•Using the Navigation Guide, we assessed the effect of long working hours on depression.•Twenty-two studies met our eligibility criteria and were included in the review.•We judged the quality of the ...body of evidence as low.•We found inadequate evidence of harmfulness of long working hours for depression risk.
The World Health Organization (WHO) and the International Labour Organization (ILO) are developing the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury (WHO/ILO Joint Estimates), supported by a large number of individual experts. Evidence from previous reviews suggests that exposure to long working hours may cause depression. In this article, we present a systematic review and meta-analysis of parameters for estimating (if feasible) the number of deaths and disability-adjusted life years from depression that are attributable to exposure to long working hours, for the development of the WHO/ILO Joint Estimates.
We aimed to systematically review and meta-analyse estimates of the effect of exposure to long working hours (three categories: 41–48, 49–54 and ≥55 h/week), compared with exposure to standard working hours (35–40 h/week), on depression (three outcomes: prevalence, incidence and mortality).
We developed and published a protocol, applying the Navigation Guide as an organizing systematic review framework where feasible. We searched electronic academic databases for potentially relevant records from published and unpublished studies, including the WHO International Clinical Trial Registers Platform, Medline, PubMed, EMBASE, Web of Science, CISDOC and PsycInfo. We also searched grey literature databases, Internet search engines and organizational websites; hand-searched reference lists of previous systematic reviews; and consulted additional experts.
We included working-age (≥15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but excluded children (aged <15 years) and unpaid domestic workers. We included randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies with an estimate of the effect of exposure to long working hours (41–48, 49–54 and ≥55 h/week), compared with exposure to standard working hours (35–40 h/week), on depression (prevalence, incidence and/or mortality).
At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. Missing data were requested from principal study authors. We combined odds ratios using random-effects meta-analysis. Two or more review authors assessed the risk of bias, quality of evidence and strength of evidence, using Navigation Guide and GRADE tools and approaches adapted to this project.
Twenty-two studies (all cohort studies) met the inclusion criteria, comprising a total of 109,906 participants (51,324 females) in 32 countries (as one study included multiple countries) in three WHO regions (Americas, Europe and Western Pacific). The exposure was measured using self-reports in all studies, and the outcome was assessed with a clinical diagnostic interview (four studies), interview questions about diagnosis and treatment of depression (three studies) or a validated self-administered rating scale (15 studies). The outcome was defined as incident depression in all 22 studies, with first time incident depression in 21 studies and recurrence of depression in one study. We did not identify any study on prevalence of depression or on mortality from depression. For the body of evidence for the outcome incident depression, we had serious concerns for risk of bias due to selection because of incomplete outcome data (most studies assessed depression only twice, at baseline and at a later follow-up measurement, and likely have missed cases of depression that occurred after baseline but were in remission at the time of the follow-up measurement) and due to missing information on life-time prevalence of depression before baseline measurement.
Compared with working 35–40 h/week, we are uncertain about the effect on acquiring (or incidence of) depression of working 41–48 h/week (pooled odds ratio (OR) 1.05, 95% confidence interval (CI) 0.86 to 1.29, 8 studies, 49,392 participants, I2 46%, low quality of evidence); 49–54 h/week (OR 1.06, 95% CI 0.93 to 1.21, 8 studies, 49,392 participants, I2 40%, low quality of evidence); and ≥ 55 h/week (OR 1.08, 95% CI 0.94 to 1.24, 17 studies, 91,142 participants, I2 46%, low quality of evidence).
Subgroup analyses found no evidence for statistically significant (P < 0.05) differences by WHO region, sex, age group and socioeconomic status. Sensitivity analyses found no statistically significant differences by outcome measurement (clinical diagnostic interview gold standard versus other measures) and risk of bias (“high”/“probably high” ratings in any domain versus “low”/“probably low” in all domains).
We judged the existing bodies of evidence from human data as “inadequate evidence for harmfulness” for all three exposure categories, 41–48, 48–54 and ≥55 h/week, for depression prevalence, incidence and mortality; the available evidence is insufficient to assess effects of the exposure. Producing estimates of the burden of depression attributable to exposure to long working appears not evidence-based at this point. Instead, studies examining the association between long working hours and risk of depression are needed that address the limitations of the current evidence.
The World Health Organization (WHO) and the International Labour Organization (ILO) are developing Joint Estimates of the work-related burden of disease and injury (WHO/ILO Joint Estimates), with ...contributions from a large network of experts. Evidence from mechanistic data suggests that exposure to long working hours may cause ischaemic heart disease (IHD). In this paper, we present a systematic review and meta-analysis of parameters for estimating the number of deaths and disability-adjusted life years from IHD that are attributable to exposure to long working hours, for the development of the WHO/ILO Joint Estimates.
