LAUSR

Oyenuga and colleagues evaluated the relationship between plasma galectin-3 (Gal-3) levels and sonographically measured carotid atherosclerosis. They found a positive correlation between this inflammatory biomarker and carotid atherosclerosis and atherosclerosis risk factors. They suggested that treatment targeting this biomarker may be important. In 2016, we investigated the association of coronary atherosclerotic burden with Gal-3 levels in 19 patients with acute coronary syndrome (ACS). The atherosclerotic burden was assessed by the Gensini score. The levels of Gal-3 in patients with ACS were high, and we found a strong correlation between the Gal-3 levels and the Gensini score. On the other hand, there was no correlation between the number of involved coronary arteries and the levels of Gal-3. Based on these findings, we assumed that the evaluation of Gal-3 levels in patients with ACS could be a promising biomarker. Similar to our study, Oyenuga et al found that higher Gal-3 levels were associated with more carotid artery atherosclerosis. Furthermore, their study is a population-based cohort with a large number of patients (n 1⁄4 5061), which provides a more reliable result. Genetic and epidemiological studies showed that Gal-3 plays a role in different physiopathological events. Indeed, it has been reported that Gal-3 messenger RNA expression can be detected at the earliest 30 minutes after acute myocardial infarction or can be delayed for up to 24 hours and can reach a peak level in 14 days. Although the researchers stated that the storage of the serum samples for a long time is a limitation, this may not be so. There are studies showing that Gal-3 remains stable in serum for 6 months at 80 C. This molecule is stable even for 10 years when samples are stored at 70 C. As stated by the authors, they analyzed the Gal-3 levels using a chemiluminescence microparticle technique, which may be a more sensitive method compared with a commonly used colorimetric enzyme-dependent immunosorbent assay.