studied. Forty-three percent of patients (N = 965) presented an inadequate response to treatment. Summarizing the different treatment approaches: 43.2% were switched to another AD, 15.5% were given an additional AD, AD dose was increased in 14.6%, and 26.7% remained with the same antidepressant agent. Healthcare/annual costs were 451.2 Euros for patients in remission vs. 826.1 Euros in those with inadequate response, and productivity losses were 991.4 versus 1,842.0 Euros, respectively (p < 0.001).ConclusionAntidepressant switch was the most common therapeutic approach performed by general practitioners in naturalistic practice. A delay in treatment change when no remission occurs and a significant heterogeneity in management of these patients were also found.

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“…The treatment of major depression remains a major challenge. Only a small portion of patients with major depression responds to treatments targeting monoamine reuptake (Souery, et al 2011; Thase, et al 2001). Moreover, patients with chronic pain and depression are poorly responsive to current antidepressant treatments (Karp, et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of neuronal kynurenine 3-monooxygenase mediates depression-like behavior in a mouse model of neuropathic pain

Laumet

Zhou

Dantzer³

et al. 2017

Brain, Behavior, and Immunity

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Pain and depression often co-occur, but the underlying mechanisms have not been elucidated. Here, we used the spared nerve injury (SNI) model in mice to induce both neuropathic pain and depression-like behavior. We investigated whether brain IL-1 signaling and activity of kynurenine 3-monoxygenase (KMO), a key enzyme for metabolism of kynurenine into the neurotoxic NMDA receptor agonist quinolinic acid, are necessary for comorbid neuropathic pain and depression-like behavior. SNI mice showed increased expression levels of Il1b and Kmo mRNA in the contralateral side of the brain. The SNI-induced increase of Kmo mRNA was associated with increased KMO protein and elevated quinolinic acid and reduced kynurenic acid in the contralateral hippocampus. The increase in KMO-protein in response to SNI mostly took place in hippocampal NeuN-positive neurons rather than microglia. Inhibition of brain IL-1 signaling by intracerebroventricular administration of IL-1RA after SNI prevented the increase in Kmo mRNA and depression-like behavior measured by forced swim test. However, inhibition of brain IL-1 signaling has no effect on mechanical allodynia. In addition, intracerebroventricular administration of the KMO inhibitor Ro 61-8048 abrogated depression-like behavior without affecting mechanical allodynia after SNI. We show for the first time that the development of depression-like behavior in the SNI model requires brain IL-1 signaling and activation of neuronal KMO, while pain is independent of this pathway. Inhibition of KMO may represent a promising target for treating depression.

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Switching Antidepressant Class Does Not Improve Response or Remission in Treatment-Resistant Depression

Abstract: In depressed nonresponders to a previous antidepressant treatment, switching to a different class of antidepressants was not associated with a better response or remission rate.

Cited by 95 publications

References 19 publications

Definitions and Predictors of Treatment‐resistant Depression

Definitions and Predictors of Treatment‐resistant Depression

Assessment of pharmacological strategies for management of major depressive disorder and their costs after an inadequate response to first-line antidepressant treatment in primary care

Upregulation of neuronal kynurenine 3-monooxygenase mediates depression-like behavior in a mouse model of neuropathic pain

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