RESUMEN
The comorbidity with anxiety disorders has profound adverse implications on the evolution, prognosis and therapeutic responsiveness of depression, it will prolong the time required to achieve remission of the depressive episode, and patients under treatment will tend to drop out of their therapeutic regimens faster than those with depression but without anxious comorbidity. The purpose of this study is to evaluate the importance of the clinical, etiopathogenetic, prognostic and especially therapeutic connotations given by the presence of psychiatric comorbidities in depression. Articles evaluating the presence of psychiatric comorbidities in depression were analyzed using PubMed, Medline, Scopus, Google Academics and WoS databases. To select the articles, we used keywords: psychiatric comorbidity, depression with anxiety disorders, depression with dysthymia, depression with psychoactive substances, depression with personality disorders. From a psychiatric perspective, the comorbidity of mental disorders can be divided into psychiatric comorbidity, when two or more distinct psychiatric conditions are present in the same individual, and medical comorbidity, when a medical-surgical illness is associated with a mental disorder. The presence of major depression is in itself a predictive factor for a later onset of generalized anxiety disorder. The comorbidity of depression in those with substance abuse or addiction has profound implications on their clinical prognosis. The association of personality disorder has a significant impact on the suicidal behavior of patients with major depression.
RESUMEN
(1) Background: The aim of this study was to analyze the impact of pharmacogenetic-guided antidepressant therapy on the 12-month evolution of the intensity of depressive symptoms in patients with recurrent depressive disorder (RDD) in comparison to a control group of depressive subjects who were treated conventionally. (2) Methods: This prospective longitudinal study was conducted between 2019 and 2022, and the patients were evaluated by employing the Hamilton Depression Rating Scale (HAM-D), Hamilton Anxiety Rating Scale (HAM-A) and the Clinical Global Impressions Scale: Severity and Improvement. We followed them up at 1, 3, 6, and 12 months. (3) Results: Of the 76 patients with RDD, 37 were tested genetically (Group A) and 39 were not (Group B). Although the patients from Group A had statistically significantly more severe MDD at baseline than those from Group B (p < 0.001), by adjusting their therapy according to the genetic testing, they had a progressive and more substantial reduction in the severity of RDD symptoms [F = 74.334; η2 = 0.674; p < 0.001], indicating a substantial association with the results provided by the genetic testing (67.4%). (4) Conclusions: In patients with RDD and a poor response to antidepressant therapy, pharmacogenetic testing allows for treatment adjustment, resulting in a constant and superior reduction in the intensity of depression and anxiety symptoms.
