Family caregiving at the intersection of private care by migrant home care workers and public care by nursing staff.

BACKGROUND: This study evaluated private family caregiving at the intersection of private migrant home care and public nursing care on the hospitalization of an older patient. METHODS: Seventy-three individuals were interviewed, including older hospitalized patients, their family members, accompanying migrant home care workers, and nursing personnel. RESULTS: There was no clear consensus concerning the role of family members. Although family members emphasized care management as their main role, the other three groups emphasized that the family members' mere physical presence was their main role. All four groups identified potential barriers to family caregiving, rather than motives for family caregiving, hence pointing to a potential discrepancy between expected and performed family caregiving roles. CONCLUSIONS: An indication of the lack of clarity concerning family caregiving roles stems from the finding that family members were frequently viewed as unengaged and neglectful, yet at times they were criticized for being overly involved in patient care. Implications for the care of hospitalized older adults are discussed.

Elder abuse: disparities between older people's disclosure of abuse, evident signs of abuse, and high risk of abuse.

OBJECTIVES: To assess and compare three types of assessment tools for identifying elder abuse: direct questions to elicit disclosure of abuse if it exists, identification of evident signs of abuse, and assessment of high risk for abuse. DESIGN: Cross-sectional. SETTING: Rambam and Hadassah medical centers, Israel. PARTICIPANTS: Seven hundred thirty persons aged 70 and older hospitalized in general hospitals in 2004/05 and their principal caregivers. MEASUREMENTS: Expanded indicator of abuse (E-IOA) tool, questionnaires looking for evident signs of abuse, and direct experience of abusive behavior. RESULTS: Although 5.9% of respondents disclosed experiencing abusive behaviors, 21.4% were identified with evident signs of abuse, and 32.6% were classified as being at high risk for abuse. More than 70% of those who disclosed abuse were identified with evident signs and were at high risk for abuse. Those who disclosed being abused suffered particularly from physical and sexual abuse. According to logistic regression, higher caregiver subjective burden was a predictor of disclosure (odds ratio (OR)=1.81, 95% confidence interval (CI)=1.19-2.74), evident signs of abuse (OR=1.86, 95% CI=1.45-2.35), and high risk of abuse (OR=1.55, 95% CI=1.27-1.88); heavier objective caregiver load was a predictor of evident signs of abuse (OR=1.14, 95% CI=1.05-1.24) and of high risk (OR=1.18, 95% CI=1.06-1.38) only; and respondent functional status was a predictor of evident signs of abuse (OR=1.88, 95% CI=1.70-2.37). CONCLUSION: The use of the three assessment tools is needed for optimal identification of abuse, whereas assessment for high risk proved an efficient method in the absence of respondent disclosure or professional detection of signs of abuse. Hospitalization provides an excellent opportunity for identifying elderly persons at risk of abuse.

Development of a screening tool for identifying elderly people at risk of abuse by their caregivers.

OBJECTIVE: This study developed and assessed an instrument to identify older people at high risk of abuse based on Reis and Nahmiash's Indicators of Abuse (IOA) screen. METHOD: A total of 108 people 65 and older, hospitalized in internal medicine departments at two major hospitals in Israel, were screened together with their principal caregivers. The interview was based on the expanded IOA (E-IOA) and a list of evident signs of abuse. RESULTS: Reliability and validity of the E-IOA were tested and confirmed. Indicators proved to be a significant predictor of evident signs of abuse. The E-IOA correctly discerned 92.7% of those at high risk for abuse and 97.9% of those who did not suffer abuse. The main indicators for risk were behavioral problems, emotional problems, and family problems of the caregiver and the elderly person. Fourteen (13%) experienced abuse. DISCUSSION: The proposed assessment tool can be an instrumental guide to identify elderly people who suffer abuse (unidentified) or who are at high risk.

Personal home care workers' role in hospital: a qualitative study.

OBJECTIVES: Unlike in most high-income countries, in Israel personal (social) care of elderly patients in hospitals is provided either by relatives or friends, or, for those patients with live-in assistance at home, by their home care workers. Our aim was to understand the explicit and implicit roles of live-in carers and whether any difficulties occurred. METHODS: Interviews in the internal medicine unit of Hadassah Hospital with 17 patients, 16 relatives, 20 home care workers and 20 nurses. Data were subjected to categorical content analysis. RESULTS: Three major themes emerged: the development of teamwork with relatives and nurses; the varied roles of home care workers including nursing care, emotional care, and monitoring and supervision of the patient; and the conflicts and challenges associated with having a care worker related to their physical presence and the care worker's own social needs. CONCLUSIONS: Israel partially addresses its nursing shortage by allowing paid home care workers to take an active role in the care of hospitalized older adults. This can have both a positive and a negative impact on the role and perception of nursing.

