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”.

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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.

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