title: Chitotriosidase genotype and serum activity in subjects with combined hyperlipidemia: effect of the lipid-lowering agents, atorvastatin and bezafibrate.
abstract: 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.
authors: Laboratorio de Investigación Molecular, Hospital Universitario Miguel Servet y Departmentos de Medicina y Bioquímica, Universidad de Zaragoza, Spain.
authors: J
authors: J
authors: Canudas
authors: A
authors: A
authors: Cenarro
authors: F
authors: F
authors: Civeira
authors: A L
authors: AL
authors: Garcí-Otín
authors: R
authors: R
authors: Arístegui
authors: C
authors: C
authors: Díaz
authors: X
authors: X
authors: Masramon
authors: J M
authors: JM
authors: Sol
authors: G
authors: G
authors: Hernández
authors: M
authors: M
authors: Pocoví
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000069059:Atorvastatin; D001629:Bezafibrate / Q000627:therapeutic use*; D004247:DNA / Q000235:genetics; D004311:Double-Blind Method; D005091:Exons; D005260:Female; D005838:Genotype; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006596:Hexosaminidases / Q000097:blood / Q000235:genetics*; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy* / Q000235:genetics*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011758:Pyrroles / Q000627:therapeutic use*
chemical_list: D006538:Heptanoic Acids; D000960:Hypolipidemic Agents; D008055:Lipids; D008074:Lipoproteins; D011758:Pyrroles; D004247:DNA; D000069059:Atorvastatin; D006596:Hexosaminidases; C086400:chitotriosidase; D001629:Bezafibrate