We aimed to systematically review and meta-analyse estimates of the effect of exposure to long working hours (three categories: 41–48, 49–54 and ≥55 h/week), compared with exposure to standard working hours (35–40 h/week), on IHD (three outcomes: prevalence, incidence and mortality).
We developed and published a protocol, applying the Navigation Guide as an organizing systematic review framework where feasible. We searched electronic databases for potentially relevant records from published and unpublished studies, including MEDLINE, Scopus, Web of Science, CISDOC, PsycINFO, and WHO ICTRP. We also searched grey literature databases, Internet search engines and organizational websites; hand-searched reference lists of previous systematic reviews; and consulted additional experts.
We included working-age (≥15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but excluded children (aged < 15 years) and unpaid domestic workers. We included randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies which contained an estimate of the effect of exposure to long working hours (41–48, 49–54 and ≥55 h/week), compared with exposure to standard working hours (35–40 h/week), on IHD (prevalence, incidence or mortality).
At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. Missing data were requested from principal study authors. We combined relative risks using random-effect meta-analysis. Two or more review authors assessed the risk of bias, quality of evidence and strength of evidence, using Navigation Guide and GRADE tools and approaches adapted to this project.
Thirty-seven studies (26 prospective cohort studies and 11 case-control studies) met the inclusion criteria, comprising a total of 768,751 participants (310,954 females) in 13 countries in three WHO regions (Americas, Europe and Western Pacific). The exposure was measured using self-reports in all studies, and the outcome was assessed with administrative health records (30 studies) or self-reported physician diagnosis (7 studies). The outcome was defined as incident non-fatal IHD event in 19 studies (8 cohort studies, 11 case-control studies), incident fatal IHD event in two studies (both cohort studies), and incident non-fatal or fatal (“mixed”) event in 16 studies (all cohort studies). Because we judged cohort studies to have a relatively lower risk of bias, we prioritized evidence from these studies and treated evidence from case-control studies as supporting evidence. For the bodies of evidence for both outcomes with any eligible studies (i.e. IHD incidence and mortality), we did not have serious concerns for risk of bias (at least for the cohort studies).
No eligible study was found on the effect of long working hours on IHD prevalence. Compared with working 35–40 h/week, we are uncertain about the effect on acquiring (or incidence of) IHD of working 41–48 h/week (relative risk (RR) 0.98, 95% confidence interval (CI) 0.91 to 1.07, 20 studies, 312,209 participants, I2 0%, low quality of evidence) and 49–54 h/week (RR 1.05, 95% CI 0.94 to 1.17, 18 studies, 308,405 participants, I2 0%, low quality of evidence). Compared with working 35–40 h/week, working ≥55 h/week may have led to a moderately, clinically meaningful increase in the risk of acquiring IHD, when followed up between one year and 20 years (RR 1.13, 95% CI 1.02 to 1.26, 22 studies, 339,680 participants, I2 5%, moderate quality of evidence).
Compared with working 35–40 h/week, we are very uncertain about the effect on dying (mortality) from IHD of working 41–48 h/week (RR 0.99, 95% CI 0.88 to 1.12, 13 studies, 288,278 participants, I2 8%, low quality of evidence) and 49–54 h/week (RR 1.01, 95% CI 0.82 to 1.25, 11 studies, 284,474 participants, I2 13%, low quality of evidence). Compared with working 35–40 h/week, working ≥55 h/week may have led to a moderate, clinically meaningful increase in the risk of dying from IHD when followed up between eight and 30 years (RR 1.17, 95% CI 1.05 to 1.31, 16 studies, 726,803 participants, I2 0%, moderate quality of evidence).
Subgroup analyses found no evidence for differences by WHO region and sex, but RRs were higher among persons with lower SES. Sensitivity analyses found no differences by outcome definition (exclusively non-fatal or fatal versus “mixed”), outcome measurement (health records versus self-reports) and risk of bias (“high”/“probably high” ratings in any domain versus “low”/“probably low” in all domains).
We judged the existing bodies of evidence for human evidence as “inadequate evidence for harmfulness” for the exposure categories 41–48 and 49–54 h/week for IHD prevalence, incidence and mortality, and for the exposure category ≥55 h/week for IHD prevalence. Evidence on exposure to working ≥55 h/week was judged as “sufficient evidence of harmfulness” for IHD incidence and mortality. Producing estimates for the burden of IHD attributable to exposure to working ≥55 h/week appears evidence-based, and the pooled effect estimates presented in this systematic review could be used as input data for the WHO/ILO Joint Estimates.
