RESUMO
Olanzapine is linked to asymptomatic, transient elevations of liver aminotransferases but is historically thought to rarely cause significant hepatotoxicity. Underlying liver disease is a risk factor for drug-induced liver injury and may complicate the differential diagnosis of acute transaminitis in patients taking medications associated with hepatotoxicity. Ms L presented with 2 months of new psychotic symptoms resulting in hospitalizations. Although psychosis previously improved with haloperidol, she reported symptoms concerning for akathisia. Restlessness improved and psychotic symptoms resolved after initiation of olanzapine. Concurrently, her alanine aminotransferase (ALT) was elevated, prompting further workup and new diagnosis of acute hepatitis C. Over the course of hospitalization, her ALT increased exponentially. Initially attributed solely to acute hepatitis C infection, ALT rapidly decreased after holding olanzapine, implying it was contributing to her liver injury. Subsequently, given her prior response, haloperidol was retrialed with close monitoring for adverse effects. Her subjective restlessness was treated with additional agents, and she was then transitioned to monthly haloperidol decanoate injections to further assist her adherence. Prior to discharge, she had resolution of psychosis and transaminitis. Olanzapine may contribute to hepatotoxicity with concurrent viral hepatitis, and clarity can be obtained by a trial of stopping the suspected medication. Furthermore, olanzapine, when combined with underlying liver disease, may have an additive effect on liver injury, resulting in accelerated elevations in liver aminotransferases.
RESUMO
Increased neural error monitoring, as measured by the error-related negativity (ERN), is a transdiagnostic neurobiological marker of anxiety. To date, little is known about whether the ERN can inform the choice between first-line anxiety disorder treatments and whether the ERN changes following treatment completion. The aim of the study was to therefore assess whether the ERN is a treatment moderator and index of symptom change during cognitive-behavioral therapy (CBT) or selective serotonin reuptake inhibitors (SSRIs). Participants included adult volunteers (M age=25.8±8.5; 67% female) with principal anxiety disorders (n=60) or no lifetime history of Axis I psychopathology (ie, healthy controls; n=26). A flanker task was used to elicit the ERN at baseline and 12 weeks later, following either CBT or SSRIs in the patient sample. Results indicated that baseline ERN was a significant treatment moderator such that a more enhanced baseline ERN was associated with greater reduction in anxiety symptoms within individuals who received CBT but not SSRIs. Results also revealed that the ERN increased pre- to post-treatment among patients randomized to SSRIs, but remained stable among patients randomized to CBT and healthy controls. Together, these novel findings highlight that ERN may help guide treatment decisions regarding engagement in CBT or SSRIs, especially among individuals with an enhanced ERN. The findings also suggest that SSRIs have the capacity to alter individual differences in the ERN, providing evidence that the ERN is not entirely static in patients with anxiety disorders.
