Fast-track for timely treatment of depression in college students

Background: Depression is a prevalent and leading issue among college students, which became worsened by the global pandemic of COVID-19. The Student Health Clinic in one of the tertiary public universities in Southern California also proved to be impacted with mental health complaints, depression being one of the most common diagnoses. The early treatment of depression is critical to avoid possible complications including suicidal ideation from untreated depression. Objectives: The primary objective was to implement a new workflow (Fast-Track) to treat students with uncomplicated depression as early as possible. Method: This project used a pre- and post-intervention design. The Fast-Track has three components: 1) reserving appointment slots from primary care providers' clinic schedules for the Fast-Track patients, 2) sending an education material about depression treatment options to the patients to read before an initial visit, 3) providing two follow-up visits at weeks 2, and 5 or 6. A descriptive analysis was performed for demographic data and secondary outcome (PHQ-9 score), Paired two sample t-Test was used for the primary outcome (time to treatment in days). Data from the participants who completed the two follow-up visits were included in the analysis. Results: A total of 24 patients met the criteria for uncomplicated depression. 16 patients completed the two follow-up visits. Time to treatment in days reduced from 19.2 days (SD 4.6) to 2.5 days (SD 1.8) (p < 0.05). The mean PHQ-9 score at the baseline visit was 13.6 (SD 4.1) and 11.4 (SD 2.5) at the second follow-up visit with a mean change of -2. 2. 81.3% (n=13) of the 16 patients reported improvement at week 5 or 6 and 18.6 % (n=3) reported worsening of their depression symptoms. Conclusion: Opening up access to provider schedules greatly improved the patient's time to treatment. Utilizing primary care providers, including APRN's, in the management of simple, uncomplicated depression for college students was safe and successful. The outcomes seen in this project offer some insight into how the pharmacological treatment for simple, uncomplicated depression can be safely initiated sooner among college students. (PsycInfo Database Record (c) 2022 APA, all rights reserved)

Antidepressant effect of prolonged twice-weekly intranasal esketamine treatments after nonresponse to electroconvulsive therapy in a patient with treatment-resistant depression

Presents a case report of a woman with depressive episodes, which began in early 2019 and was worsened by the change of her long-standing antidepressant regimen of fluoxetine to mirtazapine. Subsequently, she received 12 right unilateral ultrabrief pulse electroconvulsive therapy (ECT) treatments without any benefit. She experienced no benefit from 4 additional trials of antidepressants and during our evaluations over several weeks, her mood remained severely depressed. After 6 treatments, she experienced >50% reduction in her depression. However, her esketamine treatments were paused for 8 weeks due to COVID-19. Her depression worsened and a 4-week-long course of twice-weekly treatments was initiated, which resulted in a >50% reduction in her depression. After switching to weekly maintenance treatments, her symptoms of low mood, anhedonia, and suicidal ideation returned to her pre-treatment baseline. As she had responded well to twice-weekly treatments, the frequency of treatments was increased. In summary, this patient responded to twice-weekly esketamine treatments, experienced symptomatic worsening after switching to weekly treatments, but was able to attain remission with prolonged twice-weekly treatments. (PsycInfo Database Record (c) 2022 APA, all rights reserved)

Drug-drug interactions between COVID-19 treatments and antidepressants, mood stabilizers/anticonvulsants, and benzodiazepines: Integrated evidence from 3 databases

Introduction: The SARS-CoV-2 pandemic with psychiatric comorbidities leads to a scenario in which the use of psychotropic drugs may be required. This requires the support of evidence-based medicine to take into account possible interactions between antidepressants, mood stabilizers, benzodiazepines, and coronavirus infection treatments. Methods: Three databases were consulted: (a) Lexicomp Drug Interactions, (b) Micromedex Solutions Drugs Interactions, (c) Liverpool Drug Interaction Group for COVID-19 therapies. The CredibleMeds QTDrugs List was also queried. Hydroxychloroquine, chloroquine, azithromycin, lopinavir-ritonavir, remdesivir, favipiravir, tocilizumab, baricitinib, anakinra, and dexamethasone - drugs used for SARS-CoV-2-were analyzed, and consensus recommendations are made. Results: The potential interactions of agomelatine, desvenlafaxine, duloxetine, milnacipran, and vortioxetine with COVID-19 treatments shall be considered less risky. Antidepressant interactions with hydroxychloroquine, chloroquine, and azithromycin enhance the risk of QT prolongation, and ECG monitoring is advised for most antidepressants. Antidepressants with lopinavir/ ritonavir involve multiple CYP enzyme interactions (except with milnacipran). Gabapentin, oxcarbazepine, pregabalin, topiramate, and zonisamide are safe treatment options that have no significant interactions with COVID-19 treatments. Lithium is contraindicated with hydroxychloroquine, chloroquine, and azithromycin. Precaution should be taken in using valproic acid with lopinavir-ritonavir. The use of benzodiazepines does not present a risk of drug interaction with COVID-19 treatments, except lopinavir/ritonavir. Conclusions: Clinicians prescribing antidepressants, mood stabilizers/anticonvulsants, and benzodiazepines, should be aware of the probable risk of drug-drug interaction with COVID- 19 medications and may benefit from heeding these recommendations for use to ensure patient safety. (PsycInfo Database Record (c) 2022 APA, all rights reserved)

Neuropsychiatric drugs against COVID-19: What is the clinical evidence?