Background
Shift work is associated with insufficient sleep, which can compromise worker alertness with ultimate effects on occupational health and safety. Adapting shift work schedules may reduce ...adverse occupational outcomes.
Objectives
To assess the effects of shift schedule adaptation on sleep quality, sleep duration, and sleepiness among shift workers.
Search methods
We searched CENTRAL, PubMed, Embase, and eight other databases on 13 December 2020, and again on 20 April 2022, applying no language restrictions.
Selection criteria
We included randomised controlled trials (RCTs) and non‐RCTs, including controlled before‐after (CBA) trials, interrupted time series, and cross‐over trials. Eligible trials evaluated any of the following shift schedule components.
• Permanency of shifts • Regularity of shift changes • Direction of shift rotation • Speed of rotation • Shift duration • Timing of start of shifts • Distribution of shift schedule • Time off between shifts • Split shifts • Protected sleep • Worker participation
We included studies that assessed sleep quality off‐shift, sleep duration off‐shift, or sleepiness during shifts.
Data collection and analysis
Two review authors independently screened the titles and s of the records recovered by the search, read through the full‐text articles of potentially eligible studies, and extracted data. We assessed the risk of bias of included studies using the Cochrane risk of bias tool, with specific additional domains for non‐randomised and cluster‐randomised studies. For all stages, we resolved any disagreements by consulting a third review author. We presented the results by study design and combined clinically homogeneous studies in meta‐analyses using random‐effects models. We assessed the certainty of the evidence with GRADE.
Main results
We included 11 studies with a total of 2125 participants. One study was conducted in a laboratory setting and was not considered for drawing conclusions on intervention effects. The included studies investigated different and often multiple changes to shift schedule, and were heterogeneous with respect to outcome measurement.
Forward versus backward rotation
Three CBA trials (561 participants) investigated the effects of forward rotation versus backward rotation. Only one CBA trial provided sufficient data for the quantitative analysis; it provided very low‐certainty evidence that forward rotation compared with backward rotation did not affect sleep quality measured with the Basic Nordic Sleep Questionnaire (BNSQ; mean difference (MD) −0.20 points, 95% confidence interval (CI) −2.28 to 1.89; 62 participants) or sleep duration off‐shift (MD −0.21 hours, 95% CI −3.29 to 2.88; 62 participants). However, there was also very low‐certainty evidence that forward rotation reduced sleepiness during shifts measured with the BNSQ (MD −1.24 points, 95% CI −2.24 to −0.24; 62 participants).
Faster versus slower rotation
Two CBA trials and one non‐randomised cross‐over trial (341 participants) evaluated faster versus slower shift rotation. We were able to meta‐analyse data from two studies. There was low‐certainty evidence of no difference in sleep quality off‐shift (standardised mean difference (SMD) −0.01, 95% CI −0.26 to 0.23) and very low‐certainty evidence that faster shift rotation reduced sleep duration off‐shift (SMD −0.26, 95% CI −0.51 to −0.01; 2 studies, 282 participants). The SMD for sleep duration translated to an MD of 0.38 hours' less sleep per day (95% CI −0.74 to −0.01). One study provided very low‐certainty evidence that faster rotations decreased sleepiness during shifts measured with the BNSQ (MD −1.24 points, 95% CI −2.24 to −0.24; 62 participants).
Limited shift duration (16 hours) versus unlimited shift duration
Two RCTs (760 participants) evaluated 80‐hour workweeks with maximum daily shift duration of 16 hours versus workweeks without any daily shift duration limits. There was low‐certainty evidence that the 16‐hour limit increased sleep duration off‐shift (SMD 0.50, 95% CI 0.21 to 0.78; which translated to an MD of 0.73 hours' more sleep per day, 95% CI 0.30 to 1.13; 2 RCTs, 760 participants) and moderate‐certainty evidence that the 16‐hour limit reduced sleepiness during shifts, measured with the Karolinska Sleepiness Scale (SMD −0.29, 95% CI −0.44 to −0.14; which translated to an MD of 0.37 fewer points, 95% CI −0.55 to −0.17; 2 RCTs, 716 participants).
Shorter versus longer shifts
One RCT, one CBA trial, and one non‐randomised cross‐over trial (692 participants) evaluated shorter shift duration (eight to 10 hours) versus longer shift duration (two to three hours longer). There was very low‐certainty evidence of no difference in sleep quality (SMD −0.23, 95% CI −0.61 to 0.15; which translated to an MD of 0.13 points lower on a scale of 1 to 5; 2 studies, 111 participants) or sleep duration off‐shift (SMD 0.18, 95% CI −0.17 to 0.54; which translated to an MD of 0.26 hours' less sleep per day; 2 studies, 121 participants). The RCT and the non‐randomised cross‐over study found that shorter shifts reduced sleepiness during shifts, while the CBA study found no effect on sleepiness.
