Aspects of patient history emerged as 2 of 3 independently associated clinical predictors of whether patients currently being treated for major depressive disorder (MDD) will respond to treatment, according to a study presented here at the European Psychiatric Association (EPA) 22nd European Congress of Psychiatry.
Treating patients with treatment-resistant MDD (TRD) remains a challenge because it occurs frequently and is associated with a high number of relapses and hospitalisations plus the increased use of clinical treatments, said Georgio Di Lorenzo, MD, Department of Systems Medicine, University of Rome “Tor Vergata,” Rome, Italy, on March 2. He and colleagues conducted this analysis to identify clinical variables that could predict nonresponse in patients with MDD.
TRD was defined as the failure to respond to at least 2 different adequate trials of antidepressant treatment in the patient’s current episode, according to Dr. Di Lorenzo. He pointed out that the responder/nonresponder categories were established at the end of the hospitalisation period after treatment.
Cox regression models comparing variables in 253 patients who were hospitalised for TRD showed that patients with a history of ≥5 depressive episodes (odds ratio [OR] = 2.27) and those with a history of early-life adversities (OR = 1.60) were at increased risk of responding poorly or not at all to treatment for their current depression. Having a comorbid anxiety disorder was also determined to be predictive of poor response to current treatment (OR = 1.85).
Of the hospitalised patients with TRD, 154 were categorised as responders and 99 as nonresponders, according to whether they displayed at least a 50% decrease in the severity of their symptoms, measured by the Hamilton Rating Scale for Depression (HAM-D) 17.
The investigators concluded that the mechanisms for treatment resistance and poor response were likely to vary according to the clinical variables.
“The mechanism for treatment resistance in patients with ≥5 prior depressive episodes is probably linked to changes in brain morphology,” said Dr. Di Lorenzo, who also theorised that nonresponse in patients with early-life adversities could be linked to changes in the hypocanthus area of the brain.
Patients with a comorbid anxiety disorder showed poor response to antidepressive medication that was most likely linked to the physiological effects of GABA in the brain.
Dr. Di Lorenzo remarked that he has previously published a study showing that “dopaminergic modulation can be achieved with rotigotine and used to improve response and relieve anxiety in depressed patients.”
Treating patients with treatment-resistant MDD (TRD) remains a challenge because it occurs frequently and is associated with a high number of relapses and hospitalisations plus the increased use of clinical treatments, said Georgio Di Lorenzo, MD, Department of Systems Medicine, University of Rome “Tor Vergata,” Rome, Italy, on March 2. He and colleagues conducted this analysis to identify clinical variables that could predict nonresponse in patients with MDD.
TRD was defined as the failure to respond to at least 2 different adequate trials of antidepressant treatment in the patient’s current episode, according to Dr. Di Lorenzo. He pointed out that the responder/nonresponder categories were established at the end of the hospitalisation period after treatment.
Cox regression models comparing variables in 253 patients who were hospitalised for TRD showed that patients with a history of ≥5 depressive episodes (odds ratio [OR] = 2.27) and those with a history of early-life adversities (OR = 1.60) were at increased risk of responding poorly or not at all to treatment for their current depression. Having a comorbid anxiety disorder was also determined to be predictive of poor response to current treatment (OR = 1.85).
Of the hospitalised patients with TRD, 154 were categorised as responders and 99 as nonresponders, according to whether they displayed at least a 50% decrease in the severity of their symptoms, measured by the Hamilton Rating Scale for Depression (HAM-D) 17.
The investigators concluded that the mechanisms for treatment resistance and poor response were likely to vary according to the clinical variables.
“The mechanism for treatment resistance in patients with ≥5 prior depressive episodes is probably linked to changes in brain morphology,” said Dr. Di Lorenzo, who also theorised that nonresponse in patients with early-life adversities could be linked to changes in the hypocanthus area of the brain.
Patients with a comorbid anxiety disorder showed poor response to antidepressive medication that was most likely linked to the physiological effects of GABA in the brain.
Dr. Di Lorenzo remarked that he has previously published a study showing that “dopaminergic modulation can be achieved with rotigotine and used to improve response and relieve anxiety in depressed patients.”
