Abstract
Background: Antibiomania is a term used to describe antibiotic-induced psychosis. Triple therapy, including a PPI, amoxicillin, and clarithromycin, is commonly prescribed for patients infected with H. pylori. Acute psychotic episodes in patients undergoing this treatment regimen are found to have have been most often associated with clarithromycin. Onset of symptoms occurs within 7 days of therapy initiation and resolution occurring 24 to 48 hours after cessation. Case Presentation: A 49-year old male with no psychiatric history and recently diagnosed H. pylori gastritis was brought to the ER by his wife who noted strange behavior in the patient. The wife had found the patient on a toilet unresponsive with a blank stare. The patient abruptly stated he felt as if he was “leaving the planet” followed by cat-like screeching and movements. PMH was significant for GERD, controlled with omeprazole for 6 years. He was recently started on triple therapy for H. pylori gastritis, which included lanzoprazole, amoxicillin and clarithromycin 5 days prior. Physical Exam/Labs: In the ER, the patient was noted to have upper extremity jerky movements that resolved after 10 seconds without any intervention. Vital signs, lab studies, and CT of the head were unremarkable. The physical exam was benign except for disorientation to person and time. Hospital Course: The patient was admitted and all medications were discontinued. All organic causes were ruled out for a possible cause of acute psychosis. Symptoms began to subside within 24 hours of cessation of triple therapy with complete resolution in 36 hours. The patient became oriented and returned to his baseline mental status with no administration of anti-psychotics. Clinical Significance: Onset of psychosis days after initiation of treatment with rapid resolution with discontinuation of medications verified triple therapy to be the likely cause. Long-term PPI use disqualified this as a trigger. There have been minimal reports of amoxicillin inducing psychosis making this the less likely culprit. As widely reported, clarithromycin was the likely agent responsible for symptoms. Clarithromycin may be directly toxic to the CNS system via its lipid-soluble active metabolite 14-hydroxyclarithromycin. Clarithromycin has also been known to alter cortisol and prostaglandin metabolism, and interact with glutaminergic and GABA pathways possibly leading to CNS side effects. Though these are all plausible explanations, how clarithromycin causes psychosis remains a debate requiring further research. Clinicians should be cognizant of the psychiatric effects secondary to clarithromycin and discontinuation should be prompt for rapid recovery.
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