More compressed versus more spread out shift schedules
One RCT and one CBA trial (346 participants) evaluated more compressed versus more spread out shift schedules. The CBA trial provided very low‐certainty evidence of no difference between the groups in sleep quality off‐shift (MD 0.31 points, 95% CI −0.53 to 1.15) and sleep duration off‐shift (MD 0.52 hours, 95% CI −0.52 to 1.56).
Authors' conclusions
Forward and faster rotation may reduce sleepiness during shifts, and may make no difference to sleep quality, but the evidence is very uncertain. Very low‐certainty evidence indicated that sleep duration off‐shift decreases with faster rotation. Low‐certainty evidence indicated that on‐duty workweeks with shift duration limited to 16 hours increases sleep duration, with moderate‐certainty evidence for minimal reductions in sleepiness. Changes in shift duration and compression of workweeks had no effect on sleep or sleepiness, but the evidence was of very low‐certainty. No evidence is available for other shift schedule changes. There is a need for more high‐quality studies (preferably RCTs) for all shift schedule interventions to draw conclusions on the effects of shift schedule adaptations on sleep and sleepiness in shift workers.
Background
The term central sleep apnoea (CSA) encompasses diverse clinical situations where a dysfunctional drive to breathe leads to recurrent respiratory events, namely apnoea (complete absence of ...ventilation) and hypopnoea sleep (insufficient ventilation) during sleep. Studies have demonstrated that CSA responds to some extent to pharmacological agents with distinct mechanisms, such as sleep stabilisation and respiratory stimulation. Some therapies for CSA are associated with improved quality of life, although the evidence on this association is uncertain. Moreover, treatment of CSA with non‐invasive positive pressure ventilation is not always effective or safe and may result in a residual apnoea‐hypopnoea index.
Objectives
To evaluate the benefits and harms of pharmacological treatment compared with active or inactive controls for central sleep apnoea in adults.
Search methods
We used standard, extensive Cochrane search methods. The latest search date was 30 August 2022.
Selection criteria
We included parallel and cross‐over randomised controlled trials (RCTs) that evaluated any type of pharmacological agent compared with active controls (e.g. other medications) or passive controls (e.g. placebo, no treatment or usual care) in adults with CSA as defined by the International Classification of Sleep Disorders 3rd Edition. We did not exclude studies based on the duration of intervention or follow‐up. We excluded studies focusing on CSA due to periodic breathing at high altitudes.
Data collection and analysis
We used standard Cochrane methods. Our primary outcomes were central apnoea‐hypopnoea index (cAHI), cardiovascular mortality and serious adverse events. Our secondary outcomes were quality of sleep, quality of life, daytime sleepiness, AHI, all‐cause mortality, time to life‐saving cardiovascular intervention, and non‐serious adverse events. We used GRADE to assess certainty of evidence for each outcome.
Main results
We included four cross‐over RCTs and one parallel RCT, involving a total of 68 participants. Mean age ranged from 66 to 71.3 years and most participants were men. Four trials recruited people with CSA associated with heart failure, and one study included people with primary CSA. Types of pharmacological agents were acetazolamide (carbonic anhydrase inhibitor), buspirone (anxiolytic), theophylline (methylxanthine derivative) and triazolam (hypnotic), which were given for between three days and one week.
Only the study on buspirone reported a formal evaluation of adverse events. These events were rare and mild. No studies reported serious adverse events, quality of sleep, quality of life, all‐cause mortality, or time to life‐saving cardiovascular intervention.
Carbonic anhydrase inhibitors versus inactive control
Results were from two studies of acetazolamide versus placebo (n = 12) and acetazolamide versus no acetazolamide (n = 18) for CSA associated with heart failure. One study reported short‐term outcomes and the other reported intermediate‐term outcomes. We are uncertain whether carbonic anhydrase inhibitors compared to inactive control reduce cAHI in the short term (mean difference (MD) −26.00 events per hour, 95% CI −43.84 to −8.16; 1 study, 12 participants; very low certainty). Similarly, we are uncertain whether carbonic anhydrase inhibitors compared to inactive control reduce AHI in the short term (MD −23.00 events per hour, 95% CI −37.70 to 8.30; 1 study, 12 participants; very low certainty) or in the intermediate term (MD −6.98 events per hour, 95% CI −10.66 to −3.30; 1 study, 18 participants; very low certainty). The effect of carbonic anhydrase inhibitors on cardiovascular mortality in the intermediate term was also uncertain (odds ratio (OR) 0.21, 95% CI 0.02 to 2.48; 1 study, 18 participants; very low certainty).
