Educational inequalities in patient-centred care: patients¿ preferences and experiences

ABSTRACT: BACKGROUND: Educational attainment is strongly related to specific health outcomes. The pathway in which individual patient-provider interactions contribute to (re)producing these inequalities has yet to be studied. In this article, the focus is on differences between less and more highly educated patients in their preferences for and experiences with patient-centred care., e.g. shared decision making, receiving understandable explanations and being able to ask questions. METHODS: Data are derived from several Consumer Quality-index (CQ-index) studies. The CQ-index is a family of standardized instruments which are used in the Netherlands to measure quality of care from the patient's perspective. RESULTS: The educational level of patients is directly related to the degree of importance patients attribute to specific aspects of patient-centred care. It has a minor influence on the experienced level of shared decision making, but not on experiences regarding other aspects of patient-centred care. CONCLUSIONS: All patients regard patient-centred care as important and report positive experiences. However, there is a discrepancy between patient preferences for patient-centred care on one hand and the care received on the other. Less educated patients might receive 'too much', and more highly educated patients 'too little' in the domains of communication, information and shared decision making.     

Misregulation of human sortilin splicing leads to the generation of a nonfunctional progranulin receptor

Sortilin 1 regulates the levels of brain progranulin (PGRN), a neurotrophic growth factor that, when deficient, is linked to cases of frontotemporal lobar degeneration with TAR DNA-binding protein-43 (TDP-43)–positive inclusions (FTLD-TDP). We identified a specific splicing enhancer element that regulates the inclusion of a sortilin exon cassette (termed Ex17b) not normally present in the mature sortilin mRNA. This enhancer element is consistently present in sortilin RNA of mice and other species but absent in primates, which carry a premature stop codon within the Ex17b sequence. In the absence of TDP-43, which acts as a regulatory inhibitor, Ex17b is included in the sortilin mRNA. In humans, in contrast to mice, the inclusion of Ex17b in sortilin mRNA generates a truncated, nonfunctional, extracellularly released protein that binds to but does not internalize PGRN, essentially acting as a decoy receptor. Based on these results, we propose a potential mechanism linking misregulation of sortilin splicing with altered PGRN metabolism.     

Developments in patient activation of people with chronic illness and the impact of changes in self-reported health: results of a nationwide longitudinal study in The Netherlands

Objective

To explore how patient activation, i.e. patients’ perceived knowledge, skills and self-confidence to manage their health and healthcare, develops within chronically ill individuals over time, and to estimate the impact of self-rated health on this development.

Methods

Linear regression analyses and structural equation modeling were conducted using longitudinal data from 751 people with chronic disease(s). Patient activation was assessed by the patient activation measure; self-rated health was assessed by the SF-36 general health scale.

Results

Mean patient activation score at baseline was 60.6, and 18 months later 56.5. Baseline self-rated health had a positive, indirect effect on patient activation at 18 months. In addition, the change in self-rated health over one year (from baseline) was a significant predictor of patients’ activation scores.

Conclusion

Patient activation is not a stable characteristic of people who have been chronically ill for years. Within individuals both increases and decreases occur, but at group level patient activation slightly decreases over time. This may (partly) be due to the deterioration of health that many people with chronic illness experience in course of time.

Practice implications

Clinical practitioners should assess the activation level of chronically ill patients regularly, especially when changes in health occur.     

TARDBP mutations in Parkinson's disease

Mutations of the TARDBP gene encoding TDP-43 protein have been shown to cause amyotrophic lateral sclerosis and have been reported to present with clinical heterogeneity including parkinsonism. In addition, TDP-43 pathology has been observed across a spectrum of neurodegenerative disorders, including Alzheimer's and Parkinson's disease. Herein we report the presence of a TDP-43 mutation in a patient with a clinical diagnosis of Parkinson's disease. The TDP-43 p.N267S substitution has been previously implicated in both amyotrophic lateral sclerosis and behavioral variant frontotemporal dementia. Our findings widen the phenotypic presentation for the TDP-43 p.N267S substitution and support a possible role for rare TDP-43 mutations presenting with Parkinson's disease.     

Frontal asymmetry in behavioral variant frontotemporal dementia: clinicoimaging and pathogenetic correlates

We aimed to assess associations between clinical, imaging, pathologic, and genetic features and frontal lobe asymmetry in behavioral variant frontotemporal dementia (bvFTD). Volumes of the left and right dorsolateral, medial, and orbital frontal lobes were measured in 80 bvFTD subjects and subjects were classified into 3 groups according to the degree of asymmetry (asymmetric left, asymmetric right, symmetric) using cluster analysis. The majority of subjects were symmetric (65%), with 20% asymmetric left and 15% asymmetric right. There were no clinical differences across groups, although there was a trend for greater behavioral dyscontrol in right asymmetric compared with left asymmetric subjects. More widespread atrophy involving the parietal lobe was observed in the symmetric group. Genetic features differed across groups with symmetric frontal lobes associated with C9ORF72 and tau mutations, while asymmetric frontal lobes were associated with progranulin mutations. These findings therefore suggest that neuroanatomical patterns of frontal lobe atrophy in bvFTD are influenced by specific gene mutations.