Each GP saves 4.7 lives a year, say researchers.

save life

Each GP saves nearly five lives a year, shows the first study to estimate the impact of disease prevention by practices.

Researchers estimated the public health impact (PHI) score for all practices in England and found 139,100 lives were saved nationally as a direct result of disease preventation activities in 2009/2010.

This equated to an average, per GP, of 4.71 lives saved a year.

The research, to published be in the British Journal of General Practice next month, is the first to quantify the impact of GPs on lives saved, with the PHI score calculated based on 20 QOF indicators, including those for flu vaccination, smoking cessation advice, and HbA1c control.

QOF data was taken from 8,136 general practices in England for the study, 97.97% of all practices.

They found the mean estimated PHI score was 258.9 lives saved per 100,000 registered patients, per year. This represented 75.7% of the maximum potential PHI score of 340.9.

The researchers said they hoped the PHI score would help CCGs to assess the impact of practices more accurately and lead to better public health outcomes.

Study leader Dr Mark Ashworth, a GP in south-east London and clinical senior lecturer at King’s College London, said that the study gave GPs a real measure of how much good they are doing in the community.

He said: ‘What this is doing for the first time is giving GPs a feel that, actually, all that disease prevention work they do translates into something really tangible.

“This figure is a way of looking at how well you are doing which is not so much using the management agenda, which is so often what’s being applied to general practice. It is using something that means much more to GPs, and much more to patients. It translates into a figure for lives saved.’

He added that the score was not necessarily related to high overall QOF scores: ‘You’ve got other sets of practices that don’t do very well at QOF – so aren’t said to be doing very well in terms of care performance – and yet their PHI score is very high.

‘It gives you some sense that QOF isn’t fully rewarding the practices that have necessarily performed best in terms of saving lives out in their community.’

Source: http://www.pulsetoday.co.uk




Postpartum management of hypertension.

Hypertension in the postpartum period affects several groups of women, including those with previous chronic hypertension, gestational hypertension, pre-eclampsia, and eclampsia. In addition, pre-eclampsia may present for the first time in the postnatal period. Although the underlying causes and clinical presentation of these types of hypertension vary, patients can be investigated and treated in a similar manner. This review covers management of postpartum hypertension and its future consequences. Hypertension affects 6-10% of pregnancies,1 but few studies have reported the incidence of postpartum hypertension. This review is relevant to general practitioners, obstetricians, and specialists in secondary care who may see women with postpartum hypertension.




Use of high potency statins and rates of admission for acute kidney injury.



Objective To quantify an association between acute kidney injury and use of high potency statins versus low potency statins.

Design Retrospective observational analysis of administrative databases, using nine population based cohort studies and meta-analysis. We performed as treated analyses in each database with a nested case-control design. Rate ratios for different durations of current and past statin exposure to high potency or low potency statins were estimated using conditional logistic regression. Ratios were adjusted for confounding by high dimensional propensity scores. Meta-analytic methods estimated overall effects across participating sites.

Setting Seven Canadian provinces and two databases in the United Kingdom and the United States.

Participants 2 067 639 patients aged 40 years or older and newly treated with statins between 1 January 1997 and 30 April 2008. Each person hospitalized for acute kidney injury was matched with ten controls.

Intervention A dispensing event was new if no cholesterol lowering drug or niacin prescription was dispensed in the previous year. High potency statin treatment was defined as ≥10 mg rosuvastatin, ≥20 mg atorvastatin, and ≥40 mg simvastatin; all other statin treatments were defined as low potency. Statin potency groups were further divided into cohorts with or without chronic kidney disease.

Main outcome measure Relative hospitalization rates for acute kidney injury.

Results Of more than two million statin users (2 008 003 with non-chronic kidney disease; 59 636 with chronic kidney disease), patients with similar propensity scores were comparable on measured characteristics. Within 120 days of current treatment, there were 4691 hospitalizations for acute kidney injury in patients with non-chronic kidney injury, and 1896 hospitalizations in those with chronic kidney injury. In patients with non-chronic kidney disease, current users of high potency statins were 34% more likely to be hospitalized with acute kidney injury within 120 days after starting treatment (fixed effect rate ratio 1.34, 95% confidence interval 1.25 to 1.43). Users of high potency statins with chronic kidney disease did not have as large an increase in admission rate (1.10, 0.99 to 1.23). χ2 tests for heterogeneity confirmed that the observed association was robust across participating sites.

Conclusions Use of high potency statins is associated with an increased rate of diagnosis for acute kidney injury in hospital admissions compared with low potency statins. The effect seems to be strongest in the first 120 days after initiation of statin treatment.

