Delirium, thrombocytopenia, insomnia, and mild liver damage associated with MAOI withdrawal

Abstract

Dear Sir,Monoamine oxidase inhibitors (MAOIs) are effectivesecond-line treatment options for depression [ 1, 2]. A recentstudy showed that tranylcypromine (TCP), a nonselectiveand irreversible MAOI, remains commonly used in standardpsychiatric clinics [ 3]. The risk of hypertensive crisis due todrug  food interactions when MAOIs are prescribed iswidely known. Less well appreciated is the fact that MAOIscan cause addiction and that a particular patient populationmay be at high risk. Here we present a case of TCPdependence that brings together all signs and symptoms sofar described after TCP withdrawal, including delirium,thrombocytopenia, insomnia, and mild liver damage.CaseA 30-year-old woman diagnosed with major depressivedisorder and borderline personality disorder and with pasthistory of alcohol, marihuana, amphetamine, and cocaineabuse, presented to the emergency room. For the preceding1 2 years, she had been treated with TCP and titrated to60 mg a day, along with chlorpromazine 350 mg at nightfor “sleep. ” Two months after the initiation of TCP, shesteadily increased her dose to 170 mg a day. In order tomaintain her TCP intake, t he patient visited multiplephysicians in search for prescriptions. Three days prior toadmission,sheranoutofTCPandgraduallybecameagitated,irritable, and paranoid. When she presented to the emergencyroom, she was confused, unable to recognize her mother, andoriented to person only. She was described as responding tointernal stimuli and laughing inappropriately. On physicalexamination,she had a mild tachycardia,a severe tremor, andextensive bruising involving upper and lower extremities.Laboratory evaluation revealed a thrombocytopenia of72,000/µl.On further inpatient evaluation, her cognitive statusimproved. By the second day, her platelets had decreasedto 55,000/µl, and on the third day, these cells dropped furtherto 25,000/µl. During her third day of hospitalization, herpartial thromboplastin time (PTT) extended to 40.9 s and herliver function tests showed an aspartate transaminase (AST)of 106 IU/l. A liver ultrasound revealed fatty-acid infiltrates.On day 6, her platelets returned to normal limits. Nine daysafter admission, the patient was able to sleep 6 h without anymedication, and her tremor was completely resolved.DiscussionThis abrupt change in behavior and cognition coincideswith previously reported cases of delirium after acutewithdrawal from TCP [ 4–6]. It has been proposed thatdelirium and paranoia could result from acute removal ofthe sympathomimetic component of MAOIs on presynapticreceptors [ 7]. Under normal conditions, this presynapticeffect aims to diminish the release of catecholamines. Itis likely that when MAOIs are suddenly stopped,norepinephrine and dopamine acutely increase in thesynapse, rendering patients susceptible to psychosis anddelirium [ 6, 7].