An Open-Label Study of the Therapeutic Efficacy of High-Dose Famotidine Adjuvant Pharmacotherapy in Schizophrenia: Preliminary Evidence for Treatment Efficacy

Rosse, Richard B.; Kendrick, Kathie; Fay-McCarthy, Maureen; Prell, George D.; Rosenberg, Paul B.; Tsui, Lorraine C.; Wyatt, Richard Jed; Deutsch, Stephen I.

doi:10.1097/00002826-199619040-00007

Cited by 32 publications

(13 citation statements)

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“…4 In spite of the limited brain penetration of famotidine, a H2R antagonist, several openlabel clinical trials support an antipsychotic efficacy of this drug. [5][6][7] Recently, a polymorphism leading to an amino acid substitution within the third intracellular loop of the H2R was found to be associated with schizophrenia. 8,9 We have further examined the presence of allelic variants in the coding and promoter regions of the H2R gene and investigated their putative association with schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Histamine H2 receptor gene variants: lack of association with schizophrenia

et al. 2000

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A role of histaminergic neuronal systems in schizophrenia was suggested by an association with several polymorphisms located in the coding region of the histamine H 2 -receptor (H2R) gene (Orange et al, Mol Psychiatry 1996; 1: 466-469). Using either the reference method of direct sequencing or restriction endonuclease digestion of PCR products amplified from DNA, we could not confirm the existence of these polymorphisms in 53 Swedish controls, 52 French controls and 88 French schizophrenics. In contrast, we detected a G543A transition in the coding region of the gene that was not found in the British population. This allelic variation, which was observed in 15% of the controls with no homozygotes, did not change the amino acid sequence of the receptor. We also analyzed a 1.8-kb nucleotide sequence of the promoter region in which we detected two additional polymorphisms that may modulate the expression of the H2R gene. The first one was a A-592G transition located in the minimal promoter of the gene and found in ෂ10% of controls with no homozygotes. The second one was a G-1018A transition located in an enhancer element of the promoter and was found in ෂ20-30% of controls (with ෂ2-4% homozygotes). DNA analysis of the 88 French schizophrenic subjects revealed that the incidence of the three polymorphisms was not significantly different in this population. In conclusion, the present findings may suggest a surprisingly high variability of the H2R gene polymorphisms in different geographical areas but do not support an association of these allelic variations with schizophrenia. Molecular Psychiatry (2000) 5, 159-164.

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Section: Introductionmentioning

confidence: 99%

Histamine H2 receptor gene variants: lack of association with schizophrenia

et al. 2000

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“…5,6 (pooled N = 2) and 6 small open studies [7][8][9][10][11][12] (pooled N = 75) indicated benefits with famotidine augmentation in antipsychotic-refractory schizophrenia. 2.…”

Section: Clinical Pointsmentioning

confidence: 99%

Famotidine Augmentation in Schizophrenia: Hope or Hype?

Andrade

2013

J. Clin. Psychiatry

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“…The clinical response to H 2 R blockade remains largely unknown. It is worth noting, however, that in several open-label clinical trials, famotidine, a H 2 R inverse agonist (Alewijnse et al 1998) with limited brain penetration, displayed an antipsychotic efficacy (Kaminsky et al 1990;Oyewumi et al 1994;Rosse et al 1996), but this remains to be confirmed in double-blind studies. Several H 2 R polymorphisms have also been identified, but again none of them was associated with schizophrenia or response to clozapine (Fukushima et al 2001;Ito et al 2000;Mancama et al 2000;Mancama et al 2002).…”

Section: Involvement Of Histamine Receptors In the Antipsychotic Profmentioning

confidence: 99%