Comparison with existing evidence

According to data from the JUPITER trial, as published by the FDA,5 the maximum likelihood estimate of the relative risk was 1.11 for any renal event over a median follow-up duration of 1.9 years, and 1.19 for acute renal failure. Our rate ratio estimate was 1.15 for acute kidney injury for patients treated for one to two years. Over all treatment durations in our analysis, the average rate ratio was 1.17, or 1.20 if past treatment was excluded. The compatibility of these results with our hypothesis, their agreement with the maximum likelihood estimate observed in the large JUPITER trial, and the high degree of precision obtained from our study population, together lend meaningful support for this increased risk.

Similarity between our results and other epidemiologic studies is mixed. One multicenter study of statin use and acute kidney injury in patients with community acquired pneumonia (CAP) reported an odds ratio of 1.32 for acute kidney injury in patients with CAP who received statins compared with statin naive patients.23 By contrast, a meta-analysis of four observational studies of rosuvastatin, designed to study multiple outcomes but which included renal failure, reported no difference between rosuvatstain and other statins.24 This meta-analysis is impossible to interpret from a statin potency perspective, because the control patients received other statins of all different potencies.

It is also important to note that most statin treatment in randomized trials was of low potency. The JUPITER trial showed that about 450 patients needed to be treated with 20 mg rosuvastatin per day instead of placebo for two years to prevent one death from myocardial infarction, stroke, or cardiovascular disease (combined endpoint).4 It remains to be shown whether the number needed to treat to benefit with high potency statins instead of low potency statins (versus placebo) would outweigh the combined risk of acute kidney injury, rhabdomyolysis, and diabetes.


In this study of over two million patients newly treated with a statin, we found a significant relative increase of 34% in the rate of hospitalization for acute kidney injury within 120 days of initiation for patients receiving high potency statins versus low potency statins. Our as treated analysis was based on an expectation that less than perfect treatment persistence and a high tendency for subsequent switching to higher doses might cause a fixed cohort analysis to underestimate the risk while actually on treatment. Loss of some patients to follow-up and competing risks also could have contributed to an underestimation of the effect. The as treated analysis, which allowed quantification of risk from different durations of current exposure, indicated that risk remained elevated for at least two years.

Although we used multiplicative models to answer our study questions, it is the subsequent translation of relative risks into numbers needed to treat to harm that provides the most useful metric for prescribers, regulators, and decision makers. In this regard, we estimate that 1700 patients with non-chronic kidney disease need to be treated with a high potency statin instead of a low potency statin for 120 days to cause one additional hospitalization for acute kidney injury. A number of 1700 patients is sufficiently large for there not to be enough patients enrolled in randomized trials to find an association between acute kidney injury and statin use with high precision. However, our definition of acute kidney injury was chosen to be highly specific and thus probably excluded a number of patients with real but milder cases, which could have underestimated the absolute risk.

Further studies are necessary to determine the biological mechanism linking statins to kidney injury. The elevated risk in patients using high potency statins could be related to an increased risk of rhabdomyolysis. Another mechanism could be the statin induced suppression of coenzyme Q10, a fat soluble enzyme with antioxidant properties. Statins have been shown to block the production of coenzyme Q10,1920 and placebo controlled trials of coenzyme Q10 treatment in humans and animals with kidney disease have shown improvements in renal function within 28 days of use.20 21 Other studies have shown an association between statin treatment and proteinuria.5 22 Pleiotrophic statin effects should also be contemplated.




Use of caffeinated substances and risk of crashes in long distance drivers of commercial vehicles.

caffeinecrystalsObjective To determine whether there is an association between use of substances that contain caffeine and the risk of crash in long distance commercial vehicle drivers.

Design Case-control study.

Setting New South Wales (NSW) and Western Australia (WA), Australia.

Participants 530 long distance drivers of commercial vehicles who were recently involved in a crash attended by police (cases) and 517 control drivers who had not had a crash while driving a commercial vehicle in the past 12 months.

Main outcome measure The likelihood of a crash associated with the use of substances containing caffeine after adjustment for factors including age, health disorders, sleep patterns, and symptoms of sleep disorders as well as exposures such as kilometres driven, hours slept, breaks taken, and night driving schedules.

Results Forty three percent of drivers reported consuming substances containing caffeine, such as tea, coffee, caffeine tablets, or energy drinks for the express purpose of staying awake. Only 3% reported using illegal stimulants such as amphetamine (“speed”); 3,4 methylenedioxymethamphetamine (ecstasy); and cocaine. After adjustment for potential confounders, drivers who consumed caffeinated substances for this purpose had a 63% reduced likelihood of crashing (odds ratio 0.37, 95% confidence interval 0.27 to 0.50) compared with drivers who did not take caffeinated substances.

