Blood Biomarker Identifies Smoker's Risk of Atherosclerosis

They used a proprietary sandwich platform with minimum and maximum detection limits of 1 and 950 ng/mL, respectively. Other analytes such as tumor necrosis factor-α1 receptor (TNFR1A), myeloperoxidase (MPO), and matrix metalloproteinase-9 were measured on a similar platform.

Median SP-B levels were five-fold higher among current versus those who had never smoked and were significantly correlated with estimated pack-years smoked. Increasing levels of SP-B also associated with other traditional cardiac risk factors and higher levels of inflammatory biomarkers. An interaction was observed between SP-B, smoking status, and abdominal aortic plaque (AP) such that elevated SP-B levels were associated with AP in current smokers but not in former or non-smokers.

The SP-B assay was provided by Alere Inc (San Diego, CA, USA) is still being evaluated and is not available for commercial use. The authors concluded that circulating levels of SP-B increase with greater smoking burden and independently associate with abdominal AP among current smokers. The findings support further investigation of the role of SP-B as a marker of the vascular effects of smoking. The next step is to investigate whether SP-B causes atherosclerosis or is simply a marker of the disease, and to determine whether decreasing levels of SP-B will improve heart disease outcomes.

The study was published in October 2011, in the journal Arteriosclerosis, Thrombosis, and Vascular Biology.

Related Links:
University of Texas Southwestern Medical Center
Alere Inc.