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Acute Psychosis Following Initiation of Ruxolitinib in Post-Polycythaemia Vera Myelofibrosis
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Abstract
Polycythaemia vera (PV) is a myeloproliferative neoplasm (MPN) which can progress to myelofibrosis (MF), a phenomenon termed post-PV MF. Ruxolitinib is a Janus activated kinase (JAK) inhibitor that targets JAK mutations and is approved for treatment of high-risk MF. This is a case report of a patient with Post-PV MF who developed acute psychotic disorder five months after commencing ruxolitinib and whose mental status returned to baseline within one week of stopping ruxolitinib. Importantly, there was no history of mental health disorder and no identifiable triggers for his presentation. Ruxolitinib has not previously been implicated in the development of psychosis. Ruxolitinib is known to modulate immune responses in the central nervous system (CNS) and is thought to reduce microglia activation, thus reducing neuroinflammation. Such neuromodulation in the CNS may pose a potential mechanism by which ruxolitinib can affect mental status, however these signalling pathways are not clearly defined and future work into this theory is required.
Title: Acute Psychosis Following Initiation of Ruxolitinib in Post-Polycythaemia Vera Myelofibrosis
Description:
Abstract
Polycythaemia vera (PV) is a myeloproliferative neoplasm (MPN) which can progress to myelofibrosis (MF), a phenomenon termed post-PV MF.
Ruxolitinib is a Janus activated kinase (JAK) inhibitor that targets JAK mutations and is approved for treatment of high-risk MF.
This is a case report of a patient with Post-PV MF who developed acute psychotic disorder five months after commencing ruxolitinib and whose mental status returned to baseline within one week of stopping ruxolitinib.
Importantly, there was no history of mental health disorder and no identifiable triggers for his presentation.
Ruxolitinib has not previously been implicated in the development of psychosis.
Ruxolitinib is known to modulate immune responses in the central nervous system (CNS) and is thought to reduce microglia activation, thus reducing neuroinflammation.
Such neuromodulation in the CNS may pose a potential mechanism by which ruxolitinib can affect mental status, however these signalling pathways are not clearly defined and future work into this theory is required.
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