Since the beginning of the coronavirus disease (COVID)-19 pandemic, the need for effective treatments for COVID-19 led to the idea of "repurposing" drugs for antiviral treatment. Several antipsychotics and antidepressants have been tested for in vitro activity against the severe acute respiratory syndrome coronavirus 2. Chlorpromazine, other phenothiazine antipsychotics, and the antidepressant fluoxetine were found to be rather potent in these studies. However, whether effective plasma concentrations can be obtained with clinically accepted doses of these drugs is not clear. Data of COVID-19 patients are not yet available but several clinical studies are currently underway. The specific serotonin reuptake inhibitor fluvoxamine is a potent Sigma-1 receptor agonist and reduces inflammation in animal models of cytokine-stress. Accordingly, fluvoxamine treatment was superior to placebo in reducing impaired respiratory function and other symptoms of inflammation in COVID-19 patients in a placebo-controlled clinical study and another open clinical trial. The beneficial effects of fluvoxamine on the course of COVID-19 were recently confirmed in a large placebo-controlled double-blind trial with several hundred patients. Inflammation represents a major risk factor for many psychiatric disorders which explains the high susceptibilitiy of COVID- 19 patients for psychiatric diseases. Many antidepressants and antipsychotics possess anti-inflammatory properties independent of sigma-1 activity which might be important to reduce psychiatric symptoms of COVID-19 patients and to improve respiratory dysfunction and other consequences of inflammation. This might explain the rather unspecific benefit which has been reported for several cohorts of COVID-19 patients treated with different psychotropic drugs. (PsycInfo Database Record (c) 2022 APA, all rights reserved)

Psychotropic drugs: Therapeutic perspectives against Covid-19

Based on older reports about antiviral effects in vitro, several antipsychotics and antidepressants have recently been investigated for possible activity against the Covid-19 virus (SARS-CoV-2). A few have been found to be active in vitro, like chlorpromazine and some other phenothiazine antipsychotics as well as the antidepressants fluoxetin and fluvoxamine. For chlorpromazine, two clinical studies with Covid-19 patients are currently under way in France and Egypt, while for fluoxetine clinical data are not yet available. The specific serotonin reuptake inhibitor fluvoxamine is also a potent sigma-1 receptor agonist and has been shown to reduce inflammation in an animal model of cytokine-stress. In analogy to these findings, fluvoxamine treatment for 15 days was superior to placebo in reducing symptoms of impaired respiratory function in a first placebo-controlled clinical study. © 2021 Wissenschaftliche Verlagsgesellschaft Stuttgart.

Pharmacogenetic-Guided Antidepressant Selection as an Opportunity for Interprofessional Collaboration: A Case Report.

In the herein reported case of a 42-year-old woman diagnosed with anxiety and depression, a long history of antidepressant ineffectiveness and adverse drug reactions was decisive for an in-depth medication review including pharmacogenetic panel testing. In detail, treatment attempts with paroxetine and escitalopram were ineffective and discontinued due to subjective gastrointestinal intolerance. Due to the worsening of the depression after the failed treatment attempts, admission to our clinic became necessary. Herein, owing to the collaboration of psychiatrists with clinical pharmacists, individualized incorporation of pharmacogenetic data into the process of antidepressant selection was enabled. We identified vortioxetine as a suitable therapeutic, namely for being most likely pharmacokinetically unaffected as predicted by pharmacogenetic panel testing and taking into account the current comedication, as well as for its favorable action profile. Herein, our collaborative effort proved to be successful and resulted in the patient's depression remission and clinic discharge with the interprofessionally selected pharmacotherapy. This exemplary case not only highlights the potential benefits and challenges of pre-emptive pharmacogenetic testing in antidepressant prescription, but also proposes an approach on how to put pharmacogenetics into practice.

Drug repurposing of selective serotonin reuptake inhibitors: Could these drugs help fight COVID-19 and save lives?

The current 2019 novel coronavirus disease (COVID-19), an emerging infectious disease, is undoubtedly the most challenging pandemic in the 21st century. A total of 92,977,768 confirmed cases of COVID-19 and 1,991,289 deaths were reported globally up to January 14, 2021. COVID-19 also affects people's mental health and quality of life. At present, there is no effective therapeutic strategy for the management of this disease. Therefore, in the absence of a specific vaccine or curative treatment, it is an urgent need to identify safe, effective and globally available drugs for reducing COVID-19 morbidity and fatalities. In this review, we focus on selective serotonin reuptake inhibitors (SSRIs: a class of antidepressant drugs with widespread availability and an optimal tolerability profile) that can potentially be repurposed for COVID-19 and are currently being tested in clinical trials. We also summarize the existing literature on what is known about the link between serotonin (5-HT) and the immune system. From the evidence reviewed here, we propose fluoxetine as an adjuvant therapeutic agent for COVID-19 based on its known immunomodulatory, anti-inflammatory and antiviral properties. Fluoxetine may potentially reduce pro-inflammatory chemokine/cytokines levels (such as CCL-2, IL-6, and TNF-α) in COVID-19 patients. Furthermore, fluoxetine may help to attenuate neurological complications of COVID-19.

How Antidepressant Drugs Affect the Antielectroshock Action of Antiseizure Drugs in Mice: A Critical Review.

Depression coexists with epilepsy, worsening its course. Treatment of the two diseases enables the possibility of interactions between antidepressant and antiepileptic drugs. The aim of this review was to analyze such interactions in one animal seizure model-the maximal electroshock (MES) in mice. Although numerous antidepressants showed an anticonvulsant action, mianserin exhibited a proconvulsant effect against electroconvulsions. In most cases, antidepressants potentiated or remained ineffective in relation to the antielectroshock action of classical antiepileptic drugs. However, mianserin and trazodone reduced the action of valproate, phenytoin, and carbamazepine against the MES test. Antiseizure drug effects were potentiated by all groups of antidepressants independently of their mechanisms of action. Therefore, other factors, including brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF) modulation, should be considered as the background for the effect of drug combinations.