66 research outputs found

    Caregiver Employment Status and Time to Institutionalization of Persons with Dementia

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    Background - This study was undertaken to examine the association between caregiver employment status and the time to institutionalization of persons with dementia. No study has previously examined this association. Methods - The database of the Canadian Study of Health and Aging was used to obtain data on 326 caregiver/care-recipient dyads. Caregivers were primary, informal carers; care-recipients were diagnosed with dementia and living in the community at baseline. Care-recipients were followed from the date of their baseline screening interview until the date of institutionalization, the date of death before institutionalization, or the date of the 5-year follow-up interview. An accelerated failure time model with a Weibull distribution was used to conduct the survival analysis. Results - During the 5-year follow-up period, 139 care-recipients (45%) were institutionalized; the median time to institutionalization was 1,821 days (95% confidence interval [CI]: 1,539-1,981 days) for the care-recipients of employed caregivers and 1,542 days (95% CI: 1,284-1,653 days) for the care-recipients of unemployed caregivers (p = 0.0634). The adjusted acceleration factor was 1.85 (95% CI: 1.08-3.86), controlling for caregiver thoughts about institutionalizing the care-recipient, caregiver health, and the use of a day center to help provide care. Conclusions - For the care-recipients of employed caregivers, the adjusted time to institutionalization was longer than for the care- recipients of unemployed caregivers.dementia, caregiver, employment, time to institutionalization

    The Use of Behavior and Mood Medications by Care-recipients in Dementia and Caregiver Depression and Perceived Overall Health

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    The mental and physical health of dementia caregivers has been shown to be worse than that of non-caregivers. The present study was undertaken to investigate whether the caregivers of persons who take medications for behavior and mood problems in dementia are less depressed, and perceive their overall health to be better, than the caregivers of persons who do not take such medications. Behavior and mood medications include anti-psychotics, anti- depressants, and anti-convulsants. The Canadian Study of Health and Aging was used to identify informal, unpaid caregivers of persons with dementia (i.e., Alzheimer's disease, vascular dementia, or other dementia [e.g., Parkinson's disease]). The caregivers of persons diagnosed with cognitive impairment not dementia or no cognitive impairment were also included in the study. Care-recipient use of behavior and mood medications was not found to affect caregiver depression (OR = 1.02; 95% CI = 0.62 to 1.66) or caregiver's perceived overall health (OR = 1.35; 95% CI = 0.80 to 2.27).dementia; caregiver; medication; behavior; mood

    How Does the Canadian General Public Rate Moderate Alzheimer's Disease?

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    Objectives. The objectives of this study were to elicit health utility scores for moderate Alzheimer's disease (AD) using members of the general public. Methods. Five-hundred Canadians were chosen randomly to participate in a telephone interview. The EQ-5D was administered to estimate the health utility score for respondents' current health status (i.e., no AD) and for a hypothetical moderate AD health state. Regression analyses were conducted to explain the perceived utility decrement associated with AD. Results. The mean age of the respondents was 51 years, 60% were female, and 42% knew someone with AD. Respondents' mean EQ-5D scores for their current health status and a hypothetical moderate AD were 0.873 (SD: 0.138) and 0.638 (SD: 0.194), respectively (P < 0.001). Age, gender, and education were significant factors explaining this decrement in utility. Conclusion. Members of the general public may serve as an alternative to patients and caregivers in the elicitation of health-related quality of life in AD

    Systematic review: conservative treatments for secondary lymphedema

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    <p>Abstract</p> <p>Background</p> <p>Several conservative (i.e., nonpharmacologic, nonsurgical) treatments exist for secondary lymphedema. The optimal treatment is unknown. We examined the effectiveness of conservative treatments for secondary lymphedema, as well as harms related to these treatments.</p> <p>Methods</p> <p>We searched MEDLINE<sup>®</sup>, EMBASE<sup>®</sup>, Cochrane Central Register of Controlled Trials<sup>®</sup>, AMED, and CINAHL from 1990 to January 19, 2010. We obtained English- and non-English-language randomized controlled trials or observational studies (with comparison groups) that reported primary effectiveness data on conservative treatments for secondary lymphedema. For English-language studies, we extracted data in tabular form and summarized the tables descriptively. For non-English-language studies, we summarized the results descriptively and discussed similarities with the English-language studies.</p> <p>Results</p> <p>Thirty-six English-language and eight non-English-language studies were included in the review. Most of these studies involved upper-limb lymphedema secondary to breast cancer. Despite lymphedema's chronicity, lengths of follow-up in most studies were under 6 months. Many trial reports contained inadequate descriptions of randomization, blinding, and methods to assess harms. Most observational studies did not control for confounding. Many studies showed that active treatments reduced the size of lymphatic limbs, although extensive between-study heterogeneity in areas such as treatment comparisons and protocols, and outcome measures, prevented us from assessing whether any one treatment was superior. This heterogeneity also precluded us from statistically pooling results. Harms were rare (< 1% incidence) and mostly minor (e.g., headache, arm pain).</p> <p>Conclusions</p> <p>The literature contains no evidence to suggest the most effective treatment for secondary lymphedema. Harms are few and unlikely to cause major clinical problems.</p

    Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

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    Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all &gt;0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council
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