[Unmet needs of family dementia caregivers of persons with dementia : Primary medical care]. / Offene Versorgungsbedarfe pflegender Angehöriger von Menschen mit Demenz : Primärärztliche Versorgung.

BACKGROUND: Results of current research studies revealed that providing informal care for people with dementia (PwD) is associated with caregivers' burden and a variety of health impairments. In order to provide optimal support for family caregivers of PwD, general practitioners and specialists should be able to identify caregivers' unmet needs in primary care. OBJECTIVES: The present article provides an overview of unmet needs of family caregivers that are relevant for general practitioners as well as specialists in neurology, psychiatry, psychotherapy and psychosomatics. MATERIAL AND METHODS: The present overview is based on current reviews on unmet needs of caregivers of PwD and on results of the general practitioner-based, cluster-randomized controlled intervention trial DelpHi-MV (Life- and person-centred help in Mecklenburg-Western Pomerania, Germany; Identifier: NCT01401582). RESULTS: The article provides an overview of unmet needs of family caregivers for PwD, especially in the domains of social integration, psychological and physical health, legal and financial issues, as well as available and valid measurements. DISCUSSION: The article illustrates the importance and the possibilities for general practitioners and specialists to identify caregivers' unmet needs. The question to what extent unmet needs' assessments for family caregivers of PwD could be implemented and financed in routine care is still under debate.

Supporting family dementia caregivers: testing the efficacy of dementia care management on multifaceted caregivers' burden.

OBJECTIVES: Current research suggests that dementia care management (DCM) can decrease burden and associated health impairments of caregivers. The objective of this secondary analysis is to investigate the impact of DCM on multifaceted caregivers' burden dimensions by differentiating between objective and subjective burden. METHODS: A sample of n = 317 dyads of caregivers and community-dwelling people with dementia (PwD) participated in a general practitioner-based, cluster-randomized intervention trial (Identifier:NCT01401582) with two arms and comprehensive data assessment at baseline and 12-month follow-up. Data provided by the caregiver included an inventory with 88 items in 20 different dimensions. RESULTS: Caregivers in the intervention 'DCM' group showed decreased caregiver burden, especially in caregivers' objective burden due to caring (i.e. emotional support), caregivers' subjective burden due to behavior change (i.e. cognition, aggression and resistance, depression, late symptoms) and caregivers' subjective burden due to perceived conflicts between needs and responsibilities to care (i.e. financial losses) compared to caregivers in the control 'care as usual' group, which showed significant increased caregiver burden after 12 months. CONCLUSION: Our findings support evidence for the effectiveness of DCM to lower family dementia caregivers' burden in multifaceted dimensions.

Drug-related problems in community-dwelling primary care patients screened positive for dementia.

BACKGROUND: Older people have a higher risk of drug-related problems (DRPs). However, little is known about the prevalence of DRPs in community-dwelling people who screened positive for dementia. Our study aimed to determine (1) the prevalence and types of DRPs and (2) the socio-demographic and clinical variables associated with DRPs in people screened positive for dementia in primary care. METHODS: The Dementia: life- and person-centered help in Mecklenburg-Western Pomerania (DelpHi-MV) study is a general practitioner (GP)-based cluster-randomized controlled intervention study to implement and evaluate an innovative concept of collaborative dementia care management in the primary care setting in Germany. Medication reviews of 446 study participants were conducted by pharmacists based on a comprehensive baseline assessment that included a computer-based home medication assessment. ClinicalTrials.gov Identifier: NCT01401582. RESULTS: A total of 1,077 DRPs were documented. In 414 study participants (93%), at least one DRP was detected by a pharmacist. The most frequent DRPs were administration and compliance problems (60%), drug interactions (17%), and problems with inappropriate drug choice (15%). The number of DRPs was significantly associated with the total number of drugs taken and with a formal diagnosis of a mental or behavioral disorder. CONCLUSIONS: Degree of cognitive impairment (MMSE defined) and formal diagnosis of dementia were not risk factors for an increased number of DRPs. However, the total number of drug taken and the presence of a diagnosis of mental and behavioral disorders were associated with an increased total number of DRPs.

Analysis of oxidative DNA damage and HPRT mutant frequencies in cancer patients before and after radiotherapy.

Various markers of radiation-induced DNA damage including DNA oxidation were investigated in peripheral lymphocytes of 23 cancer patients prior to and one week after receiving radiotherapy with a cumulative dose of 54-70 Gy. Exposure to ionizing radiation nonsignificantly increased the ratio 2'deoxy-7-dihydro-8-oxoguanosine/2'deoxyguanosine (8-oxodG/dG) from 1.73 x 10(-5) to 3.33 x 10(-5). Frequencies of micronuclei significantly (p = 0.0003) increased from 6.4 to 38.9 per 1000 cells. The frequency of hypoxanthine-guanine-phosphoribosyltransferase (HPRT) mutant lymphocytes measured as 6-thioguanine resistant variant cells by 5-bromodeoxyuridine labeling, was elevated eight-fold, from 4.7 x 10(-6) to 36.2 x 10(-6) (p = 0.008) after termination of the radiotherapy, thus showing a clear response to the radiation treatment. No correlation between levels of oxidative DNA damage and frequencies of HPRT mutant lymphocytes or micronuclei could be established.

