Abstract

Background

Pay-for-performance (P4P) is increasingly implemented in the healthcare system to encourage improvements in healthcare quality. P4P is a payment model that rewards healthcare providers for meeting pre-established targets for delivery of healthcare services by financial incentives. Based on their performance, healthcare providers receive either additional or reduced payment. Currently, little is known about P4P schemes intending to improve delivery of chronic care through disease management. The objectives of this paper are therefore to provide an overview of P4P schemes used to stimulate delivery of chronic care through disease management and to provide insight into their effects on healthcare quality and costs.

Methods

A systematic PubMed search was performed for English language papers published between 2000 and 2010 describing P4P schemes related to the implementation of disease management. Wagner's chronic care model was used to make disease management operational.

Results

Eight P4P schemes were identified, introduced in the USA (n = 6), Germany (n = 1), and Australia (n = 1). Five P4P schemes were part of a larger scheme of interventions to improve quality of care, whereas three P4P schemes were solely implemented. Most financial incentives were rewards, selective, and granted on the basis of absolute performance. More variation was found in incented entities and the basis for providing incentives. Information about motivation, certainty, size, frequency, and duration of the financial incentives was generally limited. Five studies were identified that evaluated the effects of P4P on healthcare quality. Most studies showed positive effects of P4P on healthcare quality. No studies were found that evaluated the effects of P4P on healthcare costs.

Conclusion

The number of P4P schemes to encourage disease management is limited. Hardly any information is available about the effects of such schemes on healthcare quality and costs.

Abstract

Background

Primary care practices provide a gate-keeping function in many health care systems. Since depressive disorders are highly prevalent in primary care settings, reliable detection and diagnoses are a first step to enhance depression care for patients. Provider training is a self-evident approach to enhance detection, diagnoses and treatment options and might even lead to improved patient outcomes.

Methods

A systematic literature search was conducted reviewing research studies providing training of general practitioners, published from 1999 until May 2011, available on the electronic databases Medline, Web of Science, PsycINFO and the Cochrane Library as well as national guidelines and health technology assessments (HTA).

Results

108 articles were fully assessed and 11 articles met the inclusion criteria and were included. Training of providers alone (even in a specific interventional method) did not result in improved patient outcomes. The additional implementation of guidelines and the use of more complex interventions in primary care yield a significant reduction in depressive symptomatology. The number of studies examining sole provider training is limited, and studies include different patient samples (new on-set cases vs. chronically depressed patients), which reduce comparability.

Conclusions

This is the first overview of randomized controlled trials introducing GP training for depression care. Provider training by itself does not seem to improve depression care; however, if combined with additional guidelines implementation, results are promising for new-onset depression patient samples. Additional organizational structure changes in form of collaborative care models are more likely to show effects on depression care.

Keywords:

depression; primary care; training; health service

Saw Palmetto, even in high dose, has no benefit for lower urinary tract symptoms, according to this recent study.

Drats!

Abstract and Introduction

Abstract

Background Coffee contains many biologically active compounds, including caffeine and phenolic acids, that have potent antioxidant activity and can affect glucose metabolism and sex hormone levels. Because of these biological activities, coffee may be associated with a reduced risk of prostate cancer.
Methods We conducted a prospective analysis of 47 911 men in the Health Professionals Follow-up Study who reported intake of regular and decaffeinated coffee in 1986 and every 4 years thereafter. From 1986 to 2006, 5035 patients with prostate cancer were identified, including 642 patients with lethal prostate cancers, defined as fatal or metastatic. We used Cox proportional hazards models to assess the association between coffee and prostate cancer, adjusting for potential confounding by smoking, obesity, and other variables. All P values were from two-sided tests.
Results The average intake of coffee in 1986 was 1.9 cups per day. Men who consumed six or more cups per day had a lower adjusted relative risk for overall prostate cancer compared with nondrinkers (RR = 0.82, 95% confidence interval [CI] = 0.68 to 0.98, P _trend = .10). The association was stronger for lethal prostate cancer (consumers of more than six cups of coffee per day: RR = 0.40, 95% CI = 0.22 to 0.75, P _trend = .03). Coffee consumption was not associated with the risk of nonadvanced or low-grade cancers and was only weakly inversely associated with high-grade cancer. The inverse association with lethal cancer was similar for regular and decaffeinated coffee (each one cup per day increment: RR = 0.94, 95% CI = 0.88 to 1.01, P = .08 for regular coffee and RR = 0.91, 95% CI = 0.83 to 1.00, P = .05 for decaffeinated coffee). The age-adjusted incidence rates for men who had the highest (≥6 cups per day) and lowest (no coffee) coffee consumption were 425 and 519 total prostate cancers, respectively, per 100 000 person-years and 34 and 79 lethal prostate cancers, respectively, per 100 000 person-years.
Conclusions We observed a strong inverse association between coffee consumption and risk of lethal prostate cancer. The association appears to be related to non-caffeine components of coffee.

