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By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is a consultant for GlaxoSmithKline and is on the speaker's bureau of GlaxoSmithKline, 3M, Wyeth-Ayerst, Pfizer, Novartis, Bristol-Myers Squibb, AstraZeneca, Jones Pharma, and Boehringer Ingelheim.
ACCORD-MIND: Memory in Diabetes
Source: Cukierman-Yaffe T, et al. Relationship between baseline glycemic control and cognitive function in individuals with type 2 diabetes and other cardiovascular risk factors: The action to control cardiovascular risk in diabetes-memory in diabetes (ACCORD- MIND) trial. Diabetes Care 2009;32: 221-226.
The ACCORD trial has been newsworthy in the last several months primarily due to the early results of increased cardiovascular events associated with very tight glucose control. The ACCORD trial also has BP and lipid control arms, and includes a substudy on cognitive function called ACCORD-MIND: Memory in Diabetes. This cross-sectional study used a variety of cognitive tests to evaluate the relationship between glucose control and cognitive function.
In MIND (n = 2977), there was a linear relationship between baseline A1c and cognitive scores. For instance, on the Digital Symbol Substitution Test (DSST), for every 1% increase in A1c, there was a 1.75 point decreased DSST score; for comparison, in this age group each 1 year increase in age is associated with a 0.7 point DSST score decrease (and the aforementioned decrease had already been age-adjusted). Essentially, each 1% increase in A1c correlated to the same decline in cognitive function that would be seen (on average) with 2 years of aging.
Diabetes predisposes to cognitive decline, some of which is attributable to the increased risk of stroke in diabetics. Because subjects with stroke-related cognitive decline were excluded from this trial, the results suggest that hyperglycemia is negatively (inversely) related to cognitive function. Whether control of hyperglycemia has a favorable impact upon cognitive function remains to be determined.
Pulmonary embolism in acute COPD exacerbations
Source: Rizkallah J, et al. Prevalence of pulmonary embolism in acute exacerbations of COPD. Chest 2009;135: 786-793.
In contrast to most of the top 10 causes of death in the United States, the COPD mortality rate (the 4th most common cause of death) is rising. The majority of COPD deaths happen during an acute COPD exacerbation, usually attributed to an infectious agent. Still, as many as 30% of exacerbations are of uncertain etiology.
The symptoms of acute pulmonary embolism and exacerbations of COPD have some overlap. Indeed, it is easy to explain away new dyspnea, cough, and worsening of pulmonary status by simply attributing symptoms to COPD exacerbation, which is, after all, the most common explanation. Recent studies have suggested, however, that pulmonary embolus may be an overlooked etiology for symptoms that are misattributed to COPD exacerbations.
Rizkallah et al performed a meta-analysis of trials in patients (n = 550) with apparent exacerbations of COPD who underwent CT scanning, pulmonary angiography, or both. They found that in patients who were hospitalized, as many as 25% were ultimately determined to have suffered pulmonary embolus; the prevalence in studies incorporating data from both inpatients and outpatients showed only a slightly lower prevalence (24%).
Although it is tempting to accept that new onset of dyspnea and cough in a patient with COPD is most likely due to an acute exacerbation, the data from this study suggest a higher level of vigilance for pulmonary embolism in this population.
PLCO trial supports the USPSTF recommendations
Source: Andriole GL, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med 2009; 360:1310-1319.
The prostate, lung, colorectal, and Ovarian Cancer Screening Trial (PLCO) enrolled 76,693 men between 1993 and 2001, half of whom were assigned to receive annual PSA and DRE, and the other half of whom received usual care (USU). One of the endpoints of the trial was the mortality rate comparison between men in the screened and USU groups over 7-10 years of follow-up.
As might be intuitively obvious, the incidence of prostate cancer in the PSA/DRE group was somewhat higher (22% higher) than the USU group (116 vs 95 per 10,000), since men with an elevated screening PSA were referred for biopsy. Additionally, since PSA screening has become progressively more common as a component of usual care, one would not be surprised to learn that in this trial, 52% of men in the USU group had also received PSA screening.
The incidence of prostate cancer-related death per 10,000 subjects was very similar: 2 in the screening group vs 1.7 (USU). This slightly higher (but not statistically significantly different) prostate cancer-related mortality in the screened group suggests that PSA screening does not improve mortality over an interval as long as 10 years, giving credence to the recent USPSTF suggestion recommending against PSA screening in men older than age 75.