Anxiolytics versus inactive control
Results were based on one study of buspirone versus placebo for CSA associated with heart failure (n = 16). The median difference between groups for cAHI was −5.00 events per hour (IQR −8.00 to −0.50), the median difference for AHI was −6.00 events per hour (IQR −8.80 to −1.80), and the median difference on the Epworth Sleepiness Scale for daytime sleepiness was 0 points (IQR −1.0 to 0.00).
Methylxanthine derivatives versus inactive control
Results were based on one study of theophylline versus placebo for CSA associated with heart failure (n = 15). We are uncertain whether methylxanthine derivatives compared to inactive control reduce cAHI (MD −20.00 events per hour, 95% CI −32.15 to −7.85; 15 participants; very low certainty) or AHI (MD −19.00 events per hour, 95% CI −30.27 to −7.73; 15 participants; very low certainty).
Hypnotics versus inactive control
Results were based on one trial of triazolam versus placebo for primary CSA (n = 5). Due to very serious methodological limitations and insufficient reporting of outcome measures, we were unable to draw any conclusions regarding the effects of this intervention.
Authors' conclusions
There is insufficient evidence to support the use of pharmacological therapy in the treatment of CSA. Although small studies have reported positive effects of certain agents for CSA associated with heart failure in reducing the number of respiratory events during sleep, we were unable to assess whether this reduction may impact the quality of life of people with CSA, owing to scarce reporting of important clinical outcomes such as sleep quality or subjective impression of daytime sleepiness. Furthermore, the trials mostly had short‐term follow‐up. There is a need for high‐quality trials that evaluate longer‐term effects of pharmacological interventions.
Background: The World Health Organization (WHO) and the International Labour Organization (ILO) are developing Joint Estimates of the work-related burden of disease and injury (WHO/ILO Joint ...Estimates), with contributions from a large network of experts. Evidence from mechanistic data suggests that exposure to long working hours may increase alcohol consumption and cause alcohol use disorder. In this paper, we present a systematic review and meta-analysis of parameters for estimating the number of deaths and disability-adjusted life years from alcohol consumption and alcohol use disorder that are attributable to exposure to long working hours, for the development of the WHO/ILO Joint Estimates. Objectives: We aimed to systematically review and meta-analyse estimates of the effect of exposure to long working hours (three categories: 41–48, 49–54 and ≥55 h/week), compared with exposure to standard working hours (35–40 h/week), on alcohol consumption, risky drinking (three outcomes: prevalence, incidence and mortality) and alcohol use disorder (three outcomes: prevalence, incidence and mortality). Data sources: We developed and published a protocol, applying the Navigation Guide as an organizing systematic review framework where feasible. We searched electronic bibliographic databases for potentially relevant records from published and unpublished studies, including the WHO International Clinical Trials Register, Ovid MEDLINE, PubMed, Embase, and CISDOC on 30 June 2018. Searches on PubMed were updated on 18 April 2020. We also searched electronic grey literature databases, Internet search engines and organizational websites; hand-searched reference list of previous systematic reviews and included study records; and consulted additional experts. Study eligibility and criteria: We included working-age (≥15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but excluded children (<15 years) and unpaid domestic workers. We considered for inclusion randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies with an estimate of the effect of exposure to long working hours (41–48, 49–54 and ≥55 h/week), compared with exposure to standard working hours (35–40 h/week), on alcohol consumption (in g/week), risky drinking, and alcohol use disorder (prevalence, incidence or mortality). Study appraisal and synthesis methods: At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from publications related to qualifying studies. Two or more review authors assessed the risk of bias, quality of evidence and strength of evidence, using Navigation Guide and GRADE tools and approaches adapted to this project. Results: Fourteen cohort studies met the inclusion criteria, comprising a total of 104,599 participants (52,107 females) in six countries of three WHO regions (Americas, South-East Asia, and Europe). The exposure and outcome were assessed with self-reported measures in most studies. Across included studies, risk of bias was generally probably high, with risk judged high or probably high for detection bias and missing data for alcohol consumption and risky drinking. Compared to working 35–40 h/week, exposure to working 41–48 h/week increased alcohol consumption by 10.4 g/week (95% confidence interval (CI) 5.59–15.20; seven studies; 25,904 participants, I2 71%, low quality evidence). Exposure to working 49–54 h/week increased alcohol consumption by 17.69 g/week (95% confidence interval (CI) 9.16–26.22; seven studies, 19,158 participants, I2 82%, low quality evidence). Exposure to working ≥55 h/week increased alcohol consumption by 16.29 g/week (95% confidence interval (CI) 7.93–24.65; seven studies; 19,692 participants; I2 82%, low quality evidence). We are uncertain about the effect of exposure to working 41–48 h/week, compared with working 35–40 h/week on developing risky drinking (relative risk 1.08; 95% CI 0.86–1.36; 12 studies; I2 52%, low certainty evidence). Working 49–54 h/week did not increase the risk of developing risky drinking (relative risk 1.12; 95% CI 0.90–1.39; 12 studies; 3832 participants; I2 24%, moderate certainty evidence), nor working ≥55 h/week (relative risk 1.11; 95% CI 0.95–1.30; 12 studies; 4525 participants; I2 0%, moderate certainty evidence). Subgroup analyses indicated that age may influence the association between long working hours and both alcohol consumption and risky drinking. We did not identify studies for which we had access to results on alcohol use disorder. Conclusions Overall, for alcohol consumption in g/week and for risky drinking, we judged this body of evidence to be of low certainty. Exposure to long working hours may have increased alcohol consumption, but we are uncertain about the effect on risky drinking. We found no eligible studies on the effect on alcohol use disorder. Producing estimates for the burden of alcohol use disorder attributable to exposure to long working hours appears to not be evidence-based at this time.
