title: Lipoprotein apheresis reduces circulating galectin-3 in humans.
abstract: BACKGROUND
  Plasma galectin-3 (Gal-3) is elevated in, and drives, diverse systemic inflammatory disorders, including cancer, cardiovascular diseases, and diabetes. Circulating Gal-3 promotes tumorigenesis and metastasis, as well as fibrotic remodeling, and is a promising therapeutic target. Apheresis has proven utility in reducing circulating disease-promoting substances, exemplified by the success of lipoprotein apheresis (LA) in abrogating cardiovascular disease progression in drug-refractory hypercholesterolemia patients. We compared the clinical utility of two FDA-approved LA systems in reducing plasma Gal-3 in humans.
  
  
  METHODS
  Plasma Gal-3 levels were assessed by ELISA in blinded samples drawn pre- and post-apheresis from hypercholesterolemia patients (n = 10/group) undergoing therapeutic LA using either a heparin-induced extracorporeal LDL precipitation (HELP) or dextran sulfate-adsorption (DSA) system.
  
  
  RESULTS
  Mean baseline plasma Gal-3 concentrations (±SD) were 14.3 ± 5.1 (range 6.6-22.8) and 14.5 ± 2.8 (range 10.6-19.8) ng/mL in the HELP and DSA groups, respectively. Post-apheresis Gal-3 levels were respectively reduced by 19.4% and 22.7% in the HELP (P = 0.0094) and DSA (P = 0.0027) systems (paired t-tests); the difference between devices was insignificant (P = 0.5288; Mann-Whitney). Post-treatment Gal-3 levels were 11.3 ± 3.7 (HELP; range 4.5-16.3) and 11.3 ± 3.8 (DSA; range 7.5-20.7) ng/mL.
  
  
  CONCLUSIONS
  Circulating Gal-3 levels showed a statistically significant decrease in humans undergoing therapeutic LA. Although absolute Gal-3 reduction was ≈19-23%, this effect, combined with reducing atherogenic LDL and other inflammation mediators (e.g., CRP, fibrinogen, Lp-PLA2 ), may enhance apheresis clinical benefits. Applying new Gal-3-specific extraction technologies to apheresis may be advantageous in treating diverse pathologies that are promoted by elevated plasma Gal-3. J. Clin. Apheresis 31:388-392, 2016. © 2015 Wiley Periodicals, Inc.
authors.affiliation: Amitabha Medical Clinic and Healing Center, Santa Rosa, California.
authors.forename: Isaac
authors.initials: I
authors.lastname: Eliaz
authors.affiliation: Amitabha Medical Clinic and Healing Center, Santa Rosa, California.
authors.forename: Elaine
authors.initials: E
authors.lastname: Weil
authors.affiliation: University of Kansas Medical Center, Atherosclerosis and Lipid-Apheresis Center, Kansas City, Kansas.
authors.forename: Julie-Ann
authors.initials: JA
authors.lastname: Dutton
authors.affiliation: University of Kansas Medical Center, Atherosclerosis and Lipid-Apheresis Center, Kansas City, Kansas.
authors.forename: Audrey E
authors.initials: AE
authors.lastname: McCalley
authors.affiliation: Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas.
authors.forename: Barbie
authors.initials: B
authors.lastname: Nolte
authors.affiliation: University of Kansas Medical Center, Atherosclerosis and Lipid-Apheresis Center, Kansas City, Kansas.|Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas.
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Moriarty
mesh_terms: D001781:Blood Component Removal / Q000295:instrumentation / Q000379:methods* / Q000592:standards; D016264:Dextran Sulfate / Q000627:therapeutic use; D037502:Galectin 3 / Q000097:blood*; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D006937:Hypercholesterolemia / Q000628:therapy; D018836:Inflammation Mediators / Q000097:blood; D017270:Lipoprotein(a) / Q000302:isolation & purification*; D008077:Lipoproteins, LDL / Q000097:blood; D008875:Middle Aged
chemical_list: D037502:Galectin 3; D018836:Inflammation Mediators; D017270:Lipoprotein(a); D008077:Lipoproteins, LDL; D006493:Heparin; D016264:Dextran Sulfate
keywords: apheresis; biomarker; cancer; galectin; heart disease; inflammation