Response to influenza vaccination in community and in nursing home residing elderly: relation to clinical factors.

Intramuscular (IM) influenza vaccines are about 50% effective in preventing respiratory illness among the elderly. The aim of this study was to identify factors associated with immune response to influenza vaccination among nursing home and community-residing elderly. 114 nursing home (NHE) and 62 community residing elderly (CE) were vaccinated with a commercial IM vaccine. Serum antibodies were evaluated by HIA, and the impact of subjects' clinical characteristics on seroconversion was determined. Factors that were associated with low seroconversion among NHE, included: type II diabetes [for B/Harbin: p=0.044, OR 0.12, (CI: 0.015-0.94)], and antibody titer prior to vaccination A/(H1N1): p=0.03, OR 2.38, (CI: 1.09-5.22); A/(H3N2): p=0.015, OR 2.68 (CI: 1.22-5.92), B/Harbin: p=0.057, OR 4.46 (CI: 0.96-20.85)]. Factors that were associated with lower seroconversion CE elderly, included older age [A/(H1N1): p=0.008, OR 0.846, (CI 0.75-0.96), B/Harbin: p=0.016, OR 0.812, (CI:0.69-0.96)], and antibody titer prior to vaccination A/(H1N1): p=0.029, OR 4.08, (CI: 1.16-14.37); A/(H3N2): p<0.0001, OR 11.495 (CI: 3.18-41.55)]. There was no significant difference in seroconversion between nursing home residing elderly and community elderly. We conclude that Type-II diabetes and antibody titer>1:40 prior to vaccination are associated with reduced response to the influenza vaccination in nursing home elderly.

An association study of the codon 72 polymorphism in the pro-apoptotic gene p53 and Alzheimer's disease.

Recent studies have demonstrated that p53-associated apoptosis is involved in the pathogenesis of Alzheimer's disease (AD). We performed a case-control association study between sporadic AD and the common proline/arginine polymorphism at codon 72 in the pro-apoptotic gene p53, in 109 sporadic AD patients and in 111 controls. This polymorphism has been intensively investigated for association with cancer, but so far not with AD and neurodegeneration. We found no association between this locus and the risk for AD. No association was detected also for the age at disease onset and for disease progression, and no interactive effect was found with apolipoprotein E e4. These findings show no evidence for an association between p53 codon 72 polymorphism and AD in our population.

A polymorphism in the complement component C1r is not associated with sporadic Alzheimer's disease.

A growing body of evidence suggests that Alzheimer's disease (AD) is associated with local inflammation processes. Complement activation is one of the cardinal pathological features of the inflammation. Intensive AD association studies investigating polymorphisms in inflammatory-related genes have been recently performed, mainly in cytokines, but much less has been focused on AD association with polymorphisms in complement components. We performed a case-control association study between the codon 135 polymorphism in the complement component C1r gene and sporadic AD. No association was detected with AD: neither as a risk factor, and nor as a modifier gene affecting the age at disease onset and disease progression. No interactive effect was found with apolipoprotein E e4. These findings show no evidence for association between C1r codon 135 polymorphism and AD in our population.

2756GG genotype of methionine synthase reductase gene is more prevalent in rheumatoid arthritis patients treated with methotrexate and is associated with methotrexate-induced nodulosis.

OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA. METHODS: A cross-sectional study was performed on 86 MTX-treated RA patients, consisting of a clinical interview and physical examination to determine disease activity and MTX-related adverse reactions. Genotype analysis of the MTR gene was performed. Fasting plasma tHcy, serum folate, and vitamin B12 levels were measured. Allele and genotype distributions were compared to a healthy control group. RESULTS: The frequency of the 2756GG genotype (16.3%) in the RA study group was higher than that expected in the general population (3.6%; p < 0.000001). This genotype was associated with MTX-induced accelerated rheumatoid nodulosis (MIARN). No association of disease activity variables or plasma homocysteine with MTR A2756G polymorphisms was observed. The MTR 2756GG genotype, low plasma vitamin B12 levels, and the presence of rheumatoid nodules predicted MIARN. No association of nodulosis with any other indicator of disease activity or medical treatment was found. CONCLUSION: In our population of MTX-treated RA patients the 2756GG genotype of the MTR gene was more common than expected and was associated with MIARN.

