Title: Lurasidone (LATUDA)-Induced Pancreatitis: A Case Report

Background: Lurasidone (LATUDA) is a second-generation antipsychotic used in the management of schizophrenia and bipolar disorder. There have been reports of drug-induced pancreatitis (DIP) associated with antipsychotics such as haloperidol, olanzapine and clozapine. However, there is limited documented literature on the association between Lurasidone and pancreatitis. Although rare, DIP is a severe adverse effect of various medications. Here, we present a compelling case of Lurasidone-induced pancreatitis that sets itself apart from other cases of DIP.

Methods: A 60-year-old African-American woman with a past medical history of Type-1 bipolar disorder presented to the ER with complaints of nausea, multiple episodes of vomiting, and constant, sharp abdominal pain that radiates to her back. These symptoms began approximately a month after she started taking Lurasidone. A thorough examination revealed tenderness to palpation in the umbilical and lower abdominal area without rebound tenderness or guarding. Laboratory tests showed significantly elevated serum Lipase (997 U/L) and serum Amylase (533 U/L), consistent with the diagnosis of acute pancreatitis. We considered a diagnosis of Lurasidone-induced pancreatitis due to the correlation between the initiation of Lurasidone therapy and the manifestation of her symptoms. Subsequently, we discontinued the patient's Lurasidone therapy and initiated supportive management, including bowel rest, intravenous fluids, and pain control. Her symptoms improved progressively and successive laboratory assessments revealed downward trending pancreatic enzyme concentrations (serum Lipase of 25 U/L after a week).

Results: Despite the absence of documented literature linking Lurasidone specifically to pancreatitis, patient presentation and laboratory findings confirmed drug-induced pancreatitis. Much like the other antipsychotics implicated in drug-induced pancreatitis (DIP), the mechanism of this reaction, although unclear, is believed to stem from either direct toxicity on pancreatic cells, immune-mediated mechanisms, or hypertriglyceridemia.

Conclusion: Since there are no documented cases of Lurasidone-induced pancreatitis, this case report necessitates healthcare providers to maintain a high index of suspicion for DIP in patients presenting with acute abdominal pain when they are on Lurasidone therapy. The patient's clinical presentation, laboratory findings, and the temporal relationship between the start of Lurasidone treatment and the onset of symptoms, combined with the lack of any other identifiable causes for pancreatitis, established the diagnosis of Lurasidone-induced pancreatitis. Further studies are warranted to elucidate the underlying pathophysiological mechanisms and guide appropriate clinical practice for prompt patient management.