The natural history of insomnia: Focus on prevalence and incidence of acute insomnia

Despite Acute Insomnia being classified as a distinct nosological entity since 1979/1980 (ASDC/DSM III-R), there are no published estimates of its prevalence and incidence or data regarding transition to chronic insomnia or remission. This lack of data prevents an understanding of: a) the pathogenesis of insomnia and b) when and how treatment should be initiated. The aim of the present study was to provide such data from two community samples. Samples were recruited in the USA (n = 2861) and the North East of the UK (n = 1095). Additionally, 412 Normal Sleepers from the UK sample were surveyed longitudinally to determine prospectively incidence, transition, and remission rates for acute insomnia and assess whether the acute insomnia was a first episode, recurrent episode, or co-morbid with symptoms of other illnesses. The prevalence of acute insomnia was 9.5% (USA) and 7.9%(UK). The prevalence of three acute insomnia subtypes in the UK were; First-Onset Acute Insomnia 2.6%; Recurrent Acute Insomnia 3.8%; and 1.4% Co-morbid Acute Insomnia. The annual incidence of acute insomnia in the UK sample was between 31.2% and 36.6%. Remission rates fluctuated depending upon the definition of acute insomnia and whether the current episode was first-onset or recurrent. These findings provide preliminary insights into the natural history of insomnia. Such data will serve to inform how and when acute insomnia should be managed and whether such interventions may serve to diminish subsequent morbidity, particularly with respect to Major Depression. Crown Copyright (C) 2012 Published by Elsevier Ltd. All rights reserved

Eosinophil Depletion with Benralizumab for Eosinophilic Esophagitis

Background: Benralizumab is an eosinophil-depleting anti-interleukin-5 receptor α monoclonal antibody. The efficacy and safety of benralizumab in patients with eosinophilic esophagitis are unclear. Methods: In a phase 3, multicenter, double-blind, randomized, placebo-controlled trial, we assigned patients 12 to 65 years of age with symptomatic and histologically active eosinophilic esophagitis in a 1:1 ratio to receive subcutaneous benralizumab (30 mg) or placebo every 4 weeks. The two primary efficacy end points were histologic response (≤6 eosinophils per high-power field) and the change from baseline in the score on the Dysphagia Symptom Questionnaire (DSQ; range, 0 to 84, with higher scores indicating more frequent or severe dysphagia) at week 24. Results: A total of 211 patients underwent randomization: 104 were assigned to receive benralizumab, and 107 were assigned to receive placebo. At week 24, more patients had a histologic response with benralizumab than with placebo (87.4% vs. 6.5%; difference, 80.8 percentage points; 95% confidence interval [CI], 72.9 to 88.8; P<0.001). However, the change from baseline in the DSQ score did not differ significantly between the two groups (difference in least-squares means, 3.0 points; 95% CI, -1.4 to 7.4; P = 0.18). There was no substantial between-group difference in the change from baseline in the Eosinophilic Esophagitis Endoscopic Reference Score, which reflects endoscopic abnormalities. Adverse events were reported in 64.1% of the patients in the benralizumab group and in 61.7% of those in the placebo group. No patients discontinued the trial because of adverse events. Conclusions: In this trial involving patients 12 to 65 years of age with eosinophilic esophagitis, a histologic response (≤6 eosinophils per high-power field) occurred in significantly more patients in the benralizumab group than in the placebo group. However, treatment with benralizumab did not result in fewer or less severe dysphagia symptoms than placebo. (Funded by AstraZeneca; MESSINA ClinicalTrials.gov number, NCT04543409.)