Caregiving stressors and psychological distress among veteran resident and immigrant family caregivers in Israel.

The study compared caregiving stressors and psychological distress between Israeli veteran resident and immigrant family caregivers. It examined whether psychosocial variables (appraisal of caregiving, mastery, social support and coping) mediate the differences in psychological distress between these two groups. A total of 213 veteran resident and 206 immigrant (from the former Soviet Union) caregivers of chronically ill elderly were recruited from health services. The comparisons between the two groups were examined separately for spouse and adult child caregivers. The immigrant spouse and adult child caregivers reported significantly higher levels of caregiving stressors than veteran resident caregivers, but psychological distress was significantly higher only among the immigrant adult child caregivers. In multivariate analyses, the difference in psychological distress disappeared when caregiving stressors and mediating psychosocial variables were included in the regression models. Different caregiving stressors and psychosocial variables were associated with psychological distress among the spouses and among the adult child caregivers. The findings suggest that the caregiving stressors and psychosocial variables explain differences in psychological health outcomes between veteran resident and immigrant caregivers. Social work interventions should address these factors among caregivers, take into account the relationship to the care recipient, be culturally adapted to the immigrant caregivers, and target immigrant adult child caregivers in particular.

Impact of methionine synthase gene and methylenetetrahydrofolate reductase gene polymorphisms on the risk of sudden sensorineural hearing loss.

Idiopathic sudden sensorineural hearing loss (SSNHL) represents a frequently encountered otological disease of unknown etiology. In recent years, several inherited risk factors have been found in the pathogenesis of vascular diseases. In the present study, we determined whether specific polymorphism or the combination of polymorphisms in folate-dependent homocysteine metabolism genes can act as predisposing inherited vascular risk factors in the development of SSNHL. We conducted a prospective case-control study using DNA samples extracted from 81 patients diagnosed as suffering from SSNHL and 264 healthy control subjects. Three functional polymorphisms were analyzed by polymerase chain reaction amplification, restriction enzyme digestion, and DNA fragment separation by electrophoresis: methylenetetrahydrofolate reductase (MTHFR) C677T, MTHFR A1298C, and methionine synthase (MTR) A2756G polymorphisms. The prevalence of the homozygous genotype of MTR 2756GG in the SSNHL patients (9%) was significantly higher than in the control group (4%) (p = 0.011). The allelic frequency of the G allele of the MTR A2756G polymorphism among SSNHL patients (12.5%) was also significantly higher than in the control group (5%) (p = 0.033). The prevalence of patients possessing two polymorphisms (31%) and three polymorphisms (17%) in the SSNHL group was significantly higher than in the control group (23 and 9%, respectively; p = 0.019). The frequency of patients with a very high rank risk (double homozygous) was significantly higher in the SSNHL group, MTHFR 677TT/MTR 2675GG--7%, than the frequency of patients in the control group, MTHFR 677TT/MTR 2675GG--3% (p = 0.030). Certain polymorphisms in genes encoding enzymes in the folate-dependent homocysteine metabolism are associated with SSNHL. In our case-control study, a significant association between MTR 2756GG genotype and SSNHL was found which may represent an inherited vascular risk factor in the pathogenesis of SSNHL.

Association between apolipoprotein E4 and rehabilitation outcome in hospitalized ischemic stroke patients.

OBJECTIVE: To determine the value of apolipoprotein E4 (APOE*E4) allele in predicting discharge impairment and disability in ischemic stroke patients after acute rehabilitation. DESIGN: Prospective study comparing results of rehabilitation in patients with different APOE genotypes. SETTING: Acute neurologic rehabilitation department in Israel. PARTICIPANTS: One hundred one consecutive patients 75 years old or less with a first ischemic stroke. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: Impairment, as measured by the National Institutes of Health Stroke Scale (NIHSS), and disability, as assessed with the FIM trade mark instrument. RESULTS: On admission, there was no significant difference in the FIM or NIHSS measurements between the apo E4 group and other patients, but the prevalence of aphasia was 2.07 times more frequent in those with the APOE*E4 genotype (95% confidence interval, 0.98-4.4). A logistic regression model demonstrated that score measurements on admission were highly predictive of the NIHSS score at discharge (receiver operator curve=96.1%), whereas the presence of the APOE*E4 genotype did not add significantly to the model in predicting poorer rehabilitation treatment outcome as measured by the FIM or the NIHSS. CONCLUSIONS: The presence of the apo E4 allele did not predict a poorer outcome of rehabilitation treatment after ischemic stroke, but it was associated with an increased prevalence of aphasia. Further studies are warranted to confirm this association.

