BackgroundLong-term sedative use is prevalent and associated with significant morbidity, including adverse events such as falls, cognitive impairment, and sedation. The development of dependence can pose significant challenges when discontinuation is attempted as withdrawal symptoms often develop. We conducted a scoping review to map and characterize the literature and determine opportunities for future research regarding deprescribing strategies for long-term benzodiazepine and Z-drug (zopiclone, zolpidem, and zaleplon) use in community-dwelling adults.MethodsWe searched PubMed, Cochrane Central Register of Controlled Trials, EMBASE, PsycINFO, CINAHL, TRIP, and JBI Ovid databases and conducted a grey literature search. Articles discussing methods for deprescribing benzodiazepines or Z-drugs in community-dwelling adults were selected.ResultsFollowing removal of duplicates, 2797 articles were reviewed for eligibility. Of these, 367 were retrieved for full-text assessment and 139 were subsequently included for review. Seventy-four (53 %) articles were original research, predominantly randomized controlled trials (n = 52 [37 %]), whereas 58 (42 %) were narrative reviews and seven (5 %) were guidelines. Amongst original studies, pharmacologic strategies were the most commonly studied intervention (n = 42 [57 %]). Additional deprescribing strategies included psychological therapies (n = 10 [14 %]), mixed interventions (n = 12 [16 %]), and others (n = 10 [14 %]). Behaviour change interventions were commonly combined and included enablement (n = 56 [76 %]), education (n = 36 [47 %]), and training (n = 29 [39 %]). Gradual dose reduction was frequently a component of studies, reviews, and guidelines, but methods varied widely.ConclusionsApproaches proposed for deprescribing benzodiazepines and Z-drugs are numerous and heterogeneous. Current research in this area using methods such as randomized trials and meta-analyses may too narrowly encompass potential strategies available to target this phenomenon. Realist synthesis methods would be well suited to understand the mechanisms by which deprescribing interventions work and why they fail.Electronic supplementary materialThe online version of this article (doi:10.1186/s40360-015-0019-8) contains supplementary material, which is available to authorized users.

Hospital readmission is a common occurrence following kidney transplantation, but less is known about the predictors of early and recurrent hospitalization. We analyzed a cohort of adult kidney transplant recipients in Nova Scotia, Canada, from January 2010 to December 2015. Readmission rates for 30 days, 6 months, and 1 year were calculated as a proportion of total transplants. Factors independently associated with early readmission were investigated using multivariable Cox hazards models with multivariable Anderson‐Gill Cox models being used for factors independently associated with recurrent readmission. Of the 213 patients included, 41 (19.2%), 78 (36.6%), and 88 (41.3%) were readmitted to hospital within 30 days, 6 months, and 1 year, respectively. On multivariable analyses, a history of congestive heart failure (HR 1.741, 95% CI 1.039‐2.918), peptic ulcer disease (HR 2.290, 95% CI 1.054‐4.973), and liver disease (HR 2.492, 95% CI 1.162‐5.344) was associated with higher risk of first rehospitalization. Recurrent hospital admission was associated with initial hospital duration ≥ 8 days (HR 2.140, 95% CI 1.265‐3.618), congestive heart failure (HR 1.366, 95% CI 1.044‐1.787), and liver disease (HR 1.785, 95% CI 1.257‐2.534). Increasing duration of initial hospitalization, congestive heart failure, and liver disease are important to consider when evaluating a patient's risk for recurrent readmission following kidney transplant.

This report extends the clinical spectrum of neutrophilic dermatoses to include dasatinib-induced recurrent and fixed erythematous plaques.

Rationale: Primary hyperoxaluria (PH) is a rare autosomal recessive disorder more commonly diagnosed in children or adolescents. Owing to its rarity and heterogeneous phenotype, it is often underrecognized, resulting in delayed diagnosis, including diagnosis after end-stage kidney disease (ESKD) has occurred or recurrence after kidney-only transplantation. Case Presentation: A 40-year-old Caucasian Canadian woman with a history of recurrent nephrolithiasis since age 19 presented with ESKD and cutaneous symptoms. She had no known prior kidney disease and no family history of kidney disease or nephrolithiasis. Diagnosis: A diagnosis of primary hyperoxaluria type 1 (PH1) due to homozygous splice donor mutation (AGXT c.680+1G>A) was made with kidney and cutaneous pathology demonstrating calcium oxalate deposition and ultrasound suggestive of nephrocalcinosis. Interventions: She was initiated on frequent, high-efficiency, high-flux conventional hemodialysis and oral pyridoxine. Lumasiran was added 11 months later, after she developed bilateral swan-neck deformities. Outcomes: After 14 months of high-intensity dialysis and 3 months of lumasiran, there have been no signs of renal recovery, and extra-renal involvement has increased with progressive swan-neck deformities, reduced cardiac systolic function, and pulmonary hypertension. The patient has been waitlisted for kidney-liver transplantation. Teaching Points: This case report describes an adult presentation of PH1. The case highlights the importance of timely workup of metabolic causes of recurrent nephrolithiasis or nephrocalcinosis in adults which can be a presenting sign of PH and genetic testing for PH to facilitate early diagnosis and treatment especially in the era of novel therapeutics that may alter disease course and outcomes. The case also demonstrates the value of testing for PH in adults presenting with unexplained ESKD and a history of recurrent nephrolithiasis or nephrocalcinosis due to implications for organ transplantation strategy and presymptomatic family screening.

Citalopram and escitalopram have been the subject of several Health Canada and U.S. Food and Drug Administration (FDA) advisories issued since August 2011. 1-5 They raise concern over the potential for these agents to cause QT prolongation. Excessive lengthening of the heart rate-corrected QT (QTc) interval may in rare cases induce Torsade de Pointes (TdP), a tachyarrhythmia associated with ventricular fibrillation, cardiac arrest, and in about 10 to 17% of cases, death. 6,7 As patient heart rhythm is not continuously monitored and death occurs rapidly, measuring the rate of TdP and the resulting mortality is exceptionally difficult, especially in the outpatient setting. 8