Introduction

Coffee contains diverse biologically active compounds that include caffeine, minerals, and phytochemicals. Long-term coffee drinking has been associated with improved glucose metabolism and insulin secretion in observational and animal studies.^[1] Coffee is also a potent antioxidant^[2–4] and may be associated with sex hormone levels.^[5–7]

Coffee consumption has been consistently associated with a reduced risk of type 2 diabetes,^[8] and its effects on insulin, sex hormones, and antioxidants may also be relevant to prostate cancer. We hypothesized that coffee may be associated with lower risk of more advanced prostate cancers because the associations of insulin, antioxidants, and androgens with incidence of prostate cancer are stronger for advanced disease than for overall disease.^[9–15]

Epidemiological studies of coffee consumption and prostate cancer have generally reported null results,^[16–30] although most lacked a wide range of coffee intakes and a large number of case subjects and none specifically examined advanced disease. The two studies of coffee consumption and prostate cancer mortality^[31,32] found no statistically significant associations, but these were limited by a narrow range of intake, small number of cancer deaths, and inadequate adjustment for potential confounding.

We investigated the relationship between coffee intake and risk of overall prostate cancer and of aggressive disease, defined as lethal, advanced, or high-grade cancer, in the Health Professionals Follow-up Study.

Section 1 of 4

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Table 1. Age-adjusted characteristics of the Health Professionals Follow-up Study population at baseline in 1986, by coffee consumption*

Characteristic	Category of total coffee intake
	None (n = 7890)	<1 cup per day (n = 9533)	1–3 cups per day (n = 21 261)	4–5 cups per day (n = 6735)	≥6 cups day (n = 2492)
Mean age, y	52	55	55	54	53
White race, %	95	94	96	98	98
Mean BMI, kg/m2	25	25	26	26	26
Mean BMI at age 21, kg/m2	23	23	23	23	23
Mean height, inches	70	70	70	70	70
Former smoker, quit >10 y ago, %	20	28	32	34	31
Former smoker, quit ≤10 y ago, %	6	10	14	17	17
Current smokers, %	4	6	10	16	25
Vigorous activity (% highest quintile)	17	17	15	15	11
Diabetes, %	3	3	3	3	3
Family history of prostate cancer, %	13	11	12	12	12
PSA test, 1994, %	35	39	38	38	33
PSA test, 2004, %	60	64	66	66	58
Mean dietary intakes
Energy, kcal/d	1960	1895	1990	2069	2159
Alcohol, g/d	6	9	13	14	15
Calcium, mg/d	973	931	866	881	873
Alpha-linolenic acid, g/d	1.1	1.1	1.1	1.1	1.1
Supplemental vitamin E, mg/day	41.5	45.1	36.1	33.3	33.0
Multivitamin use, %	42	44	41	40	38
Processed meat, servings per week	2.1	2.1	2.6	2.9	3.4
Tomato sauce, servings per week	0.9	0.9	0.9	0.9	0.9
Total coffee, servings per day	0.0	0.5	1.9	4.2	6.3
Regular coffee, servings per day	0.0	0.2	1.3	2.9	4.2
Decaffeinated coffee, servings per day	0.0	0.2	0.6	1.3	2.0

* All variables (except age) are standardized to the age distribution of the cohort at baseline. BMI = body mass index; PSA = prostate-specific antigen.

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Table 2. Relative risk (RR) with 95% confidence interval (95% CI) of prostate cancer by category of total coffee intake, 1986–2006*