Local and systemic immune response in nursing-home elderly following intranasal or intramuscular immunization with inactivated influenza vaccine.

Intramuscular (IM) influenza vaccines are only 30-40% effective in preventing clinical illness among the elderly, and their effectiveness in eliciting mucosal response may be even lower. The aim of the present study was to evaluate the immunological effect of a novel inactivated intranasal (IN) trivalent whole influenza virus vaccine among nursing-home elderly. Twenty-one institutionalized elderly subjects were vaccinated IN with an inactivated novel vaccine, twice, 21 days apart, and with no adverse effects. Twenty-two subjects were vaccinated once with a commercial IM vaccine. Viral strains used in the 1998/9 vaccine (20 microg of each per dose) were A/Beijing/262/95, A/Sydney/5/97 and B/Harbin/7/94. Serum antibodies (IgG and IgM) and nasal IgA were determined by the hemagglutination inhibition (HI) test and enzyme-linked immunosorbent assay (ELISA), respectively. Mucosal antibody response to the three vaccine strains was detected in 47.6-71.4% and 18.1-31.8% of IN and IM immunized subjects, respectively. Serum antibody response to the three antigens tested was detected in 20.0-61.9% and 18.2-72.7% of IN and IM immunized subjects, respectively. Seroconversion was not significantly different after IN or IM vaccination for both A/Sydney and B/Harbin, but higher for A/Beijing following IM vaccination. On study completion, 57.1, 65.0 and 50.0% of IN vaccinees were seroprotected to A/Beijing, A/Sydney and B/Harbin, respectively. Similarly, 68.1, 77.2 and 54.5% were immune after IM vaccination. The IN vaccine tested was significantly more effective than the IM vaccine in inducing mucosal IgA response. This may prevent influenza at its early stages and thus contribute to the reduction of morbidity and complications in nursing-home elderly.

The Fas promoter polymorphism at position -670 is not associated with late-onset sporadic Alzheimer's disease.

The Fas antigen is a cell surface receptor-mediating cell apoptosis. Recent studies have demonstrated that Fas-associated apoptosis is involved in the pathogenesis of Alzheimer's disease (AD). Moreover, the Fas gene is located on chromosome 10q24.1, a region of linkage to late-onset AD (LOAD). These two criteria, pathobiological and positional, make the Fas antigen an interesting candidate for an association with AD. We performed a case-control association study between the common A/G polymorphism at position -670 in the Fas gene (TNFSRF6) promoter and sporadic AD in Jews, investigating whether this locus acts as a risk factor or whether it has a modifying effect. An association has recently been detected by Feuk et al. in the Scottish population between this locus and the risk of early-onset AD (EOAD), but not of LOAD. In agreement with Feuk et al., we found no association between this locus and the risk of LOAD (n = 86). However, in our small sample of patients with EOAD (n = 19), no association was found either. No interactive effect was found between the Fas promoter polymorphism at position -670 and the known risk factor of LOAD, apolipoprotein E epsilon4, and no association was detected with disease progression. These findings show no evidence for an association between the Fas promoter polymorphism at position -670 and AD in our population.

An association study of a polymorphism in the heparan sulfate proteoglycan gene (perlecan, HSPG2) and Alzheimer's disease.

Accumulating evidence indicates that the heparan-sulfate-proteoglycan (perlecan, HSPG2), as well as other specific proteoglycans, are involved in amyloidogenesis and tau aggregation in Alzheimer's disease (AD). Moreover, the HSPG2 is located on chromosome 1p36, a region of linkage to late-onset AD (LOAD). These two criteria, pathological and positional, make the HSPG2 an interesting candidate for an association with AD. We performed a case-control association study between the common intron 6 BamHI polymorphism at a region of putative heparan-sulfate (HS) attachment sites in the HSPG2 gene and sporadic AD in Jews. No association was detected with AD, neither as a risk factor nor as a modifier gene affecting the age at disease onset and disease progression. In addition, no interactive effect was found with the known risk factor for AD, the apolipoprotein E (APOE) epsilon4. These findings show no evidence for association between HSPG2 intron 6 BamHI polymorphism and AD in our population.