{'fraction_non_alphanumeric': 0.02936096718480138, 'fraction_numerical': 0.03195164075993091, 'mean_word_length': 5.660919540229885, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Famotidine augmentation in schizophrenia: hope or hype?

J Clin Psychiatry 2013;74(9):e855–e858 (doi:10.4088/JCP.13f08707) © Copyright 2013 Physicians Postgraduate Press, Inc. A medication does not always result in the remission of positive symptoms in patients with schizophrenia. Furthermore, in many patients in whom positive symptoms substantially or completely remit, negative symptoms, cognitive disturbances, and other impairments often remain. Antipsychotic augmentation is one of many strategies to which clinicians turn in an attempt to reduce the burden of these residual symptoms, and famotidine is one of many unconventional augmentation agents that has been studied in this context. Histamine mechanisms may play a role in schizophrenia.1,2 Famotidine is a potent, selective histamine H2 receptor antagonist that poorly penetrates the blood-brain barrier.3,4 Although H2 receptors are present in the brain, there does not seem to be a strong argument made for the involvement of the H2 receptor in schizophrenia; nevertheless, many case reports and small open studies suggest that famotidine may improve outcomes in patients with schizophrenia.