| Autor: |
Mestre TA; Division of Neurology The Parkinson's Disease and Movement Disorder Center The Ottawa Hospital Ottawa Ontario Canada., Shah BB; Department of Neurology University of Virginia Health Sciences Center McKim Hall Charlottesville Virginia USA., Connolly BS; Division of Neurology Department of Medicine McMaster University, Hamilton Health Sciences Hamilton Ontario Canada., de Aquino C; Division of Neurology Movement Disorders Center and Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network, University of Toronto Toronto Canada., Al Dhakeel A; Division of Neurology Movement Disorders Center and Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network, University of Toronto Toronto Canada., Walsh R; Movement Disorders Unit Tallaght Hospital and Trinity College Dublin Dublin Ireland., Ghate T; Division of Neurology Movement Disorders Center and Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network, University of Toronto Toronto Canada., Lui JP; Department of Pharmacy Toronto Western Hospital Toronto Ontario Canada., Fox SH; Division of Neurology Movement Disorders Center and Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network, University of Toronto Toronto Canada. |
| Jazyk: |
angličtina |
| Zdroj: |
Movement disorders clinical practice [Mov Disord Clin Pract] 2014 Jun 26; Vol. 1 (3), pp. 219-224. Date of Electronic Publication: 2014 Jun 26 (Print Publication: 2014). |
| DOI: |
10.1002/mdc3.12061 |
| Abstrakt: |
The neural mechanisms underlying levodopa-induced dyskinesia (LID) in Parkinson's disease (PD) may involve histamine (H 2 ) receptors on striatopallidal pathways. We recently demonstrated that the clinically available oral histamine H 2 receptor antagonist (H 2 RA), famotidine, can reduce l-dopa-induced chorea in MPTP-lesioned macaques. We hypothesized that famotidine may be useful in the treatment of LID in PD patients. We performed a proof-of-concept, double-blind, randomized, multiple cross-over (4×) trial. Seven PD subjects with bothersome dyskinesia were randomized to oral famotidine 80, 120, and 160 mg/day and placebo. Each subject was randomized to receive each of the four treatment phases for 14 days followed by a 7-day wash-out period between each treatment phase. The primary outcome measure was change in the Unified Dyskinesia Rating Scale (UDysRS; part III) between placebo and famotidine. Secondary outcomes were UDysRS (parts I and II), Global Impression of Change, Lang-Fahn Activities of Daily Living Dyskinesia Scale, Unified Parkinson's Disease Rating part III, and adverse events (AEs). Outcomes were evaluated pre- and post-treatment per dose and analyzed using a mixed-effects linear model. There was no significant effect of famotidine treatment on any of the primary or secondary outcome measures compared to placebo (each dose and all doses combined). There were no significant AEs. Even though the sample size of the current study is limited, famotidine seems to be safe in patients with PD and LID, but showed no potential as an antidyskinetic agent. |
| Databáze: |
MEDLINE |
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