Changing practice as a quality indicator for primary care: analysis of data on voluntary disenrollment from the English GP Patient Survey

Background: Changing family practice (voluntary disenrollment) without changing address may indicate dissatisfaction with care. We investigate the potential to use voluntary disenrollment as a quality indicator for primary care. Methods: Data from the English national GP Patient Survey (2,169,718 respondents), the number of voluntary disenrollments without change of address, data relating to practice characteristics (ethnicity, deprivation, gender of patients, practice size and practice density) and doctor characteristics were obtained for all family practices in England (n = 8450). Poisson regression analyses examined associations between rates of voluntary disenrollment, patient experience, and practice and doctor characteristics. Results: Mean and median rates of annual voluntary disenrollment were 11.2 and 7.3 per 1000 patients respectively. Strongest associations with high rates of disenrollment were low practice scores for doctor-patient communication and confidence and trust in the doctor (rate ratios 4.63 and 4.85). In a fully adjusted model, overall satisfaction encompassed other measures of patient experience (rate ratio 3.46). Patients were more likely to move from small practices (single-handed doctors had 2.75 times the disenrollment rate of practices with 6–9 doctors) and where there were other local practices. After allowing for these, substantial unexplained variation remained in practice rates of voluntary disenrollment. Conclusion: Family practices with low levels of patient satisfaction, especially for doctor patient communication, are more likely to experience high rates of disenrollment. However substantial variation in disenrollment rates remains among practices with similar levels of patient satisfaction, limiting the utility of voluntary disenrollment as a performance indicator for primary care in England

Copper uptake and trafficking in the brain

The aim of this chapter is to give a general view on the current status of the scientific basis for the role of copper in human health and disease, outlining the roles of copper in human metabolism and bioenergetics, its coordination chemistry as well as the biological ligands involved in the multiple steps of metal incorporation. In particular, our attention has been focused towards the interaction of copper status and brain function in health and disease, with particular consideration to the role of copper in the pathogenesis of Wilson’s, of Menkes’s, and of human neurodegenerative diseases. Data on interactions between essential trace elements and copper, from the level of absorption in the gut to other systems in the body, are also presented. Particular attention is paid to copper-dependent enzymes in the central nervous system and to copper uptake and trafficking in brain cells