Risk of prostate cancer	Category of coffee intake					P trend
	None	<1 cup/d	1–3 cups/d	4–5 cups/d	≥6 cups/d
All prostate cancers, No.	587	1139	2438	719	152
Age-adjusted RR (95% CI)	1.00	0.96 (0.87 to 1.06)	0.97 (0.88 to 1.06)	0.95 (0.85 to 1.06)	0.81 (0.67 to 0.96)	.08
Fully adjusted RR (95% CI)	1.00	0.94 (0.85 to 1.05)	0.94 (0.86 to 1.04)	0.93 (0.83 to 1.04)	0.82 (0.68 to 0.98)	.10
Lethal prostate cancers†, No.	89	150	298	93	12
Age-adjusted RR (95% CI)	1.00	0.76 (0.58 to 0.99)	0.73 (0.58 to 0.93)	0.83 (0.62 to 1.11)	0.43 (0.24 to 0.80)	.08
Fully adjusted RR (95% CI)	1.00	0.76 (0.58 to 1.00)	0.71 (0.55 to 0.92)	0.76 (0.56 to 1.04)	0.40 (0.22 to 0.75)	.03
Advanced prostate cancers†, No.	122	211	422	122	19
Age-adjusted RR (95% CI)	1.00	0.81 (0.65 to 1.02)	0.78 (0.63 to 0.95)	0.79 (0.61 to 1.01)	0.49 (0.30 to 0.80)	.01
Fully adjusted RR (95% CI)	1.00	0.81 (0.64 to 1.02)	0.75 (0.60 to 0.93)	0.73 (0.56 to 0.95)	0.47 (0.28 to 0.77)	.004
Nonadvanced prostate cancers†, No.	353	729	1554	483	102
Age-adjusted RR (95% CI)	1.00	1.04 (0.91 to 1.18)	1.04 (0.92 to 1.16)	1.04 (0.91 to 1.20)	0.88 (0.71 to 1.10)	.60
Fully adjusted RR(95% CI)	1.00	1.01 (0.88 to 1.15)	0.99 (0.87 to 1.12)	1.02 (0.88 to 1.18)	0.93 (0.74 to 1.16)	.77
Grade 8–10 cancers, No.	61	111	255	78	11
Age-adjusted RR (95% CI)	1.00	0.86 (0.63 to 1.18)	0.93 (0.70 to 1.23)	0.96 (0.69 to 1.35)	0.57 (0.30 to 1.09)	.58
Fully adjusted RR (95% CI)	1.00	0.84 (0.61 to 1.16)	0.87 (0.65 to 1.18)	0.88 (0.61 to 1.26)	0.53 (0.27 to 1.02)	.29
Grade 7 cancers, No.	174	295	641	226	41
Age-adjusted RR (95% CI)	1.00	0.86 (0.72 to 1.04)	0.88 (0.74 to 1.04)	0.98 (0.80 to 1.20)	0.69 (0.49 to 0.97)	.58
Fully adjusted RR (95% CI)	1.00	0.85 (0.70 to 1.04)	0.85 (0.71 to 1.02)	0.94 (0.76 to 1.16)	0.69 (0.49 to 0.99)	.50
Grade 2–6 cancers, No.	232	489	1045	298	70
Age-adjusted RR (95% CI)	1.00	1.08 (0.92 to 1.26)	1.07 (0.93 to 1.24)	0.99 (0.83 to 1.18)	0.94 (0.72 to 1.23)	.34
Fully adjusted RR (95% CI)	1.00	1.02 (0.87 to 1.20)	1.01 (0.87 to 1.18)	0.96 (0.80 to 1.15)	1.00 (0.75 to 1.31)	.53

* All relative risks are from an age-adjusted model adjusted for age in months and calendar time. The multivariable model was additionally adjusted for: race (White, African American, Asian American, Other), height (quartiles), BMI at age 21 (<20, 20 to <22.5, 22.5 to <25, ≥25), current BMI (<21, 21 to <23, 23 to <25, 25 to <27.5, 27.5 to <30, ≥30 kg/m²), vigorous physical activity (quintiles), smoking (never, former quit >10 years ago, former quit <10 years ago, current), diabetes (type I or II, yes/no), family history of prostate cancer in father or brother (yes/no), multivitamin use (yes/no), intakes of processed meat, tomato sauce, calcium, alpha linolenic acid, supplemental vitamin E, alcohol intake (all quintiles), and energy intake (continuous), and history of PSA testing (yes/no, lagged by one period to avoid counting diagnostic PSA tests as screening; collected frsom 1994 onwards). All P values were from two-sided tests. BMI = body mass index; PSA, prostate-specific antigen.
† Lethal prostate cancer: Prostate cancer death or bone metastases at diagnosis or during follow-up. Advanced: Lethal, or stage T3b, T4, N1, or M1 at diagnosis, or spread to lymph nodes or other metastases during follow-up. Nonadvanced: T1 or T2 and N0/M0 at diagnosis with no spread to lymph nodes or other metastases or death during follow-up.