Background
Obstructive sleep apnoea syndrome (OSAS) is associated with several chronic diseases, including erectile dysfunction (ED). The association of OSAS and ED is far more common than might be ...found by chance; the treatment of OSAS with non‐invasive positive airway pressure therapy is associated with improvement of respiratory symptoms, and may contribute to the improvement of associated conditions, such as ED.
Objectives
To assess the effectiveness and acceptability of non‐invasive positive airway pressure therapy for improving erectile dysfunction in OSAS.
Search methods
We identified studies from the Cochrane Airways Trials Register, CENTRAL, MEDLINE, Embase, PsycINFO, CINAHL, AMED EBSCO, and LILACS, the US National Institutes of Health ongoing trials register ClinicalTrials.gov, and the World Health Organisation international clinical trials registry platform to 14 June 2021, with no restriction on date, language, or status of publication. We checked the reference lists of all primary studies, and review articles for additional references, and relevant manufacturers' websites for study information. We also searched specific conference proceedings for the British Association of Urological Surgeons; the European Association of Urology; and the American Urological Association to 14 June 2021.
Selection criteria
We considered randomised controlled trials (RCTs) with a parallel or cross‐over design, or cluster‐RCTs, which included men aged 18 years or older, with OSAS and ED. We considered RCTs comparing any non‐invasive positive airway pressure therapy (such as continuous positive airways pressure (CPAP), bilevel positive airway pressure (BiPAP), variable positive airway pressure (VPAP), or similar devices) versus sham, no treatment, waiting list, or pharmacological treatment for ED. The primary outcomes were remission of ED and serious adverse events; secondary outcome were sex‐related quality of life, health‐related quality of life, and minor adverse events.
Data collection and analysis
Two review authors independently conducted study selection, data extraction, and risk of bias assessment. A third review author solved any disagreement. We used the Cochrane RoB 1 tool to assess the risk of bias of the included RCTs. We used the GRADE approach to assess the certainty of the body of evidence. To measure the treatment effect on dichotomous outcomes, we used the risk ratio (RR); for continuous outcomes, we used the mean difference (MD). We calculated 95% confidence intervals (CI) for these measures. When possible (data availability and homogeneous studies), we used a random‐effect model to pool data with a meta‐analysis.
Main results
We included six RCTs (all assessing CPAP as the non‐invasive positive airway pressure therapy device), with a total of 315 men with OSAS and ED. All RCTs presented some important risk of bias related to selection, performance, assessment, or reporting bias. None of included RCTs assessed the ED remission rate, and we used the provided ED mean scores as a proxy.
CPAP versus no CPAP
There is uncertainty about the effect of CPAP on mean ED scores after 4 weeks, using the International index of erectile function (IIEF‐5, higher = better; MD 7.50, 95% CI 4.05 to 10.95; 1 RCT; 27 participants; very low‐certainty evidence), and after 12 weeks (IIEF‐ED, ED domain; MD 2.50, 95% CI ‐1.10 to 6.10; 1 RCT; 57 participants; very low‐certainty evidence, downgraded due to methodological limitations and imprecision). There is uncertainty about the effect of CPAP on sex‐related quality of life after 12 weeks, using the Self‐esteem and relationship test (SEAR, higher = better; MD 1.00, 95% CI ‐8.09 to 10.09; 1 RCT; 57 participants; very low‐certainty evidence, downgraded due to methodological limitations and imprecision); no serious adverse events were reported after 4 weeks (1 RCT; 27 participants; very low‐certainty evidence, downgraded due to methodological limitations and imprecision).
