Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2021
The efficacy of add-on ramelteon and subsequent dose reduction in benzodiazepine derivatives/Z-drugs for the treatment of sleep-related eating disorder and night eating syndrome: a retrospective analysis of consecutive patients.
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Matsui Kentaro, Kuriyama Kenichi, Kobayashi Mina, Inada Ken, Nishimura Katsuji, Inoue Yuichi
Аннотация
STUDY OBJECTIVES: The objective of this study was to determine the efficacy of ramelteon in treating abnormal eating behavior in patients with sleep-related eating disorder and/or night eating syndrome.
METHODS: We retrospectively reviewed the medical records of patients with sleep-related eating disorder/night eating syndrome at the Yoyogi Sleep Disorder Center from November 2013 to November 2018. We categorized patients as ramelteon treatment responders when the frequency of nighttime eating per week decreased to less than half of that before treatment.
RESULTS: Forty-nine patients were included in the analysis. The mean frequency of eating behavior (per week) (standard deviation) at baseline and post-ramelteon treatment was significantly different, at 5.3 (2.2) and 3.2 (3.0), respectively (P < .001). Twenty-one patients (42.9%) were classified as responders. Adverse events, all of which were mild daytime somnolence, were observed in 5 patients. There were significantly more individuals using benzodiazepine derivatives and Z-drugs before treatment and those with coexisting delayed sleep-wake phase disorder in the responder group than in the nonresponder group (P < .001 and P < .05, respectively). The mean benzodiazepine derivatives and Z-drugs dose significantly decreased from baseline to post-ramelteon treatment within the responder group (P < .05). This trend was not observed in the nonresponder group. Meanwhile, the sleep midpoint of patients with sleep-related eating disorder/night eating syndrome and delayed sleep-wake phase disorder did not significantly change after treatment.
CONCLUSIONS: Our results indicate that ramelteon is a candidate treatment for sleep-related eating disorder/night eating syndrome. The effects of ramelteon might have occurred primarily through the reduction in benzodiazepine derivatives and Z-drugs rather than through the improvement in sleep-wake rhythm dysregulation.
METHODS: We retrospectively reviewed the medical records of patients with sleep-related eating disorder/night eating syndrome at the Yoyogi Sleep Disorder Center from November 2013 to November 2018. We categorized patients as ramelteon treatment responders when the frequency of nighttime eating per week decreased to less than half of that before treatment.
RESULTS: Forty-nine patients were included in the analysis. The mean frequency of eating behavior (per week) (standard deviation) at baseline and post-ramelteon treatment was significantly different, at 5.3 (2.2) and 3.2 (3.0), respectively (P < .001). Twenty-one patients (42.9%) were classified as responders. Adverse events, all of which were mild daytime somnolence, were observed in 5 patients. There were significantly more individuals using benzodiazepine derivatives and Z-drugs before treatment and those with coexisting delayed sleep-wake phase disorder in the responder group than in the nonresponder group (P < .001 and P < .05, respectively). The mean benzodiazepine derivatives and Z-drugs dose significantly decreased from baseline to post-ramelteon treatment within the responder group (P < .05). This trend was not observed in the nonresponder group. Meanwhile, the sleep midpoint of patients with sleep-related eating disorder/night eating syndrome and delayed sleep-wake phase disorder did not significantly change after treatment.
CONCLUSIONS: Our results indicate that ramelteon is a candidate treatment for sleep-related eating disorder/night eating syndrome. The effects of ramelteon might have occurred primarily through the reduction in benzodiazepine derivatives and Z-drugs rather than through the improvement in sleep-wake rhythm dysregulation.