Incentivizing preventive services in primary care: perspectives on Local Enhanced Services.

BACKGROUND: General practitioners in the UK play a key role in prevention but provision of preventive services is variable. The 2004 General Medical Services contract allows Primary Care Trusts (PCTs) to address health needs through providing locally agreed payments for Local Enhanced Services (LESs). This study identifies how this contractual flexibility is used for preventive services and explores its perceived effectiveness. METHODS: Semi-structured interviews were carried out (2008-09) in 10 purposively selected case study sites in England. Details of LESs for these sites were collected (2009) through Freedom of Information requests or local contacts. A national on-line survey of PCTs (2009) provided a national context for case study findings. RESULTS: LESs were considered to be effective in incentivizing preventive activity. However, specifications and performance management were often weak, awareness of how to optimize incentives was low and, as optional services, LESs were perceived to be at risk in a financial downturn. CONCLUSIONS: Using LESs for preventive services highlights gaps in 'core' primary care responsibilities and in the national pay-for-performance framework. Current incentive arrangements are complex, could increase inequalities and provide only a partial, short-term solution to developing a proactive approach to prevention in primary care.

Public health governance: views of key stakeholders.

OBJECTIVES: To identify views of key stakeholders on public health governance. STUDY DESIGN: Focus groups and interviews. METHODS: Key national and regional stakeholders in England were invited to participate in focus groups. Three focus groups and four additional interviews were transcribed and a thematic analysis was carried out. RESULTS: Focus groups and interviewees identified points of transition in public health governance including changes in the notion of stewardship, governance across a local public health system and a shift from organizational governance to 'governance of place'. CONCLUSIONS: Different governance arrangements and approaches to governance can influence health outcomes through their impact on commissioning strategies, public health practice and performance management regimes. Failure to address these issues will hamper the development of a stewardship role in local organizations and across a local public health system.

An alpha1-antitrypsin enhancer polymorphism is a genetic modifier of pulmonary outcome in cystic fibrosis.

Lung disease is the direct cause of death in over 90% of cystic fibrosis (CF) patients. Excess neutrophil elastase is an important determinant of pulmonary disease in CF. alpha1-antitrypsin (AAT), also known as alpha1-proteinase inhibitor (alpha1PI) is a major modulator of elastase activity. We investigated the hypothesis that an enhancer polymorphism in the AAT gene would contribute to pulmonary prognosis in CF. Respiratory function, chest X-ray scores, bacterial colonisation and infective exacerbation were assessed to evaluate pulmonary disease severity in the CF group. Sixteen patients were found to have the 1237A allele, and 108 the more frequent G allele. Contrary to expectation, the patients with the 1237A allele were found to have better indices of pulmonary disease progression than those without, as indicated by less change in X-ray score (1237A: 0.2+/-0.1; 1237G: 1.2+/-0.1; P = 0.002) and fewer infective exacerbations (1237A: 2.8+/-0.6; 1237G: 4.6+/-0.3; P = 0.03) over the preceding 2 years. Also, a higher proportion of the 1237A (25%) than the 1237G (6.5%) were not colonised by Pseudomonas Aeruginosa (P = 0.04). Prospective monitoring of infections for a further 2 years confirmed a lesser propensity to infection in patients with the 1237A allele. These trends were also observed in a tightly matched sub-set of CF genotypes of similar age and sex, thus confirming that these effects were independent of the CF genotype. These results indicate that this AAT enhancer polymorphism is associated with better pulmonary prognosis in CF. Though the number of CF patients with the polymorphism is small, and these data need to be confirmed in larger studies, they suggest that a cautious approach should perhaps be taken to treatment of CF patients with supplemental AAT.

A polymorphism in the tumor necrosis factor-alpha gene promoter region may predispose to a poor prognosis in COPD.

STUDY OBJECTIVES: To determine whether the adenine (A)-guanine (G) substitution polymorphism at position - 308 on the tumor necrosis factor-alpha gene confers susceptibility to COPD or to the development of a more severe form of disease. DESIGN: A cross-sectional study was undertaken to compare the frequency of the A allele in a group of 106 patients with COPD with that in a control population (n = 99). Patients were followed up prospectively for a period of 2 years. PARTICIPANTS AND SETTING: Participants included 106 COPD patients recruited from a respiratory outpatient clinic and 99 control subjects recruited from patients admitted for cardiac catheterization. MEASUREMENTS AND RESULTS: DNA was extracted from venous blood, and each subject was genotyped for the polymorphism by polymerase chain reaction amplification and restriction digestion using Nco1. There was no increased frequency of the A allele in patients compared to control subjects. AA homozygous patients had less reversible airflow obstruction (p<0.05) and a significantly greater mortality (both all-cause and respiratory deaths) on follow-up (p<0.001), despite a shorter cigarette smoking history. CONCLUSIONS: This study suggests that homozygosity for this A allele predisposes to more severe airflow obstruction and a worse prognosis in COPD.

Fibroblast growth factor, epidermal growth factor and insulin exert a neuronal-like influence on acetylcholine receptors in aneurally cultured human muscle.

Fibroblast growth factor (FGF), epidermal growth factor (EGF) and insulin added in combination to the culture medium in which normal human muscle was cultured caused a 4.0-fold (P less than 0.005) increase of the total number of nicotinic acetylcholine receptors (AChRs) and a 4.5-fold (P less than 0.001) increase in AChR aggregation. Individually, only FGF caused a 3.0-fold increase (P less than 0.005) in AChR aggregation, without influencing the total number of AChRs. To the contrary, insulin alone caused a 2.0-fold increase (P less than 0.05) in the total number of AChRs without influencing AChR aggregation. These findings show that these three polypeptide growth factors exert a neuronal-like influence on cultured human muscle in regard to AChRs.

Pulp-test responses in orthodontic patients.

The diagnosis of orofacial pain is complicated in the orthodontic patient as treatment-induced alterations to pulpal physiology may result in altered responses to pulp-test stimuli. Thirty-three subjects commencing fixed orthodontic treatment and another 15 subjects not undergoing orthodontic treatment were used in this study. Cold and electrical stimuli were applied to the maxillary incisor teeth prior to treatment, after the placement of fixed appliances and at regular intervals for both groups for up to 252 days. At baseline, response thresholds to electric testing were typically higher for orthodontic subjects, particularly for the lateral incisors. For the non-orthodontic group, the response threshold over the 252 days was relatively constant. For the orthodontic group, application of force immediately increased the response threshold to electric pulp testing, which peaked after two months. By day 252, response means for lateral incisors still remained elevated. Responses to thermal testing were more consistent and reliable. The results of this study indicate that dental practitioners should interpret responses to electric pulp testing cautiously in orthodontic patients and that thermal testing with carbon dioxide snow may be more reliable.

Microsatellite polymorphism of the alpha 1-antichymotrypsin gene locus associated with sporadic Alzheimer's disease.

A variant of the apolipoprotein E gene, APOE*4, is associated with both sporadic Alzheimer's disease (AD) and a subset of familial AD and this association is stronger with early as opposed to late onset AD. Both APOE*4 and alpha 1-antichymotrypsin (ACT) will accelerate the rate of amyloid filament formation and are major constituents of the plaques associated with AD. We now show that a dinucleotide microsatellite allele in the 5'-flanking sequence of the ACT gene, designated A10, in association with APOE*4 significantly increases the risk of developing sporadic AD, which accounts for the majority of AD cases.