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Table 3. Relative risk (RR) and 95% confidence interval (95% CI) of prostate cancer by category of regular coffee intake*

Risk of prostate cancer	No coffee at all†	Category of regular (with caffeine) coffee intake				P trend	No regular, some decaf
		<1 cup per day	1–3 cups per day	4–5 cups per day	≥6 cups per day
Lethal prostate cancers‡, No.	89	207	209	52	6		79
Fully adjusted RR (95% CI)*	1.00	0.81 (0.61 to 1.07)	0.71 (0.54 to 0.93)	0.77 (0.53 to 1.10)	0.46 (0.20 to 1.08)	.07	0.72 (0.51 to 1.01)
Advanced prostate cancers‡, No.	122	298	293	65	12		106
Fully adjusted RR (95% CI)*	1.00	0.86 (0.69 to 1.09)	0.74 (0.59 to 0.93)	0.70 (0.51 to 0.95)	0.69 (0.38 to 1.27)	.01	0.75 (0.56 to 1.00)
Nonadvanced prostate cancers‡, No.	353	1042	1164	270	43		349
Fully adjusted RR (95% CI)*	1.00	0.98 (0.86 to 1.12)	0.99 (0.87 to 1.12)	1.00 (0.84 to 1.18)	0.93 (0.67 to 1.29)	.97	1.10 (0.93 to 1.29)

* All relative riskss are from a multivariable model adjusted for: age in months, calendar time, race (White, African American, Asian American, Other), height (quartiles), BMI at age 21 (four categories), current BMI (six categories), vigorous physical activity (quintiles), smoking (never, former quit >10 years ago, former quit <10 years ago, current), diabetes (type I or II, yes/no), family history of prostate cancer in father or brother (yes/no), multivitamin use (yes/no), intakes of processed meat, tomato sauce, calcium, alpha linolenic acid, supplemental vitamin E, alcohol intake (all quintiles), energy intake (continuous), and history of prostate-specific antigen testing. Models for regular coffee are also adjusted for decaffeinated coffee intake (continuous). All P values are from two-sided tests. BMI = body mass index.
† Reference group is men who drink no regular or decaffeinated coffee.
‡ Lethal prostate cancer: Prostate cancer death or bone metastases at diagnosis or during follow-up. Advanced: Lethal, or stage T3b, T4, N1, or M1 at diagnosis, or spread to lymph nodes or other metastases during follow-up. Nonadvanced: T1 or T2 and N0/M0 at diagnosis with no spread to lymph nodes or other metastases or death during follow-up.

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Table 4. Relative risk (RR) and 95% confidence interval (CI) of prostate cancer by category of decaffeinated coffee intake*

	No coffee at all†	Category of decaffeinated coffee intake			P trend	No decaf, some regular
		<1 cup/d	1–3 cups/d	≥4 cups/d
Lethal prostate cancers‡, No.	89	264	125	15		149
Fully adjusted RR*	1.00	0.81 (0.62 to 1.06)	0.68 (0.50 to 0.91)	0.53 (0.30 to 0.94)	.01	0.71 (0.52 to 0.98)
Advanced prostate cancers‡, No	122	374	171	25		204
Fully adjusted RR*	1.00	0.85 (0.68 to 1.07)	0.70 (0.54 to 0.89)	0.67 (0.43 to 1.05)	.02	0.77 (0.59 to 1.01)
Nonadvanced prostate cancers‡, No.	353	1455	688	86		639
Fully adjusted RR*	1.00	0.99 (0.87 to 1.13)	1.04 (0.90 to 1.19)	0.94 (0.74 to 1.20)	.88	0.98 (0.85 to 1.14)

* All relative riskss are from a multivariable model adjusted for: age in months, calendar time, race (White, African American, Asian American, Other), height (quartiles), BMI at age 21 (four categories), current BMI (six categories), vigorous physical activity (quintiles), smoking (never, former quit >10 years ago, former quit <10 years ago, current), diabetes (type I or II, yes/no), family history of prostate cancer in father or brother (yes/no), multivitamin use (yes/no), intakes of processed meat, tomato sauce, calcium, alpha linolenic acid, supplemental vitamin E, alcohol intake (all quintiles), and energy intake (continuous), and history of prostate-specific antigen testing. Models for decaffeinated coffee are also adjusted for regular coffee intake (continuous). All P values are from two-sided tests. BMI = body mass index.
† Reference group is men who drink no regular or decaffeinated coffee. ‡ Lethal prostate cancer: Prostate cancer death or bone metastases at diagnosis or during follow-up. Advanced: Lethal, or stage T3b, T4, N1 or M1 at diagnosis, or spread to lymph nodes or other metastases during follow-up. Nonadvanced: T1 or T2 and N0/M0 at diagnosis with no spread to lymph nodes or other metastases or death during follow-up.