CPAP versus sham CPAP
One RCT assessed this comparison (61 participants), but we were unable to extract outcomes for this comparison due to the factorial design and reporting of this trial.
CPAP versus sildenafil (phosphodiesterase type 5 inhibitors)
Sildenafil may slightly improve erectile function at 12 weeks when compared to CPAP, measured with the IIEF‐ED (MD ‐4.78, 95% CI ‐6.98 to ‐2.58; 3 RCTs; 152 participants; I² = 59%; low‐certainty evidence, downgraded due to methodological limitations).
There is uncertainty about the effect of CPAP on sex‐related quality of life after 12 weeks, measured with the Erectile Dysfunction Inventory of Treatment Satisfaction questionnaire (EDITS, higher = better; MD ‐1.24, 95% CI ‐1.80 to ‐0.67; 2 RCTs; 122 participants; I² = 0%; very low‐certainty evidence, downgraded due to methodological limitations). No serious adverse events were reported for either group (2 RCTs; 70 participants; very low‐certainty evidence, downgraded due to methodological limitations and imprecision). There is uncertainty about the effects of CPAP when compared to sildenafil for the incidence of minor adverse events (RR 1.33, 95% CI 0.34 to 5.21; 1 RCT; 40 participants; very low‐certainty evidence, downgraded due to methodological limitations and imprecision). The confidence interval was wide and neither a significant increase nor reduction in the risk of minor adverse events can be ruled out with the use of CPAP (4/20 men complained of nasal dryness in the CPAP group, and 3/20 men complained of transient flushing and mild headache in the sildenafil group).
Authors' conclusions
When compared with no CPAP, we are uncertain about the effectiveness and acceptability of CPAP for improving erectile dysfunction in men with obstructive sleep apnoea. When compared with sildenafil, there is some evidence that sildenafil may slightly improve erectile function at 12 weeks.
To evaluate the impact of the coronavirus disease 2019 (COVID-19) pandemic on insomnia and other sleep disturbances in health care professionals.
A survey was distributed using social media and ...organizational emails to Brazilian active health care professionals during the COVID-19 outbreak. We explored potential associated factors including age, sex, occupation, workplace, work hours, income, previous infection with COVID-19, recent/current contact with COVID-19 patients, regional number of incident deaths, anxiety, and burnout. We evaluated new-onset/previous insomnia worsening episodes (primary outcome), new pharmacological treatments, sleep quality, duration, nightmares, and snoring (secondary outcomes).
A total of 4,384 health professionals from all regions of the country were included in the analysis (44 ± 12 years, 76% females, 53.8% physicians). Overall, 55.7% were assisting patients with COVID-19, and 9.2% had a previous COVID-19 infection. The primary outcome occurred in 32.9% of respondents in parallel to 13% new pharmacological treatments for insomnia. The sleep quality worsened for 61.4%, while 43.5% and 22.8% reported ≥ 1-hour sleep duration reduction and worsening or new-onset nightmares, respectively. Multivariate analyses showed that age (odds ratio OR: 1.008; 95% confidence interval CI 1.001-1.015), females (OR: 1.590; 95% CI 1.335-1.900), weight change (decrease: OR: 1.772; 95% CI 1.453-2.161; increase: OR: 1.468; 95% CI 1.249-1.728), prevalent anxiety (OR: 3.414; 95% CI 2.954-3.948), new-onset burnout (OR: 1.761; 95% CI 1.489-2.083), family income reduction > 30% (OR: 1.288; 95% CI 1.069-1.553), and assisting patients with COVID-19 (OR: 1.275; 95% CI 1.081-1.506) were independently associated with new-onset or worsening of previous insomnia episodes.
We observed a huge burden of insomnia episodes and other sleep disturbances in health care professionals during the COVID-19 pandemic.
Drager LF, Pachito DV, Moreno CRC, et al. Insomnia episodes, new-onset pharmacological treatments, and other sleep disturbances during the COVID-19 pandemic: a nationwide cross-sectional study in Brazilian health care professionals.
. 2022;18(2):373-382.
Abstract
Background
Management of patient flow within a healthcare network, allowing equitable and qualified access to healthcare, is a major challenge for universal health systems. Implementation of ...telehealth strategies to support referral management has been shown to increase primary care resolution and to promote coordination of care. The objective of this study was to assess the impact of telehealth strategies on waiting lists and waiting times for specialized care in Brazil.
