Quetiapine, a pharmacological agent within the class of atypical antipsychotics, is characterized by its efficacy in mood stabilization and its role in the modulation of serotonergic and dopaminergic pathways. Its therapeutic utility is broad, encompassing the management of acute psychotic episodes, schizophrenia, bipolar disorder, and treatment-resistant depressive states. Quetiapine\'s effectiveness extends to depressive disorders that do not exhibit classic psychotic features, with a side effect profile that is less burdensome than many alternative psychotropic medications. Its versatility in addressing a range of psychiatric conditions is useful in the psychopharmacological management of mood and thought disorders. However, like all drugs, quetiapine may have different effects relative to the individual. It is imperative to approach the administration of quetiapine carefully, ensuring any adverse effects are ameliorated for beneficial therapeutic outcomes. In this case report, we present a psychosis-naive 42-year-old male who developed psychotic symptoms after beginning a quetiapine regimen in order to manage major depressive disorder with suicidal ideation. Clinical suspicion of quetiapine-induced psychosis was a diagnosis considered due to symptom remission secondary to ziprasidone in the place of quetiapine. The determination of a suspected adverse drug reaction can utilize the Naranjo scale to demonstrate the likelihood of an adverse drug reaction. This patient scored a three on the Naranjo scale, indicating a possible adverse effect from quetiapine. Other potential etiologies of psychosis include medication-induced psychosis, major depressive disorder exacerbation, cocaine use/withdrawal, and brief psychotic disorder. Quetiapine-induced psychosis has not been described in the current literature, and therefore, this case report is solely based on clinical evaluation and is intended for educational purposes due to possible confounding factors and etiologies.

Some people who experience substance-induced psychosis later develop an enduring psychotic disorder such as schizophrenia. This study examines the proportion of people with substance-induced psychoses who transition to schizophrenia, compares this to other brief and atypical psychoses, and examines moderators of this risk. A search of MEDLINE, PsychINFO, and Embase identified 50 eligible studies, providing 79 estimates of transition to schizophrenia among 40 783 people, including 25 studies providing 43 substance-specific estimates in 34 244 people. The pooled proportion of transition from substance-induced psychosis to schizophrenia was 25% (95% CI 18%-35%), compared with 36% (95% CI 30%-43%) for brief, atypical and not otherwise specified psychoses. Type of substance was the primary predictor of transition from drug-induced psychosis to schizophrenia, with highest rates associated with cannabis (6 studies, 34%, CI 25%-46%), hallucinogens (3 studies, 26%, CI 14%-43%) and amphetamines (5 studies, 22%, CI 14%-34%). Lower rates were reported for opioid (12%), alcohol (10%) and sedative (9%) induced psychoses. Transition rates were slightly lower in older cohorts but were not affected by sex, country of the study, hospital or community location, urban or rural setting, diagnostic methods, or duration of follow-up. Substance-induced psychoses associated with cannabis, hallucinogens, and amphetamines have a substantial risk of transition to schizophrenia and should be a focus for assertive psychiatric intervention.