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Table 5. Relative risk (RR) and 95% confidence interval (95% CI) of prostate cancer by category of total coffee intake for various latency periods between exposure and diagnosis*

	Total prostate cancer		Advanced cancer†		Nonadvanced cancer†
	N	RR (95% CI)	N	RR (95% CI)	N	RR (95% CI)
0 to 4-year lag, cups per day
None	810	1.00 (referent)	160	1.00 (referent)	493	1.00 (referent)
<1	1003	.95 (.87 to 1.05)	180	.78 (.62 to.97)	655	1.05 (.93 to 1.18)
1–3	2501	.96 (.89 to 1.05)	436	.77 (.63 to.93)	1592	1.01 (.91 to 1.13)
4–5	587	.97 (.87 to 1.09)	100	.73 (.56 to.95)	389	1.08 (.93 to 1.24)
≥6	134	.81 (.67 to.98)	20	.52 (.33 to.84)	92	.96 (.76 to 1.21)
P trend		.20		.008		.91
4 to 8-year lag, cups per day
None	745	1.00 (referent)	131	1.00 (referent)	468	1.00 (referent)
<1	886	.92 (.83 to 1.02)	152	.84 (.66 to 1.07)	589	1.00 (.88 to 1.13)
1–3	2267	.93 (.85 to 1.02)	329	.72 (.58 to.89)	1519	1.00 (.89 to 1.11)
4–5	594	.92 (.82 to 1.03)	99	.81 (.61 to 1.07)	397	.97 (.85 to 1.12)
≥6	153	.80 (.67 to.96)	18	.47 (.28 to.78)	102	.88 (.71 to 1.10)
P trend		.06		.008		.34
8 to 12-year lag, cups per day
None	551	1.00 (referent)	79	1.00 (referent)	360	1.00 (referent)
<1	664	.98 (.87 to 1.10)	91	.85 (.62 to 1.17)	458	1.06 (.92 to 1.22)
1–3	1687	.99 (.89 to 1.10)	181	.68 (.51 to.91)	1175	1.06 (.93 to 1.20)
4–5	465	.91 (.80 to 1.03)	63	.82 (.58 to 1.17)	329	.98 (.83 to 1.14)
≥6	154	.93 (.77 to 1.12)	18	.71 (.42 to 1.21)	111	1.04 (.83 to 1.30)
P trend		.17		.18		.70
12 to 16-year lag, cups per day
None	389	1.00 (referent)	41	1.00 (referent)	268	1.00 (referent)
<1	448	.97 (.84 to 1.11)	49	.90 (.58 to 1.39)	307	.96 (.81 to 1.14)
1–3	1046	.93 (.82 to 1.06)	93	.72 (.48 to 1.07)	742	.94 (.81 to 1.10)
4–5	353	.97 (.83 to 1.13)	41	.97 (.61 to 1.55)	260	1.02 (.85 to 1.23)
≥6	115	.93 (.75 to 1.16)	8	.59 (.27 to 1.29)	84	.98 (.76 to 1.26)
P trend		.61		.43		.78

* All relative riskss are from multivariable models adjusted for: age in months, calendar time, race (White, African American, Asian American, Other), height (quartiles), BMI at age 21 (<20, 20 to <22.5, 22.5 to <25, .25 kg/m²), current BMI (<21, 21 to <23, 23 to <25, 25 to <27.5, 27.5 to <30, .30 kg/m²), vigorous physical activity (quintiles), smoking (never, former quit >10 years ago, former quit <10 years ago, current), diabetes (type I or II, yes/no), family history of prostate cancer in father or brother (yes/no), multivitamin use (yes/no), intakes of processed meat, tomato sauce, calcium, alpha linolenic acid, supplemental vitamin E, alcohol intake (all quintiles), and energy intake (continuous), and history of PSA testing (yes/no, lagged by one period to avoid counting diagnostic PSA tests as screening; collected from 1994 onwards). All P values are from two-sided tests. BMI = body mass index; PSA = prostate-specific antigen.
† Advanced: Lethal, or stage T3b, T4, N1, or M1 at diagnosis, or spread to lymph nodes or other metastases during follow-up. Nonadvanced: T1 or T2 and N0/M0 at diagnosis with no spread to lymph nodes or other metastases or death during follow-up.

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Authors and Disclosures

Kathryn M. Wilson, Julie L. Kasperzyk, Jennifer R. Rider, Stacey Kenfield, Rob M. van Dam, Meir J. Stampfer, Edward Giovannucci and Lorelei A. Mucci

Department of Epidemiology (KMW, JLK, SK, MJS, EG, LAM) and Department of Nutrition (RMvD, MJS, EG), Harvard School of Public Health, Boston, MA; Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (KMW, JLK, JRR, SK, MJS, EG, LAM); Department of Urology, Örebro University Hospital, Örebro, Sweden (JRR); Department of Epidemiology and Department of Public Health and Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore (RMvD)

Correspondence to
Kathryn M. Wilson, ScD, Department of Epidemiology, Harvard School of Public Health, 677 Huntington Ave, Boston, MA 02115 (e-mail: kwilson@hsph.harvard.edu).