Methods
Before-and-after study with measures obtained between January 2019 and February 2020. Baseline measurements of waiting lists were obtained immediately before the implementation of a remotely operated referral management system. Post-interventional measurements were obtained monthly, up to six months after the beginning of operation. Data was extracted from the database of the project. General linear models were applied to assess interaction of locality and time over number of cases on waiting lists and waiting times.
Results
At baseline, the median number of cases on waiting lists ranged from 2961 to 12,305 cases. Reductions of the number of cases on waiting lists after six months of operation were observed in all localities. The magnitude of the reduction ranged from 54.67 to 88.97 %. Interaction of time measurements was statistically significant from the second month onward. Median waiting times ranged from 159 to 241 days at baseline. After six months, there was a decrease of 100 and 114 waiting days in two localities, respectively, with reduction of waiting times only for high-risk cases in the third locality.
Conclusions
Adoption of telehealth strategies resulted in the reduction of number of cases on waiting lists. Results were consistent across localities, suggesting that telehealth interventions are viable in diverse settings.
Obstructive sleep apnea (OSA) is a highly prevalent chronic disease, associated with morbidity and mortality. Although effective treatment for OSA is commercially available, their provision is not ...guaranteed by lines of care throughout Brazil, making legal action necessary. This study aimed at presenting data related to the volume of legal proceedings regarding the access to diagnosis and treatment of OSA in Brazil.
This was a descriptive study of national scope, evaluating the period between January of 2016 and December of 2020. The number of lawsuits was analyzed according to the object of the demand (diagnosis or treatment). Projections of total expenses were carried out according to the number of lawsuits.
We identified 1,462 legal proceedings (17.6% and 82.4% related to diagnosis and treatment, respectively). The projection of expenditure for OSA diagnosis in the public and private spheres were R$575,227 and R$188,002, respectively. The projection of expenditure for OSA treatment in the public and private spheres were R$2,656,696 and R$253,050, respectively. There was a reduction in the number of lawsuits between 2017 and 2019.
Legal action as a strategy for accessing diagnostic and therapeutic resources related to OSA is a recurrent practice, resulting in inefficiency and inequity. The reduction in the number of lawsuits between 2017 and 2019 might be explained by the expansion of local health care policies or by barriers in the journey of patients with OSA, such as difficulties in being referred to specialized health care and low availability of diagnostic resources.
The World Health Organization (WHO) and the International Labour Organization (ILO) are developing a joint methodology for estimating the national and global work-related burden of disease and injury ...(WHO/ILO joint methodology), with contributions from a large network of experts. In this paper, we present the protocol for two systematic reviews of parameters for estimating the number of deaths and disability-adjusted life years from alcohol consumption and alcohol use disorder attributable to exposure to long working hours, to inform the development of the WHO/ILO joint methodology.
We aim to systematically review studies on exposure to long working hours (Systematic Review 1) and systematically review and meta-analyse estimates of the effect of exposure to long working hours on alcohol consumption and alcohol use disorder (Systematic Review 2), applying the Navigation Guide systematic review methodology as an organizing framework.
Separately for Systematic Reviews 1 and 2, we will search electronic academic databases for potentially relevant records from published and unpublished studies, including MEDLINE, Embase, Web of Science, CISDOC and PsychINFO. We will also search electronic grey literature databases, Internet search engines and organizational websites; hand-search reference list of previous systematic reviews and included study records; and consult additional experts.
We will include working-age (≥15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but exclude children (<15 years) and unpaid domestic workers. For Systematic Review 1, we will include quantitative prevalence studies of relevant levels of exposure to long working hours (i.e., 35–40, 41–48, 49–54 and ≥55 h/week) stratified by country, sex, age and industrial sector or occupation. For Systematic Review 2, we will include randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies with an estimate of the relative effect of a relevant level of exposure to long working hours on total amount of alcohol consumed and on the incidence of, prevalence of or mortality from alcohol use disorders, compared with the theoretical minimum risk exposure level (i.e., worked 35–40 h/week).
At least two review authors will independently screen titles and abstracts at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. At least two review authors will assess risk of bias and quality of evidence, using the most suited tools currently available. For Systematic Review 2, if feasible, we will combine relative risks using meta-analysis. We will report results using the guidelines for accurate and transparent health estimates reporting (GATHER) for Systematic Review 1 and the preferred reporting items for systematic reviews and meta-analyses guidelines (PRISMA) for Systematic Review 2.
PROSPERO registration number: CRD42018084077.
•Long working hours have been associated with increased alcohol consumption.•We report the protocol for a systematic review on the topic.•The methodology for the systematic review is explained in detail.•This research is part of the joint methodology of the WHO and ILO.
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