Clozapine: An Updated Overview of Pharmacogenetic Biomarkers, Risks, and Safety-Particularities in the Context of COVID-19.
Ana Miruna DragoiIoana RadulescuBogdana Adriana NăsuiAnca Lucia PopValentin Nicolae VarlasSimona TrifuPublished in: Brain sciences (2020)
we considered RCTs and CCS from two databases, limited to the search topics. Conclusions and implications of key findings: (a) clozapine doses should be personalized for each patient based on pharmacogenetics testing when available; the genetic vulnerability postulates predictors of adverse reactions' severity; patients with a lower genetic risk could have less frequent hematological monitoring; (b) a CLZ-associated risk of pulmonary embolism imposes prophylactic measures for venous thromboembolism; (c) convulsive episodes are not an indication for stopping treatment; the plasma concentration of clozapine is a better side effect predictor than the dosage; (d) COVID-19 infection may enhance clozapine toxicity, generating an increased risk of pneumonia. Therapy must be continued with the proper monitoring of the white blood count, and the clozapine dose decreased by half until three days after the fever breaks; psychiatrists and healthcare providers must act together.
Keyphrases
- pulmonary embolism
- venous thromboembolism
- healthcare
- coronavirus disease
- sars cov
- inferior vena cava
- genome wide
- oxidative stress
- climate change
- emergency department
- case report
- copy number
- machine learning
- stem cells
- peripheral blood
- dna methylation
- direct oral anticoagulants
- human health
- social media
- electronic health record
- deep learning
- extracorporeal membrane oxygenation
- acute respiratory distress syndrome
- atrial fibrillation
- chemotherapy induced