The NHS needs a major overhaul if the UK is to cope with the needs of people with long term conditions, according to Sir John Oldham.

Sir John is in charge of the team which aims to improve how the national health service deals with Long Term Conditions and Urgent Care.

Sir John established the collaboratives in the UK and was instrumental in their introduction to Australia.

Cf http://www.inpharm.com/news/163372/chronic-problem-health-service

also

http://www.guardian.co.uk/healthcare-network/2011/jun/14/nhs-reform-around-lo...

The STOPP criteria are available at http://www.em-consulte.com/showarticlefile/245669/main.pdf

Did you know that low fitness kills more Americans than smoking, obesity and diabetes combined?

Implementation, Knowledge, Translation, Dissemination - How can research move from the shelf to actually improve health outcomes?

(This article from the British Journal of Sports Medicine)

Ovarian Cancer Mortality is not decreased by annual screening with Ca-125 and vaginal ultrasound. There is more morbidity in the screened group from the complications of investigating false positive cases.

The Limitations of Using FEV₁ in Evaluating COPD: A Discussion of Patient-Centered Outcomes

Symptom assessment and Quality of Life as measures of COPD

Correcting excessive anticoagulation in Warfarin treatment - If INR 4.5 -10 and no active bleeding, withhold Warfarin and consider 1.25mg stat dose oral Vit K (not IMI).
However, Vit K tablets are hard to source!

April 28, 2011 (San Diego, California) — In an effort to address the dangerous comorbid conditions that often accompany diabetes, as well as the symptoms of the disease itself, the American Association of Clinical Endocrinology (AACE) has released new clinical practice guidelines that emphasize individualized, comprehensive healthcare for patients with diabetes. Until now, that comprehensive care has been a missing piece in the healthcare that patients with diabetes receive, said 2 experts here at the AACE 20th Annual Meeting and Clinical Congress.

Guidelines available at http://aace.metapress.com/content/t7g5335740165v13/fulltext.pdf

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Table 1. Comparison of Primary Prevention Trials of Aspirin That Enrolled Patients With Diabetes (N=11 787)

Study/Year (Ref.)	Aspirin Dose (Study Design)	Follow-Up (Years)	Number Enrolled With Diabetes	% Female	Age (Years) (Minimum/Mean)	CHD Endpoint	CHD Endpoint Event Rate (Control vs. Aspirin)	10-Year Extrapolated CHD Event Ratesi	RR (95% CI)ii	Stroke Events for Aspirin vs. Control: RR (95% CI)
PHS DM/1989 (12)	325 mg every other day (2 × 2 factorial design with 50 mg beta carotene)	5.0	533	70	>40/NA	Fatal + nonfatal MI	10.5% vs. 6.2%iii (27/258 vs. 17/275)	21% vs. 12.4%	0.59 (0.33–1.06)	16 vs. 10: 1.50 (0.69–3.25)
ETDRS/1992 (18)	650 mg daily	5.0	3711	44	>18/NA	Fatal + nonfatal MI	15.3% vs. 13.0% (283/1855 vs. 241/1856)	30.6% vs. 26.0%	0.85 (0.73–1.00)	92 vs. 78: 1.18 (0.88–1.58)
PPP DM/2003iv (16)	100 mg daily (2 × 2 design with 30 mg vitamin E)	3.7	1031	52	>50/64	Fatal + nonfatal MI	2.0% vs. 1.0% (10/512 vs. 5/519)	5.4% vs. 2.7%	0.49 (0.17–1.43)	10 vs. 11: 0.90 (0.38–2.09)
WHS DM/2005 (17)	100 mg every other day (2 × 2 factorial design with 600 IU vitamin E every other day)	10.1	1027	100	>45/55	Fatal + nonfatal MIv	5.9% vs. 7.9% (29/494 vs. 42/533)	5.9% vs. 7.9%	1.34 (0.85–2.12)	15 vs. 31: 0.45 (0.25–0.82)
JPAD/2008 (10)	81–100 mg daily (open label treatment assignment, blinded endpoint assessment)	4.4	2539	46	>30/65	Fatal + nonfatal MI	1.1% vs. 1.0% (14/1277 vs. 12/1262)	2.5% vs. 2.3%	0.87 (0.40–1.87)	22 vs. 34: 0.65 (0.39–1.11)
POPADAD/2008 (9)	100 mg daily (2 × 2 factorial design including anti-oxidants)	6.7	1276	56	>40/60	CHD death + nonfatal MI	12.9% vs. 13.9% (82/638 vs. 89/638)	19.3% vs. 20.7%	1.09 (0.82–1.44)	37 vs. 50: 0.74 (0.49–1.12)
TPT DM/1998 (data from ATT) (5)	75 mg daily	6.7	68	0	>45/58	MCE	15.4% vs. 13.8% (6/39 vs. 4/29)	23.0% vs. 20.6%	0.90 (0.28–2.89)	1 vs. 2: 0.67 (0.06–7.06)
BMD/1988 (data from ATT) (5)	500 mg daily	5.6	101	0	>50/NA	MCE	18.8% vs. 18.8% (6/32 vs. 13/69)	33.48% vs. 33.6%	1.00 (0.42–2.40)	3 vs. 1: 1.39 (0.15–12.86)
HOT DM/1998 (data from ATT) (5)	75 mg daily (co-randomized to one of three diastolic BP goals)	3.8	1501	47	>50/62	MCE	3.6% vs. 2.8% (27/749 vs. 21/752)	9.5% vs. 7.3%	0.77 (0.44–1.36)	22 vs. 24: 0.91 (0.52–1.61)