Oxidative DNA damage and cytogenetic effects in flight engineers exposed to cosmic radiation.

This study set out to analyze biomarkers for genotoxic events, e.g., oxidative DNA damage, chromosomal damage and hprt mutations, among flight personnel, who are known to be occupationally exposed to ionizing radiation of cosmic origin. Twenty-three flight engineers were recruited while ground personnel served as a matched control group. Cumulative radiation doses during flight were calculated on the basis of subjects' flight records assuming an exposure rate of 6 microSv per hour of flight. Oxidative DNA damage in peripheral lymphocytes from flight engineers appeared significantly increased in comparison with controls and was associated with cumulative exposure to cosmic radiation. Frequencies of peripheral lymphocyte chromosome aberrations, micronuclei and hprt mutations appeared also to be increased in flight engineers, but not significantly. It was also observed that DNA damage was higher in flight engineers with a relatively shorter flight history in comparison with flight engineers with higher cumulative exposures to radiation, suggesting adaptation to DNA damage caused by ionizing radiation. DNA repair activities measured as unscheduled DNA synthesis were clearly increased in the higher-exposed subgroup of flight engineers, and appeared significantly correlated with cumulative radiation dose, as well as inversely with oxidative DNA damage. The implications for cancer risk assessment in relation to exposure to cosmic radiation are discussed.

B[a]P-DNA adduct formation and induction of human epithelial lung cell transformation.

In this study we tested the suitability of the human epithelial lung cell line BEAS-2B for in vitro studies of lung carcinogenesis. The human bronchial epithelial lung cell line BEAS-2B, immortalized with an SV-40/Ad-12 hybrid virus construct, was treated for 24 hours with five different concentrations of the lung carcinogen benzo(a)pyrene (B[a]P) to assess the relationship between DNA adduct levels, cell cycle distribution, micronuclei formation (MN), colony forming efficiency (CFE), and anchorage independent growth (AIG). There appeared to be a strong linear correlation between B[a]P concentration and DNA adduct formation, but no difference in cell cycle distribution was observed after incubation with various concentrations of B[a]P. In the incubation range of 4 to 100 nM B[a]P, the number of DNA adducts was linearly correlated with colony formation in AIG and with the number of cells within individual colonies but not the number of colonies in the CFE test. At higher B[a]P concentrations, the clonal expansion of cells in the CFE and the number of colonies in the AIG declined. Also, the number of micronuclei increased with the formation of DNA adducts. It is concluded that after 24 hours of incubation with 100 nM B[a]P, the formation of BPDE-DNA adducts in the human epithelial lung cells BEAS-2B results in maximal induction of cell transformation. Because of this correlation between DNA adduct formation and lung epithelial cell transformation, the BEAS-2B cells seem suitable for in vitro studies on lung carcinogens.

Induction of oxidative DNA damages and enhancement of cell proliferation in human lymphocytes in vitro by butylated hydroxyanisole.

The food additive butylated hydroxyanisole (BHA) has been shown to induce gastrointestinal hyperplasia in rodents by an unknown mechanism. The relevance of this observation for human risk assessment is not clear. We therefore analysed the effect of BHA and its primary metabolites tert-butylhydroquinone (TBHQ) and tert-butylquinone (TBQ) on 8-oxo-deoxyguanosine formation and labelling induces in human lymphocytes in vitro. Analysis of culture medium and cell lysate fractions after administration of BHA or metabolites of BHA revealed that BHA and TBHQ undergo biotransformation in whole blood cultures. Moreover, TBQ can be reduced to TBHQ. While in cultures treated with BHA 50-60% of the dose administered was recovered, a much lower dose recovery was found in cultures treated with either TBHQ or TBQ. This indicates a considerable binding of these compounds to macromolecules. BHA and TBHQ, as well as TBQ, induced a dose-dependent increase in cell proliferation of phytohaemagglutinin-stimulated lymphocytes, 50 microM being the optimal dose. Since BHA is metabolized to TBHQ, it is not clear which compound is responsible for the proliferation enhancing effects observed in culture. Inhibition of IBHQ metabolism to its semiquinone radical by acetylsalicylic acid (ASA) reduced the increase in labelling indices induced by TBHQ. This indicates that this metabolic pathway is involved in the enhancement of cell proliferation induced by the hydroquinone. HPLC-ECD analysis of oxidative DNA damage in lymphocytes exposed to 10, 50 and 100 microM BHA, TBHQ or TBQ respectively showed that BHA was not capable of inducing oxidative DNA damage to a significant degree. TBQ and, in particular, TBHQ at a dose of 50 microM (the optimal dose for induction of cell proliferation), however, increased lymphocyte 7-hydroxy-8-oxo-2'-deoxyguanosine formation by 320 and 680% respectively. Inhibition of prostaglandin H synthase by ASA in cultures treated with TBHQ decreased the oxidation ratio significantly, confirming the significance of this enzyme system in the mechanism of toxicity of BHA.