Chitotriosidase, an
enzyme involved in the degradation of
chitin-containing pathogens with unclear function in humans, has been proposed as a marker of
lipid accumulation in macrophages in different
lipid-storage diseases, including
atherosclerosis. To evaluate (1) if
lipid-lowering treatment could modify serum
chitotriosidase activity and (2) be useful in monitoring
lipid-lowering treatment, we have analyzed this
enzyme activity in the participants in the Atozvastatin Versus
Bezafibrate in Mixed
Hyperlipidemia (ATOMIX) study, a double-blind, comparative, and randomized study comparing the efficacy of
atorvastatin and
bezafibrate in mixed
hyperlipidemia. Because a common genetic deficiency of
chitotriosidase modifies serum quitotriosidase activity, this genetic variation was also studied. Seven subjects of 116 (6.03%) were homozygous, and 46 (39.6%) were heterozygous for the defective allele. Mean serum quitotriosidase activity correlated with allele dosage, as it was found to be of 0, 59.8 +/- 52.6 and 81.2 +/- 41.6 nmol/mL/h, in homozygotes for the defective allele, heterozygotes, and homozygotes for the wild-type allele, respectively (P =.0011 for the difference between the last 2 groups). However, this
enzyme activity was not found to correlate with
lipid levels before and
after treatment with either
atorvastatin or
bezafibrate, and neither with the intensity of the
lipid lowering. These results do not support the use of serum
chitotriosidase activity as a
biologic marker of
atherosclerotic plaque modification related to hypolipidemic treatment.