Conclusions Caffeinated substances are associated with a reduced risk of crashing for long distance commercial motor vehicle drivers. While comprehensive mandated strategies for fatigue management remain a priority, the use of caffeinated substances could be a useful adjunct strategy in the maintenance of alertness while driving.




Cardiovascular events after clarithromycin use in lower respiratory tract infections:.



Objective To study the association of clarithromycin with cardiovascular events in the setting of acute exacerbations of chronic obstructive pulmonary disease and community acquired pneumonia.

Design Analysis of two prospectively collected datasets.

Setting Chronic obstructive pulmonary disease dataset including patients admitted to one of 12 hospitals around the United Kingdom between 2009 and 2011; Edinburgh pneumonia study cohort including patients admitted to NHS Lothian Hospitals between 2005 and 2009.

Population 1343 patients admitted to hospital with acute exacerbations of chronic obstructive pulmonary disease and 1631 patients admitted with community acquired pneumonia.

Main outcome measures Hazard ratios for cardiovascular events at one year (defined as hospital admissions with acute coronary syndrome, decompensated cardiac failure, serious arrhythmia, or sudden cardiac death) and admissions for acute coronary syndrome (acute ST elevation myocardial infarction, non-ST elevation myocardial infarction, and unstable angina). Secondary outcomes were all cause and cardiovascular mortality at one year.

Results 268 cardiovascular events occurred in the acute exacerbations of chronic obstructive pulmonary disease cohort and 171 in the community acquired pneumonia cohort over one year. After multivariable adjustment, clarithromycin use in acute exacerbations of chronic obstructive pulmonary disease was associated with an increased risk of cardiovascular events and acute coronary syndrome—hazard ratios 1.50 (95% confidence interval 1.13 to 1.97) and 1.67 (1.04 to 2.68). After multivariable adjustment, clarithromycin use in community acquired pneumonia was associated with increased risk of cardiovascular events (hazard ratio 1.68, 1.18 to 2.38) but not acute coronary syndrome (1.65, 0.97 to 2.80). The association between clarithromycin use and cardiovascular events persisted after matching for the propensity to receive clarithromycin. A significant association was found between clarithromycin use and cardiovascular mortality (adjusted hazard ratio 1.52, 1.02 to 2.26) but not all cause mortality (1.16, 0.90 to 1.51) in acute exacerbations of chronic obstructive pulmonary disease. No association was found between clarithromycin use in community acquired pneumonia and all cause mortality or cardiovascular mortality. Longer durations of clarithromycin use were associated with more cardiovascular events. Use of β lactam antibiotics or doxycycline was not associated with increased cardiovascular events in patients with acute exacerbations of chronic obstructive pulmonary disease, suggesting an effect specific to clarithromycin.

Conclusions The use of clarithromycin in the setting of acute exacerbations of chronic obstructive pulmonary disease or community acquired pneumonia may be associated with increased cardiovascular events. These findings require confirmation in other datasets.



This is the first study showing that use of clarithromycin in the context of exacerbations of chronic obstructive pulmonary disease and community acquired pneumonia may be associated with excess cardiovascular events that last beyond the period of prescription. Clarithromycin is the most widely used macrolide in the UK and is strongly recommended for use in patients with severe community acquired pneumonia. Previous studies have suggested an excess cardiovascular morbidity after clarithromycin use,14 but these patients were selected on the basis of pre-existing cardiovascular risk rather than having a defined infective episode requiring treatment with this drug. Other studies have shown a short term association seen only during the time of administration.12 13 The observed association with cardiovascular events is of a similar magnitude to that seen in stable non-infected patients with established coronary artery disease.14 Our data suggest that the increased risk may persist beyond the time when clarithromycin is stopped.


Possible explanations for findings

Although short term events may be associated with clarithromycin’s pro-arrhythmic effects mediated through prolongation of the QT interval,27 this would not affect outcome after cessation of the drug and would support an ischaemic mechanism. Clarithromycin may activate macrophages, leading to an inflammatory cascade resulting in more vulnerable plaques that over time may lead to acute coronary syndromes or sudden cardiac death by plaque rupture.25 This may explain why clarithromycin seems to increase cardiovascular events and mortality beyond the time of prescription.

We did several hypothesis generating analyses to explore the relation between clarithromycin use and cardiovascular events in these cohorts. We found a strong association between prolonged (more than seven days) courses of clarithromycin and cardiovascular events, which strengthens the case for a true biological cause. The association between duration of antibiotic treatment and cardiovascular events could also represent residual confounding by severity of illness. Although prolonged courses of antibiotics are common for respiratory tract infections in clinical practice, a considerable body of evidence suggests that short courses of antibiotics are equivalent to prolonged courses in community acquired pneumonia and other respiratory tract infections.