ⁱ 10-year extrapolated CHD event rate calculated by (10 ÷ study duration) × event rate. ⁱⁱ Calculated based on event counts. ⁱⁱⁱ Values slightly different from original PHS report based on updated ICD-9 coding information obtained by the ATT trialists. ^iv Data used from 2003 PPP diabetic substudy (16); number with diabetes is discrepant from original PPP publication (15) due to continued enrollment and follow-up of diabetic patients beyond the original study period. ^v Event rates slightly different than original 2005 report due to 11 extra MI/CHD deaths (6 in aspirin group and 5 in placebo) reported to the ATT study group vs. original publication.
ATT indicates Antithrombotic Trialists' Collaboration; CHD, coronary heart disease; DM, diabetes mellitus; IU, international unit; MCE, major coronary event (CHD death + nonfatal MI + sudden death); MI, myocardial infarction; NA, not available; and RR, relative risk.

The effect of aspirin for primary prevention of CVD events in adults with diabetes is currently unclear. Trials to date have reached mixed results, but overall suggest that aspirin modestly reduces risk of cardiovascular events. More research is needed to better define the specific effects of aspirin in diabetes, including any sex-specific differences. For now, we recommend the following:

Low-dose (75 to 162 mg/day) aspirin use for prevention is reasonable for adults with diabetes and no previous history of vascular disease who are at increased CVD risk (10 year risk of CVD events over 10%) and who are not at increased risk for bleeding (based on a history of previous gastrointestinal bleeding or peptic ulcer disease or concurrent use of other medications that increase bleeding risk, such as NSAIDS or warfarin). Those adults with diabetes at increased CVD risk include most men over age 50 years and women over age 60 years who have one or more of the following additional major risk factors: smoking, hypertension, dyslipidemia, family history of premature CVD, and albuminuria. (ACCF/AHA Class IIa, Level of Evidence: B) (ADA Level of Evidence: C)
Aspirin should not be recommended for CVD prevention for adults with diabetes at low CVD risk (men under age 50 years and women under 60 years with no major additional CVD risk factors; 10-year CVD risk under 5%) as the potential adverse effects from bleeding offset the potential benefits. (ACCF/AHA Class III, Level of Evidence: C) (ADA Level of Evidence: C)
Low-dose (75 to 162 mg/day) aspirin use for prevention might be considered for those with diabetes at intermediate CVD risk (younger patients with one or more risk factors, or older patients with no risk factors, or patients with 10-year CVD risk of 5% to 10%) until further research is available. (ACCF/AHA Class IIb, Level of Evidence: C) (ADA Level of Evidence: E)

THE oral thrombin inhibitor dabigatran has been approved for listing on the PBS for use in patients with atrial fibrillation (AF) under a new pilot, fast-track regulatory process.

Dabigatran (Pradaxa) reimbursement was approved at the March meeting of the Pharmaceutical Benefits Advisory Committee (PBAC) for use in patients with AF at risk of stroke on the basis of “acceptable cost-effectiveness”.

  Brain scans suggest doctors learn to shut down empathy  

Research is revealing what goes on in the brains of health care workers when they see patients as objects

Recent research on how medical professionals’ brains function sheds light on these questions. Specifically, two experiments by Jean Decety and colleagues of the University of Chicago have examined the neuroscientific basis of pain empathy in physicians.

 

Chronic fatigue syndrome: where to PACE from here?

