Intravenous (iv) insulin does not prevent rises in inflammatory or oxidative stress markers after percutaneous coronary intervention (PCI) in patients with diabetes compared with standard insulin treatment, study findings suggest.

Diabetic patients who have undergone PCI are usually managed with insulin administered subcutaneously, which generally fails to attain plasma glucose targets, note the researchers from Hospital de Clínicas de Porto Alegre in Brazil.

They examined the value of iv insulin in an open-label, randomized trial in 70 patients with diabetes and stable coronary artery disease who had a mean age of 60.5 years and had undergone angioplasty with bare metal stent implantation.

Participants were randomly assigned to a standard approach, where hyperglycemia was managed with subcutaneous regular insulin as needed with a target of 250 mg/dl or less, or to 24 hours of continuous iv insulin infusion, targeting glucose levels of 80 to 100 mg/dl in premeal periods and lower than 140 mg/dl in random glucose measurements.

Blood samples were collected immediately after PCI and again 24 hours later.

At 24 hours after PCI, mean glycemia was significantly lower and insulinemia higher among patients receiving iv versus subcutaneous insulin, report Beatriz D’Agord Schaan and co-workers in the Journal of Clinical Endocrinology and Metabolism.

Levels of the inflammatory marker C-reactive protein doubled in the 24 hours after PCI in both groups, and interleukin-6 levels doubled with iv-insulin and tripled with standard treatment, but differences between the groups were not statistically significant.

Endothelin 1 levels were approximately 30% higher 24 hours after PCI compared with immediately after the procedure in both groups, with no significantly between-group differences.

The treatment groups also did not significantly differ in protein oxidation, with the plasma carbonyl content not significantly changing in either group in the 24 hours after PCI and total serum antioxidant status rising in both.

The authors conclude that despite the fact that “continuous iv insulin effectively increased insulin levels and prevented hyperglycemia, a clear rise in inflammatory markers was observed after PCI.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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Researchers say that high levels of plasma lactate are strongly associated with increased prevalence of Type 2 diabetes in older adults.

Plasma lactate level is an indicator of the gap between oxidative capacity and energy expenditure, and evidence suggests that insufficient oxidative capacity may be indicated in the development of Type 2 diabetes.

To investigate this further, Jeffery Young (John Hopkins University, Baltimore, Maryland, USA) and colleagues tested plasma lactate levels in 1709 participants (18% with Type 2 diabetes) of the Atherosclerosis Risk in Communities Study Carotid Magnetic Resonance Imaging (ARIC CAR-MRI), aged 60-84 years.

The participants were divided into quartiles of lactate concentration, namely, less than 5.9 (n=378), 5.9-7.2 (n=480), 7.3-9.1 (n=458), and 9.2 mg/dl or above (n=393).

The team found that the prevalence of Type 2 diabetes increased significantly across increasing lactate quartiles, at 11%, 14%, 20%, and 30%, from the lowest to the highest quartile.

After adjustment for body mass index, physical activity, demographic factors, and waist circumference, risk for having Type 2 diabetes was a significant 1.64- and 2.23-fold higher for participants in the third and fourth quartiles, respectively, than for those in the first.

Young and team note that high lactate was also linked to increased levels of fasting glucose in those without Type 2 diabetes.

“Further work must be carried out to reassess the prospective association of plasma lactate and Type 2 diabetes in a modern cohort,” say the researchers.

However, “if confirmed, blood lactate measurement could be used as a marker of oxidative capacity in clinical and population studies,” they conclude.

The results of this study are published in the International Journal of Epidemiology.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

Free abstract

Women with current or previous asthma or chronic obstructive pulmonary disease (COPD) have an increased risk for developing Type 2 diabetes, show study findings.

Respiratory conditions have been reported as comorbidities with Type 2 diabetes, but whether prior or current asthma or COPD actively increase the risk for developing Type 2 diabetes is less clear.

Writing in the journal Diabetes Research and Clinical Practice, Yiqing Song (Harvard Medical School, Boston, Massachusetts, USA) and colleagues report results from the Women’s Health Study.

Overall, 1808 women had COPD alone, 3368 had asthma alone, and 32,248 had no history of COPD or asthma at enrollment in 1991. The participants were all aged 45 years or above.

They found that women with a history of asthma or COPD at enrollment had a respective 37% and 38% increased risk for Type 2 diabetes 12.2 years later at study completion compared with those without such a history.

These associations were not altered by adjustment for age, smoking status, physical activity, body mass index, alcohol intake, hormone replacement therapy, or randomized treatment.

“Our study provides clear information on the relation of asthma and COPD with comorbid diabetes mellitus, indicating the importance of increasing awareness and promotion of diabetes risk reduction for patients with these chronic lung diseases,” write the authors.

“Future evidence-based preventive strategies should be developed and implemented to improve the overall health burden in adults with asthma and/or COPD who are also at high risk for other chronic comorbidities,” they conclude.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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