Original Text

Gijs Bleijenberg a, Hans Knoop a

 

In The Lancet, Peter White and colleagues1 report the four-group PACE randomised trial in adults with chronic fatigue syndrome. PACE stands for “Pacing, graded Activity, and Cognitive behaviour therapy: a randomised Evaluation”. The investigators report the efficacy of three behaviour interventions and specialist medical care. The Article provides a useful panel to summarise the interventions.

PACE tested the safety of the interventions. Concerns about the safety of cognitive behaviour therapy and graded exercise therapy have been raised more than once by patients' advocacy groups. Few patients receiving cognitive behaviour therapy or graded exercise therapy in the PACE trial had serious adverse reactions and no more than those receiving adaptive pacing therapy or standard medical care, which for cognitive behavioural therapy has already been shown.2 This finding is important and should be communicated to patients to dispel unnecessary concerns about the possible detrimental effects of cognitive behaviour therapy and graded exercise therapy, which will hopefully be a useful reminder of the potential positive effects of both interventions.

Another important aspect of PACE (the largest randomised trial of cognitive behaviour therapy and graded exercise therapy to date) is that the efficacy of both interventions was compared with another therapy and specialist medical care alone. Also, for the first time, adaptive pacing therapy was empirically tested. Both graded exercise therapy and cognitive behaviour therapy assume that recovery from chronic fatigue syndrome is possible and convey this hope more or less explicitly to patients. Adaptive pacing therapy emphasises that chronic fatigue syndrome is a chronic condition, to which the patient has to adapt. Although PACE was not intended to compare cognitive behaviour therapy and graded exercise therapy with each other, there was actually no difference between the two. Both were more effective than adaptive pacing.

Graded exercise therapy and cognitive behaviour therapy might assume that recovery from chronic fatigue syndrome is possible, but have patients recovered after treatment? The answer depends on one's definition of recovery.3 PACE used a strict criterion for recovery: a score on both fatigue and physical function within the range of the mean plus (or minus) one standard deviation of a healthy person's score. In accordance with this criterion, the recovery rate of cognitive behaviour therapy and graded exercise therapy was about 30%—although not very high, the rate is significantly higher than that with both other interventions.

Although the PACE trial shows that recovery from chronic fatigue syndrome is possible, there is clearly room for improvement with both interventions (cognitive behaviour therapy and graded exercise therapy). Both interventions could be improved if more was known about the mechanisms of change. These mechanisms could differ between the interventions, but we think this is unlikely. The rationale behind graded exercise therapy is that increasing the level of physical activity and fitness will cause symptoms to be reduced. The basis of cognitive behaviour therapy is described in PACE as the fear-avoidance theory. There is little empirical support for these proposed mechanisms of change. Mediation analysis of a randomised trial4 which tested the efficacy of graded exercise therapy for chronic fatigue syndrome showed that a decrease in symptom focusing, rather than an increase in fitness, mediated the reduction in fatigue. Wiborg and colleagues5 have shown that the effect of cognitive behaviour therapy on fatigue in chronic fatigue syndrome is not mediated by a persistent increase in physical activity. We noted that a decrease in focus on fatigue mediated the effect of cognitive behaviour therapy on fatigue and impairments in patients with the syndrome.6 Similarly, we have shown that higher levels of perceived activity and an increased sense of control over symptoms contribute to the treatment effect.

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Full-size image (69K) Science Photo Library

The central role of cognition in relation to fatigue might explain why graded exercise therapy is effective and adaptive pacing therapy is not. Both treatments aim to increase activity, but the activity-related cognition is probably different in adaptive pacing therapy—“I have to focus on how fatigued I am in order to stop in time, I can't do more, I have to stop”—from that in graded exercise therapy—“I am able to do more than I thought I could” (ie, less focused). Remarkably in this context, confidence in the treatment at the start is substantially lower with cognitive behaviour therapy than it is with adaptive pacing therapy. Despite lowered confidence in cognitive behaviour therapy, this therapy is more effective than is adaptive pacing therapy. Patient's confidence in treatment can only change if a change in abilities is perceived, which generally seems to happen in cognitive behaviour therapy.

Future studies into mechanisms of change are urgently needed and could help to improve the efficacy of the interventions, by focusing on the elements that are crucial for change.

We have received funding from The Netherlands Organisation for Health Research and Development, the Dutch Cancer Society, the Dutch MS Research fund, and the Princess Beatrix Foundation.

Children with infrequent intermittent asthma require no preventer therapy. Current evidence suggests that non-steroidal preventers should be trialled first in children with frequent intermittent or mild persistent asthma, while inhaled corticosteroids are indicated as first-line preventer treatment in children with moderate–severe persistent asthma. Long-acting β-agonists or montelukast are add-on options in children with persistent symptoms despite adequate inhaled corticosteroid treatment.